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Year : 2021  |  Volume : 8  |  Issue : 4  |  Page : 446-448

Boerhaave’s syndrome in a sixty-two-year-old Nigerian man: delayed diagnosis secondary to premorbid symptomatology

Division of Nephrology and Hypertension, Department of Internal Medicine, Babcock University/Babcock University Teaching Hospital, Ilishan-Remo, Nigeria

Date of Submission25-Jun-2021
Date of Acceptance15-Sep-2021
Date of Web Publication22-Dec-2021

Correspondence Address:
Dr. Peter K Uduagbamen
Division of Nephrology and Hypertension, Department of Internal Medicine, Babcock University/Babcock University Teaching Hospital, Ilishan-Remo.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/mgmj.mgmj_40_21

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Boerhaave’s syndrome is a rare spontaneous transmural esophageal rupture from forceful vomiting. It is commonly misdiagnosed either from the non-specific presentation or its mimicking known premorbid conditions. Mortality could be very high and early with delayed diagnosis. We present a rare occurrence of this syndrome in which delayed diagnosis was due to premorbid conditions of bronchial asthma and hypertension and not symptom presentation and with a very good treatment outcome.

Keywords: Boerhaave syndrome, delayed diagnosis, mortality, spontaneous transmural esophageal rupture

How to cite this article:
Ngubor TD, Omokore T, Nwachukwu NO, Uduagbamen PK. Boerhaave’s syndrome in a sixty-two-year-old Nigerian man: delayed diagnosis secondary to premorbid symptomatology. MGM J Med Sci 2021;8:446-8

How to cite this URL:
Ngubor TD, Omokore T, Nwachukwu NO, Uduagbamen PK. Boerhaave’s syndrome in a sixty-two-year-old Nigerian man: delayed diagnosis secondary to premorbid symptomatology. MGM J Med Sci [serial online] 2021 [cited 2022 Aug 13];8:446-8. Available from: http://www.mgmjms.com/text.asp?2021/8/4/446/333314

  Introduction Top

Boerhaave’s syndrome (BS) is a transmural esophageal rupture precipitated by vomiting, which increases the intraesophageal pressure against a close glottis, particularly in defective relaxation of the cricopharyngeal muscles.[1] First described in a Dutch naval Admiral, Baron Jan van Wassenaer, by Dutch Physician, Hermann Boerhaave, in 1724, it is commonly misdiagnosed, and with delayed treatment, mortality could be up to 75%.[2] Fatality approaches 100% without treatment. It could be complicated by mediastinitis, shock, and acute kidney injury (AKI).[3]

  Case study Top

A 62-year-old man, known hypertensive and asthmatic, was referred from a private facility on account of a 5-day history of vertigo and vomiting and 2 days of upper abdominal pain and breathlessness. He was febrile (T-37.8°C) and dyspneic. Percussion notes and breath sounds were dull and diminished bilaterally in the middle and lower lung zones, respectively. His oxygen saturation (SPO2) and pulse were normal and blood pressure was 170/111 mmHg. He had epigastric tenderness and hepatomegaly.

An initial assessment of vestibular neuritis with background chest infection was made. Laboratory investigations ordered at presentation showed leukocytosis (15.5×109/L) with neutrophilia (87.0%), hematocrit (39.8%), and platelets (156 x 109/L).

Chest X-ray showed left hydropneumothorax with right pleural effusion.

He was commenced on intravenous antibiotics and had two doses of nebulized salbutamol with no significant improvement. He had bilateral chest drainage tubes inserted which drained 150 mL of serosanguinous fluid from the right and 800 mL of hemorrhagic fluid from the left that contained pasty and liquid materials.

The possibility of lung cancer was also considered on account of his age and the unilateral hemorrhagic effusion. Further history revealed a chronic (20 years) occupational exposure to gasoline fumes and silica dust working in petrochemical companies with gas flaring and exposure to fumes, further heightening our suspicion of lung cancer.

A chest computed tomography (CT) scan after chest tube insertion showed bilateral pneumothorax and left lung collapse. A repeat chest X-ray showed a loop of bowel in the chest, suggestive of a diaphragmatic hernia [Figure 1]. An esophagogram showed a narrowed distal esophagus and a minor leak of contrast material [Figure 2].
Figure 1: Chest X-ray showing bowel loop in the chest

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Figure 2: Esophagoscope showing distal esophageal narrowing

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An assessment of a perforated viscus (esophagus), oral feeding was withheld.

