Boerhaave Syndrome Diagnosis: Recognizing and Responding to Esophageal Rupture

Introduction

Boerhaave syndrome is a critical medical emergency defined by a transmural esophageal perforation, most frequently arising from a sudden increase in intraesophageal pressure, often due to forceful vomiting or retching. It’s crucial to distinguish Boerhaave syndrome from Mallory-Weiss syndrome, which involves a non-transmural esophageal tear also linked to vomiting. While the term “spontaneous” is sometimes used, Boerhaave syndrome in the context of emesis isn’t truly spontaneous, differentiating it from iatrogenic perforations. Vomiting remains the most prevalent cause, but any activity elevating intraesophageal pressure can precipitate this syndrome. Although it can occur in individuals with a healthy esophagus, underlying esophageal conditions or pathologies are sometimes identified in affected patients. Boerhaave syndrome accounts for a significant portion of esophageal perforations, ranging from 10% to 15%.1

Diagnosing Boerhaave syndrome presents a considerable challenge due to its variable clinical presentations, necessitating a high index of suspicion. The classic Mackler triad—vomiting, chest pain, and subcutaneous emphysema—is rarely fully present, and patients often exhibit non-specific symptoms, contributing to diagnostic delays and poorer outcomes. Boerhaave syndrome is considered among the most lethal gastrointestinal disorders, with mortality rates reaching up to 60% even with intervention, and nearly 100% without timely treatment.2 Management approaches are diverse, ranging from conservative medical care to extensive surgical procedures, depending on the timing of diagnosis and the patient’s clinical status at presentation. Prompt diagnosis and tailored therapeutic strategies are essential for improving patient outcomes in Boerhaave syndrome.3

Etiology of Boerhaave Syndrome

Boerhaave syndrome is fundamentally a barogenic injury, resulting from a rapid and significant rise in pressure within the esophagus against a closed cricopharyngeus muscle. This neuromuscular dysfunction leads to a failure of the cricopharyngeus to relax properly, causing a dramatic increase in pressure that overwhelms the esophageal wall at its weakest point.4 In adults, perforation most commonly occurs in the left posterolateral aspect of the distal esophagus, just above the diaphragm. However, in younger patients, esophageal rupture more frequently results in perforation into the right pleural cavity.

Alcoholism and dietary indiscretion are well-established risk factors. Both can precipitate episodes of sudden, forceful emesis, which is the most common trigger. Other activities that elevate intraesophageal pressure, potentially leading to Boerhaave syndrome, include strenuous weightlifting, defecation straining, epileptic seizures, blunt abdominal trauma, compressed air injuries, and childbirth.5 While most cases arise in individuals with a previously normal esophagus, pre-existing conditions such as esophagitis and esophageal ulcers have been identified in a subset of patients. Currently, there is no known genetic predisposition for Boerhaave syndrome.

Epidemiology of Boerhaave Syndrome

Boerhaave syndrome constitutes approximately 15% of all traumatic esophageal ruptures. The estimated global incidence is around 3.1 cases per 1,000,000 individuals annually, a figure likely underestimated due to underreporting and diagnostic challenges. This condition has been documented across all racial and ethnic groups globally, with a marked predominance in males, exhibiting male-to-female ratios from 2:1 to 5:1. While the peak incidence is observed in men during their sixth and seventh decades of life, Boerhaave syndrome can occur across all age ranges, from neonates to individuals over 90 years old. Children aged 1 to 17 years appear to be the least affected demographic group.4

Pathophysiology of Esophageal Rupture in Boerhaave Syndrome

Effort rupture of the esophagus in Boerhaave syndrome is primarily caused by a rapid, extreme increase in intraesophageal pressure, most commonly due to forceful vomiting. This pressure surge is thought to originate from neuromuscular incoordination, specifically a failure of the cricopharyngeal muscle to relax during vomiting, leading to a full-thickness tear in the esophageal wall. Overeating and excessive alcohol consumption are frequently associated factors.6

Typically, these perforations are linear, ranging from 3 to 8 cm in length, and are predominantly located in the posterolateral lower third of the esophagus, approximately 2 to 3 cm proximal to the gastroesophageal junction. This area is considered weaker due to a higher density of neurovascular structures and a relative paucity of longitudinal muscle fibers.1, 7 The upper thoracic or subdiaphragmatic esophagus is the second most common site for perforation in Boerhaave syndrome.

