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CASE REPORT
Year : 2020  |  Volume : 9  |  Issue : 4  |  Page : 264-266

Delayed and atypical presentation of Boerhaave's syndrome as epigastric mass


Department of General Surgery, Pt. BDS PGIMS, Rohtak, Haryana, India

Date of Submission15-Apr-2020
Date of Acceptance28-Jul-2020
Date of Web Publication6-Jan-2021

Correspondence Address:
Dr. Mahavir Singh
11/11J (UH), Medical Campus, Pt. B.D. Sharma PGIMS, Rohtak - 124001, Haryana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_55_20

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  Abstract 


Boerhaave's syndrome (BS), also known as “spontaneous rupture of the esophagus,” is an emergent condition requiring early diagnosis and management to prevent associated morbidity and mortality. Mortality ranges between 20% and 40% with timely treatment but this rises to virtually 100% if treatment is delayed by more than 48 h.[1] The classical clinical triad of vomiting, chest pain, and subcutaneous emphysema classically described symptoms for BS, which is actually uncommon accounting for the frequently delayed diagnosis.[2] This article describes a case of this syndrome in which the actual diagnosis was made 1 month after the esophageal perforation because of delayed atypical presentation with epigastrium mass and was successfully managed.

Keywords: Boerhaave syndrome, epigastric mass, esophageal perforation


How to cite this article:
Singh M, Dalal S, Dhiman B, Raman S. Delayed and atypical presentation of Boerhaave's syndrome as epigastric mass. J NTR Univ Health Sci 2020;9:264-6

How to cite this URL:
Singh M, Dalal S, Dhiman B, Raman S. Delayed and atypical presentation of Boerhaave's syndrome as epigastric mass. J NTR Univ Health Sci [serial online] 2020 [cited 2021 Jan 18];9:264-6. Available from: https://www.jdrntruhs.org/text.asp?2020/9/4/264/306126




  Introduction Top


Boerhaave's syndrome (BS) is also known as spontaneous esophageal rupture or effort rupture of the esophagus. The adjective “spontaneous” does not imply absence of a precipitating factor, but instead the fact that the rupture is not a consequence of direct trauma.[3] Although vomiting is thought to be the most common cause, other causes include weightlifting, defecation, epileptic seizures, abdominal trauma, compressed air injury, and childbirth, all of which can increase the pressure in the esophagus and cause a barogenic esophageal rupture.[4] BS was first described by the Dutch physician, Harmann Boerhaave in 1724. Although the actual incidence of esophageal perforation worldwide is unclear, some studies estimate an incidence of approximately 3.1 per 1 million per year. However, many cases of BS are diagnosed postmortem resulting in under-reporting and thus an underestimate both with regards to its incidence and mortality.[5]

Symptoms consist of vomiting, lower thoracic pain, and subcutaneous emphysema (Mackler's triad).[6] We should suspect BS when a patient presents with retrosternal chest pain with or without subcutaneous emphysema when associated with heavy alcohol intake and severe or repeated vomiting. The actual clinical presentation of Boerhaave syndrome will depend on the level of the perforation, the degree of leakage, and the time since onset of injury. Cervical perforations can present with neck pain, dysphagia, or dysphonia; intrathoracic perforations with chest pain; and intra-abdominal perforations with epigastric pain radiating to the shoulder or back.[7] Physical exam findings may include abnormal vitals (tachycardia, tachypnea, fever), decreased breath sounds on the perforated side, mediastinal emphysema, and Hamman's sign (mediastinal “crackling” accompanying every heart beat) in left lateral decubitus position.


  Case Report Top


A 57-year-old man presented to emergency department with complaints of severe respiratory difficulty associated with severe abdominal pain in the epigastrium region with epigastrium fullness and recurrent vomiting. About 1 month back patient had moderate grade fever (101°F) for which he took medicine; after that the patient developed several episode of vomiting associated with severe epigastrium pain radiating to back. Vomiting was nonbillious, nonprojectile, and contains recently taken food particles. For these complaints patient took treatment from a private practitioner and his symptoms got somewhat relieved. Now patient developed severe respiratory difficulty and was brought to the emergency department. On chest X-ray, the patient was found to be having pleural effusion on the left side. About 400 ml of straw colored fluid was aspirated from pleural cavity and surgeon opinion was taken. On per abdominal examination, the patient was having epigastrium tenderness with an ill-defined lump, mainly in epigastrium region extending into bilateral hypochondium and umbilical region. A nasogastric tube was put which was having purulent aspirate. A CECT abdomen and thorax was done which gave impression of lower esophageal perforation with collection in lesser sac [Figure 1]. Exploratory laparotomy was done. On exploratory laparotomy, a large collection was present posterior to stomach in lesser sac pushing it anteriorly [Figure 2]. About 2 l of frank pus was drained from lesser sac. Some food particles were also noted in the collection. Fingers were pushed behind stomach to break any loculi and to identify gastroesophageal junction. Whole of the cavity was drained and a drain was put in the drained cavity. A feeding jejunostomy was done. Postoperatively feed was started through jejunostomy after 5 days when there was evidence of gut motility. On 7th postop day, a CECT abdomen was done revealing no evidence of any residual collection. Patient continued to have purulent drainage for 3 weeks and drain was removed after that. Now after the follow-up of about 1 year, the patient is totally asymptomatic and doing well.
Figure 1: Axial CT film showing collection in lesser sac pushing the stomach anteriorly

