Chest pain after vomiting

A 66 year old man, previously fit and well, was admitted to the emergency department with sudden pain in his left chest and abdomen after vomiting. He had woken in the early hours of the morning, vomited three times, and started getting progressively worsening pain in the left side of his chest and abdomen, radiating to the shoulder. He was a non-smoker and occasional drinker. He had no history of operations or similar episodes.

Fig 1 X ray image of the posteroanterior view of the chest, showing left hydropneumoth orax

On arrival he was pale, sweaty, clammy, and had fever. His pulse was 106 beats/min and regular. His blood pressure was 92/52 mm Hg. Jugular venous pulse and heart sounds were normal.

Trachea was central, and respiratory rate was 40 breaths/min. Left lung base was dull on percussion, and air entry was diminished. His abdomen was soft, with generalised tenderness and normal bowel sounds.

Full blood count, liver function tests, serum electrolytes and serum amylase were normal. His troponin I concentration was below 0.03 (normal range 0-0.1) ng/ml and the concentration of C reactive protein was less than 1 (<10) mg/l. Blood gas analysis showed mild metabolic acidosis, and an electrocardiogram showed sinus tachycardia. Attending doctors took an urgent x ray scan of his chest (fig 1) and a computed tomograph of his chest and abdomen (fig 2).

Fig 2 Computed tomography, showing mediastinal air and left hydropneumoth orax

Questions

Imagine you are managing this patient.

1. What are the possible differential diagnoses, and what is the most likely cause?
2. How would you interpret the radiograph of the chest (fig 1)?
3. What should be the initial management, and how would you reach a definitive diagnosis?
4. How would you interpret the computed tomograph of the chest (fig 2)?

Answers

1. Differential diagnoses include cardiovascular (myocardial infarction, aortic dissection), respiratory (pulmonary embolism, pneumothorax, and pneumonia), or gastrointestinal conditions (acute pancreatitis, acute cholecystitis, mesenteric ischaemia, ruptured or perforated viscus, and peptic ulceration.¹ The final diagnosis in this case was oesophageal rupture secondary to vomiting (Boerhaave's syndrome). He was initially treated as having acute coronary syndrome and was given aspirin on presentation, which was subsequently found in the left pleural cavity at the time of operation.
2. The erect portable chest x ray (fig 1) shows a pneumothorax at the left apex and mid-zone with considerable left pleural effusion - that is, hydropneumothrax. There is no free gas under the diaphragm.
3. Initial management included resuscitation with oxygen, and attending doctors gave intravenous fluids, analgesics, antiemetics, and antibiotics, keeping nil by mouth. A computed tomography with oral contrast of the abdomen and chest allowed rapid confirmation of the diagnosis.
4. This is a contrast enhanced computed tomograph confirming a left sided pleural effusion and pneumothorax. The posterior mediastinum contains air, outside the oesophagus. These findings are consistent with a diagnosis of ruptured oesophagus. Computed tomography can easily exclude differentials such as aortic dissection, pulmonary embolism, acute pancreatitis, and pneumonia.

Discussion

A Dutch physician called Herman Boerhaave first described postemetic oesophageal rupture in 1724, hence the eponym. This rare but life threatening condition demands early diagnosis and management. The condition is associated with high mortality as its presentation often mimics other conditions or is not considered in the differential diagnoses and is thus diagnosed late.¹

The condition is caused by barotrauma to the oesophagus during vomiting, when the intraluminal pressure rises due to a closed upper oesophageal sphincter. This can leads to a tear in the left posterolateral wall of the lower third of the oesophagus.¹ The reasons for predilection for this site include lack of adjacent support structures, thinning of the musculature, and the entrance of vessels and nerves, which weaken the wall.

Diagnosis

The incidence of diagnostic error can be 50% or higher.^{2 3} The typical history is of a middle aged man who has been drinking and eating excessively, leading to vomiting followed by severe chest pain. The pain is usually pleuritic and poorly relieved by narcotics. If subcutaneous emphysema accompanies the above symptoms then this constitutes Mackler's triad.¹ Other symptoms include dyspnoea, tachypnoea, tachycardia, fever, hypotension, and abdominal pain.

Chest examination may show a pneumothorax or an effusion. Pneumomediastinum may be confirmed by mediastinal crackling heard on auscultation, which is known as Hamman crunch. People presenting late may be in septic shock.

Useful investigations include a chest x ray, which may show hydropneumothorax, pneumomediastinum, and subcutaneous emphysema. A pleural tap may find a pH below six, food particles, and a high amylase concentration.

Definitive investigations include contrast studies in the form of a gastrograffin swallow, computed tomography with contrast of the chest and abdomen, or upper gastrointestinal endoscopy. These will help to confirm the size and location of the perforation, to identify the underlying oesophageal disease, and to exclude other differentials.