The clinical manifestations of Boerhaave syndrome are largely determined by the anatomical location of the esophageal rupture. The middle esophagus is in proximity to the right pleura, while the lower esophagus is adjacent to the left pleura, which explains why ruptures more frequently occur into the left pleural cavity. Perforations in the intrathoracic esophagus can lead to severe mediastinal inflammation, empyema, emphysema, or even necrosis as gastric contents leak into the mediastinal space. However, rupture can also occur in the cervical or upper thoracic regions. Upper thoracic and midesophageal perforations are more likely to result in right-sided pleural effusion or hydropneumothorax. Cervical ruptures often remain localized and are generally less severe, as the spread to the mediastinum through the retroesophageal space is slower and more contained.8, 9, 10

History and Physical Examination in Boerhaave Syndrome Diagnosis

The classic clinical presentation of Boerhaave syndrome, traditionally described as the Mackler triad—vomiting, lower thoracic pain, and subcutaneous emphysema in middle-aged men with a history of overindulgence in food or alcohol—is infrequently observed in its entirety. More commonly, the presentation is non-specific, with a wide array of potential symptoms.11 This variability is due to the esophagus’s anatomical course through cervical, thoracic, and abdominal compartments. Notably, 25% to 45% of patients do not report a history of vomiting upon presentation, and Boerhaave syndrome can affect individuals of any age, ethnicity, and gender.12

Clinical presentation also varies depending on the time elapsed since the esophageal injury and the extent of leakage. Patient complaints can range significantly, including the sudden onset of chest, neck, or abdominal pain, odynophagia (painful swallowing), dysphagia (difficulty swallowing), hoarseness, dysphonia (voice changes), vomiting, hematemesis (vomiting blood), and respiratory distress. Physical examination findings may include subcutaneous crepitation (a crackling sensation due to air under the skin), mediastinal crunching sounds synchronous with the heartbeat in the left lateral decubitus position (Hamman sign), fever, hypotension, tachycardia, tachypnea, cyanosis, decreased breath sounds, abdominal pain, abdominal rigidity, neck pain, tracheal shift, proptosis, and altered mental status. The subtle and varied nature of these signs underscores the importance of considering Boerhaave syndrome in the differential diagnosis of patients presenting with chest or abdominal pain, especially in the context of recent vomiting.

Comprehensive Evaluation and Boerhaave Syndrome Diagnosis

The cornerstone of Boerhaave Syndrome Diagnosis relies on a combination of thorough physical examination and advanced radiographic assessments. A focused physical examination is crucial to evaluate the patient’s overall distress and physiological stability. However, given the non-specific nature of the early symptoms, imaging techniques play a pivotal role in confirming the diagnosis and determining the extent of esophageal perforation.

Imaging Modalities for Boerhaave Syndrome Diagnosis

Imaging is indispensable in diagnosing Boerhaave syndrome. Several modalities are used, each providing unique diagnostic information:

Plain Radiography: Initial radiographic assessment often includes plain films of the chest and abdomen. These may reveal indicative signs such as subcutaneous or mediastinal emphysema, mediastinal widening, and pleural effusion. A less common but highly specific finding is the Nacleario V-sign, seen in up to 20% of cases, where radiolucent streaks dissect the retrocardiac fascia, forming a V-shape. While specific, this sign is not sensitive for esophageal perforation.

Contrast Esophagography: A contrast esophagogram is a critical diagnostic tool. Water-soluble contrast agents like Gastrografin are preferred initially to minimize mediastinitis risk should extravasation occur, as barium leakage can exacerbate inflammation and fibrosis. The sensitivity of this study depends on the perforation size, location, and technique. False-negative rates range from 10% to 38%.13 If the initial water-soluble contrast study is negative but clinical suspicion remains high, repeating the study with barium contrast may be considered to increase sensitivity, provided the risks are carefully weighed.