Seventh day on admission (7DOA), dyspnea worsened necessitating higher oxygen flow. His daily serum electrolyte check showed, among other derangements, a 62% rise in serum creatinine from baseline 106 to 177 mmol/L (167% of baseline), which meets the criteria for the diagnosis of AKI (stage 1).[4]

He had intravenous fluid and low-dose furosemide challenge and kidney function gradually improved, returning to baseline 9 days later (16DOA), without dialysis.

On the 10DOA, the patient had a thoracotomy and an exploratory laparotomy on account of a suspected ruptured esophagus and a diaphragmatic hernia. Intraoperative findings included a 2 cm linear postero-lateral distal esophageal rupture (esophageal hiatus), 1.5 L of purulent foul-smelling materials, and food substances trapped in the left hemithorax, with a trapped, non-expanding left lung.

An intraoperative assessment of BS was made. The esophageal rupture was repaired, the left lung was decorticated, the gastroesophageal junction was ligated, and a diverting cervical esophagostomy was done, with the placement of a jejunostomy feeding tube. He was taken off intensive care post-operative day 2 (POD2). Post-operative, chest tubes drained 5820 mL of serosanguinous fluids and the jejunostomy tube drained 1100 mL of bilious exudates.

On account of hypokalemia, the patient developed paralytic ileus 7th-day post-op, which was managed with potassium chloride-containing intravenous fluids. He had antihypertensives, proton pump inhibitors, antibiotics, analgesics, anticoagulants, total parenteral nutrition, and active breathing exercises and was ambulated.

He had another surgery for esophagostomy closure and removal of the gastroesophageal junction band 6 weeks later, which was well tolerated. Repeat esophagogram showed a successful repair without leakage [Figure 3]. The patient is recuperating well, but yet feeding via gastrostomy tube.
Figure 3: Esophagogram (transverse view) showing the repaired esophagus without leakages

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  Discussion Top

BS is rare and commonly misdiagnosed as pneumothorax, pleural effusion, myocardial infarction (MI), or aortic dissection due to its diverse symptom presentation.[2] The common risk factors of overeating and alcohol intake seen in BS were absent in our patient, same as left-sided chest pain which to some extent ruled out MI despite being a known hypertensive. Added to our diagnostic dilemma was vertigo that started with the illness and the history of bronchial asthma prompted our earlier consideration of this diagnosis. Despite these diagnostic challenges, the prominence of vomiting, advancing age, and the male gender are common associates of BS. Without imaging findings, the prominence of abdominal symptoms in our patient could have suggested a sub-diaphragmatic rupture.[5]

AKI in BS can result from severe dehydration, shock, and sepsis; prompt recognition and treatment, as were done for our patient, are often effective.[6] Esophagostomy is a reliable diagnostic investigative tool. CT and X-ray are important supportive investigative tools and were also used in this index case. Barium meal was used in the index patient at esophagostomy; sweetened Methylene blue and gastrografin can also be used.[7] Delayed diagnosis, as was the case in this patient management, is commonly associated with poor treatment outcomes including case fatality; hence, treatment involves mediastinal and pleural cavity clearance (with extensive lavage), esophagostomy with feeding jejunostomy while esophageal tissue replacement (with colon or stomach) was done 6 weeks after the first surgery.[8]

  Conclusion Top

A rarer case of BS with delayed diagnosis, despite this treatment outcome, was very satisfactory.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Harikrishnan S, Murugesan CS, Karthikeyan R, Manickavasagam K, Singh B. Challenges faced in the management of complicated Boerhaave syndrome: A tertiary care center experience. Pan Afr Med J 2020;36:65.  Back to cited text no. 1
Whyte RI. Boerhaave’s syndrome. N Engl J Med 2001;344:139.  Back to cited text no. 2
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
Rokicki M, Rokicki W, Rydel M. Boerhaave’s syndrome—Over 290 yrs of surgical experiences. Epidemiology, pathophysiology, diagnosis. Pol Przegl Chir 2016;88:359-64.  Back to cited text no. 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. 5
Rassameehiran S, Klomjit S, Nugent K. Right-sided hydropneumothorax as a presenting symptom of Boerhaave’s syndrome (spontaneous esophageal rupture). Proc (Bayl Univ Med Cent) 2015;28:344-6.  Back to cited text no. 6
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
Tzeng CH, Chen WK, Lu HC, Chen HH, Lee KI, Wu YS, et al. Challenges in the diagnosis of Boerhaave syndrome: A case report. Medicine (Baltimore) 2020;99:e18765.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]


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