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Figure 2: Coronal CT film showing collection in lesser sac

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  Discussion Top


BS is an uncommon condition so the diagnosis can easily be missed or delayed, leading to complications like dehydration, mediastinitis, sepsis, and shock. Diagnostic delay carries a very high risk of death. Similar to other acute esophageal disorders, the mortality of BS is exceedingly high and rises steeply with time. It is reported to be in the order of 25% if treatment is started within 24 h but reaches almost 100% at 48 h.[1] These exceedingly high mortality figures illustrate the critical importance of timely diagnosis of BS. Any diagnostic delay is very likely to lead to patient death. Although history alone will sometimes give away the diagnosis, more often than not, this is not the case. Radiological investigations most commonly provide the diagnosis in BS but clinical suspicion is essential so as to request these in time and look for the relevant signs.

The first radiological investigation to be requested is a simple chest radiograph. Chest X-ray is readily available; it is normal for approximately 15% of cases and cannot be used to exclude the diagnosis. Potential chest X-ray findings include subcutaneous or mediastinal emphysema, mediastinal widening, pleural effusion, and in 20% of cases, the “V sign” (radiolucent streak of air dissecting the retrocardiac fascial planes).[8] The diagnostic tool of choice is the contrast esophagogram using a water-soluble contrast agent such as gastrograffin. Such a study will show extravasation of contrast material at the site of the perforation. Other investigations for BS include CT with or without oral contrast and needle thoracentesis if a pleural effusion exists. In the latter, biochemical and cytological examination of the pleural fluid can give the diagnosis by revealing the presence of salivary amylase and undigested food contents, respectively.[9]

Treatment is typically tailored to the patient's presentation, the type, and extent of rupture, the time to diagnosis, and the viability of the esophageal wall. Early perforations, those diagnosed within 12–24 h, have the best outcomes.[10] Three common treatment options include conservative, endoscopic, or surgical. The mainstay of treatment includes volume replacement, broad-spectrum antibiotic coverage, and surgical evaluation. Surgical intervention includes primary esophageal repair through open thoracotomy versus VATS with fundic reinforcement, which is the gold standard within the first 24 h. Endoscopic placement of stents has been used to prevent fistula formations or seal esophageal leaks in both patients with delayed diagnoses and those with the early diagnosis without widespread contamination. Conservative measurements are usually reserved for small or contained ruptures. Controversy occurs when a late perforation, those diagnosed after 24 h, is diagnosed, as the wound edges are typically edematous, stiff, or friable rendering primary repair risky. Taking this into consideration, many manage late perforations through debridement of pleural cavity and mediastinum, esophagostomy, and feeding gastrostomy. Esophageal replacement is usually done after 6 weeks.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Korn O, Onate JC, Lopez R. Anatomy of the Boerhaave syndrome. Surgery 2007;141:222-8.  Back to cited text no. 1
    
2.
de Schipper JP, Pull ter Gunne AF, Oostvogel HJ, van Laarhoven CJ. Spontaneous rupture of the oesophagus: Boerhaave's syndrome in 2008. Literature review and treatment algorithm. Dig Surg 2009;26:1-6.  Back to cited text no. 2
    
3.
Vidarsdottir H, Blondal S, Alfredsson H, Geirsson A, Gudbjartsson T. Oesophageal perforations in Iceland: A whole population study on incidence, aetiology and surgical outcome. Thorac Cardiovasc Surg 2010;58:476-80.  Back to cited text no. 3
    
4.
Garas G, Zarogoulidis P, Efthymiou A, Athanasiou T, Tsakiridis K, Mpaka S, et al. Spontaneous esophageal rupture as the underlying cause of pneumothorax: Early recognition is crucial. J Thorac Dis 2014;6:1655-8.  Back to cited text no. 4
    
5.
Bladergroen MR, Lowe JE, Postlethwait RW. Diagnosis and recommended management of esophageal perforation and rupture. Ann Thorac Surg 1986;42:235-9.  Back to cited text no. 5
    
6.
Rochford M, Kiernan TJ. Images in emergency medicine, Boerhaave's syndrome (spontaneous esophageal rupture). Ann Emerg Med 2007;49:746-77.  Back to cited text no. 6
    
7.
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.  Back to cited text no. 7
    
8.
Yang ST, Devanand A, Tan KL, Eng PC. Boerhaave's syndrome presenting as a right-sided pleural effusion. Ann Acad Med Singapore 2003;32:415-7.  Back to cited text no. 8
    
9.
Søreide JA, Viste A. Esophageal perforation: Diagnostic work-up and clinical decision-making in the first 24 hours. Scand J Trauma Resusc Emerg Med 2011;19:66.  Back to cited text no. 9
    
10.
Schweigert M, Beattie R, Solymosi N, Booth K, Dubecz A, Muir A, et al. Endoscopic stent insertion versus primary operative management for spontaneous rupture of the esophagus (Boerhaave syndrome): An international study comparing the outcome. Am Surg 2013;79:634-40.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2]



 

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