Computed Tomography (CT) Imaging: CT scanning of the chest and abdomen is invaluable for a more definitive diagnosis and is often better tolerated by acutely ill patients. CT provides detailed anatomical information, aiding in identifying the location of fluid collections and precisely localizing the rupture site. Contrast enhancement can further delineate the extent of injury and expedite diagnosis. Key CT findings suggestive of Boerhaave syndrome include periesophageal and mediastinal gas, mediastinal fluid collections, esophageal wall thickening, pleural effusion, pneumothorax, and hydrothorax.13 CT scanning is particularly useful for evaluating the mediastinum and pleural spaces, areas not well visualized by esophagography.

Endoscopy: While potentially diagnostic, endoscopy is considered controversial in Boerhaave syndrome due to the risk of exacerbating the perforation. It is generally reserved for cases where the perforation location is uncertain and when endoscopic therapeutic interventions are being considered. Endoscopy allows direct visualization of the esophageal mucosa and can sometimes identify the perforation site, but it must be performed with extreme caution to avoid further injury.

Laboratory Findings in Boerhaave Syndrome Diagnosis

Laboratory tests are generally non-specific in diagnosing Boerhaave syndrome but can support clinical suspicion and assess the patient’s overall condition. Common findings include leukocytosis with a left shift, indicating an inflammatory response. Hemoconcentration, reflected by hematocrit values around 50%, is often seen due to fluid loss and dehydration. Pleural fluid analysis, if effusion is present, may reveal undigested food particles and gastric fluid, with a characteristic low pH (less than 6) and elevated salivary amylase levels, confirming esophageal content leakage into the pleural space.

Treatment and Management Strategies for Boerhaave Syndrome

Management of Boerhaave syndrome is complex and requires a multidisciplinary approach. The three primary treatment modalities include non-surgical (conservative), endoscopic, and surgical interventions (both open and minimally invasive). The optimal treatment strategy is determined by an interprofessional team experienced in managing esophageal perforations.14 Treatment typically involves a combination of medical and procedural interventions. The foundational principles of management include nil per os (NPO) status, aggressive fluid resuscitation, broad-spectrum antibiotic therapy, nutritional support (usually parenteral), source control of leaks (via interventional radiology or video-assisted thoracoscopic surgery – VATS), and timely surgical or endoscopic intervention as indicated. Treatment plans are highly individualized, based on the perforation’s location and size, the time from injury to diagnosis, and the patient’s overall clinical status. Early diagnosis, within 12 to 24 hours of perforation, is a critical determinant of positive outcomes.

Non-Surgical Management

Conservative management may be considered in highly select patients meeting strict criteria:15

Contained Leak: The esophageal leak must be contained within the neck, mediastinum, or between the mediastinum and visceral lung pleura.
Spontaneous Re-entry: Contrast medium must be able to flow back into the esophagus from the cavity surrounding the perforation, indicating some degree of sealing.
Non-Neoplastic, Non-Obstructed Perforation: The perforation should not be associated with neoplastic tissue, located in the abdomen, or proximal to an esophageal obstruction.
Minimal Symptoms, No Sepsis: Patients should exhibit minimal symptoms without signs of systemic sepsis.
Immediate Access to Imaging and Surgery: Contrast studies should be readily available at any time, and surgical specialists must be immediately accessible should the patient’s condition deteriorate.

Medical management includes strict NPO status for at least 7 days, parenteral nutrition to provide necessary caloric intake, broad-spectrum intravenous antibiotics for 7 to 14 days to combat infection, and drainage of any mediastinal or pleural fluid collections, often guided by interventional radiology. Close monitoring is essential. Patients showing clinical deterioration under conservative management require prompt surgical intervention.

Surgical and Endoscopic Interventions

Surgical intervention is indicated if conservative management fails or if the patient presents with:15

Progression to Free Perforation: A contained perforation evolves into a free perforation.
Extension of Injury: The esophageal injury extends.
Persistent Sepsis: Patient exhibits persistent fevers or develops sepsis.
Clinical Deterioration: Overall clinical condition worsens.
Progression of Pneumothorax/Pneumomediastinum: Worsening air leak in the chest or mediastinum.
Development of Empyema: Pus collection in the pleural space.

Primary esophageal repair is often the most effective surgical approach, particularly when performed within the first 4 hours of perforation. This can be accomplished via open thoracotomy or VATS, frequently with fundic reinforcement to buttress the repair, now considered the gold standard surgical treatment.