Treatment

Recommendations about treatment are controversial. Multiple options exist for treating the perforated oeso- phagus, including primary closure, drainage alone, exclusion and diversion, or oesophageal resection, with none being clearly superior.³

Classical teaching says to treat patients presenting within 24 hours from the start of symptoms with surgery in the form of a two layer primary closure with buttressing of the suture line with pericardial fat, pleura, omentum, or other tissues. Chest drains are inserted after careful mediastinal and pleural cleansing and a feeding jejunostomy fashioned for nutrition. The most feared complication of primary repair is anastomotic leakage leading to an empyema or an oesophagopleural fistula. This can be treated conservatively if there is no distal obstruction, infection, foreign body or malignancy.

Historically, people presenting late (after 24 hours after symptoms started) are treated conservatively by giving oxygen, fluids, and intravenous antibiotics, provid- ing nutrition and keeping nil by mouth. The prognosis in these patients is poor. Recent studies provide hope for patients presenting late as they show that primary repair can be safely done in late presenters with better results.^{4 5} Any benefit of primary repair in addition to proper mediastinal toilet and drainage and nutritional support is controversial.

Critically ill late presentations have been successfully treated with desperate surgical measures, such as T tube intubation, with high mortality and reasonable success.⁶ Oesophageal stenting has been used successfully in a critically ill patient.²

Our patient presented within 24 hours of symptoms starting and was discharged home after uneventful recovery.

The cornerstones of a successful outcome include prompt diagnosis, aggressive resuscitation, and then a patient specific treatment based on patient's presentation, physiological condition, comorbidities, and underlying condition (the degree of sepsis and his haemodynamic and nutritional status). The mediastinal toilet (cleaning of the mediastinum by irrigation with saline and opening pockets of any collection in the mediastenum), proper drainage, and nutritional support in the form of jejunal feeding or parental nutrition remain the mainstay of surgical treatment, irrespective of the actual surgical technique.⁴

Many conditions mimic oesophageal rupture, and you should have a high index of clinical suspicion in any patient presenting with vomiting and chest and upper abdominal pain.
 

Competing interests: None declared.

Nazam Mohammed, senior house officer

Manoj Purohit, clinical fellow
Email: drpurohitm@yahoo.com
Andrew Duncan, consultant cardiothoracic surgeon, Department of Cardiothoracic Surgery, Blackpool Victoria Hospital, Blackpool, United Kingdom



studentBMJ 2006;14:309-352 September ISSN 0966-6494

1. Shields W. General thoracic surgery. 6th ed. Philadelphia: Lippincott, Williams, and Wilkins, 2005.
2. Davies AP, Vaughan R. Expanding mesh stent in the emergency treatment of Boerhaave's syndrome. Ann Thorac Surg 1999;67:1482-3.
3. Brinster CJ, Singhal S, Lee L, Marshall MB, Kaiser LR, Kucharczuk JC. Evolving options in the management of esophageal perforation. Ann Thorac Surg 2004;77:1475-83.
4. Jougon J, McBride T, Delcambre F, Minniti A, Velly JF. Primary esophageal repair for Boerhaave's syndrome whatever the free interval between perforation and treatment. Eur J Cardiothorac Surg 2004;25:475-9.
5. Wang N, Razzouk AJ, Safavi A, Gan K, Van Arsdell GS, Burton PM, et al. Delayed primary repair of intrathoracic esophageal perforation: is it safe? J Thorac Cardiovasc Surg 1996;111:114-22.
6. Naylor AR, Walker WS, Dark J, Cameron EW. T tube intubation in the management of seriously ill patients with oesophagopleural fistulae. Br J Surg 1990;77:1074.

       

           

	EDUCATION Chest pain after vomiting       Nazam Mohammed, Manoj Purohit, Andrew Duncan (September 2006)
	Dr Avinash Aujayeb (August 28th, 2006)       F2, North Tyneside Hospital, Newcastle avinash.aujayeb@ncl.ac.uk
	I read with great interest your case presentation on oesophageal rupture and I just wanted to briefly make the student population aware of a case that i have come across during my house officer year. A female patient was admitted under the medical team with shortness of breath and pleuritic chest pain of aboutt 2 days duration.The fact that she had been vomiting quite violently for a 3-4 days prior to her start of her symptoms was put down to a simple gastro-enteritis and considered an entirely different problem. Blood gases showed a respiratory alkalosis with hypoxia and chest x-ray was normal. With a possible diagnosis of a pulmonary embolism being entertained,a CTPA was performed and imagine our untmost surprise when showed that there was no blood clot but a pneumomediastinum from a small tear in her oesphagus. The patient was treated conservatively after that and made a full recovery. A diagnosis of an oesophageal tear is certainly not entertained very frequently,but as the author of the article points out we should keep a high index of suspicion for anyone presenting with chest pain after vomiting,just like we always think of a Mallory-Weiss tear if there is haematemesis after severe retching or vomiting.