In cases of a severely diseased or nonviable esophageal segment, resection may be the preferred surgical strategy. For late presentations, diagnosed after 24 hours, the tissue edges are typically edematous, stiff, and friable, making primary repair more challenging and risky. In these scenarios, management may involve debridement of the pleural cavity and mediastinum, esophagostomy (creating an opening in the esophagus), and feeding gastrostomy to provide nutritional access. Definitive esophageal reconstruction can be performed at a later stage, typically after 6 weeks.

Esophageal stenting across the perforation site has emerged as a less invasive alternative to surgery in certain cases, showing promising results.16 Stenting may be particularly considered in patients with significant comorbidities who are poor surgical candidates. Advanced endoscopic techniques are also increasingly utilized for minimally invasive therapeutic interventions. These include placement of fully covered esophageal stents, through-the-scope clips, over-the-scope clips, endoscopic suturing, and in rare cases, endoscopic esophageal resection and diversion.17 The choice between surgical and endoscopic approaches depends on the specifics of each case, including the location and size of the perforation, the time since injury, and patient factors.

Differential Diagnosis of Boerhaave Syndrome

The symptoms of Boerhaave syndrome are often non-specific and can mimic a variety of other acute medical conditions, necessitating a broad differential diagnosis. Conditions to consider include:

Aortic Dissection: Presents with sudden, severe chest pain, which can be similar to Boerhaave syndrome. However, aortic dissection often has associated symptoms like pulse deficits, blood pressure discrepancies, and specific ECG findings. CT angiography is crucial for differentiation.
Acute Pancreatitis: Can cause epigastric and chest pain, often associated with nausea and vomiting. Elevated serum lipase and amylase levels and abdominal CT findings help distinguish it from Boerhaave syndrome.
Myocardial Infarction (MI): Presents with chest pain, potentially radiating to the arm or jaw, and may be accompanied by nausea and vomiting. ECG changes and elevated cardiac enzymes are key diagnostic features.
Pulmonary Embolism (PE): Can cause sudden chest pain and respiratory distress, mimicking Boerhaave syndrome, especially if there is associated hemoptysis. CT pulmonary angiography is used to diagnose PE.
Perforated Peptic Ulcer: Causes sudden, severe abdominal pain that can radiate to the chest. Free air on abdominal X-ray and upper endoscopy are diagnostic.
Spontaneous Pneumothorax: Presents with sudden onset chest pain and shortness of breath. Chest X-ray readily diagnoses pneumothorax.
Pneumonia and Empyema: Can present with chest pain, fever, and respiratory symptoms. Chest X-ray and CT can differentiate these from esophageal perforation by demonstrating lung consolidation or pleural effusion without mediastinal air in typical pneumonia.
Pericarditis: Causes chest pain, often pleuritic in nature, which can be confused with esophageal perforation. ECG findings, pericardial rub on auscultation, and echocardiography are helpful in diagnosis.
Mallory-Weiss Tear: Involves a mucosal tear of the esophagus, typically presenting with hematemesis after vomiting. Unlike Boerhaave syndrome, it is non-transmural and generally less severe. Upper endoscopy is diagnostic.

A careful history, thorough physical examination, appropriate laboratory tests, electrocardiogram, and targeted imaging are essential to differentiate Boerhaave syndrome from these other conditions.18 The key to accurate diagnosis is maintaining a high index of suspicion for Boerhaave syndrome in patients presenting with chest or abdominal pain, particularly after episodes of forceful vomiting or retching.

Prognosis of Boerhaave Syndrome

The prognosis of Boerhaave syndrome is strongly correlated with the time elapsed between esophageal injury and diagnosis, as well as the promptness and appropriateness of treatment. Delayed diagnosis and treatment are associated with significantly worse outcomes and increased mortality. When diagnosis is made and appropriate treatment initiated within 12 to 24 hours of perforation, patient survival rates can approach 75%, indicating a reasonably good prognosis. However, untreated Boerhaave syndrome carries a mortality rate exceeding 90%, underscoring the critical need for timely recognition and intervention.19

Complications of Untreated or Delayed Boerhaave Syndrome

Boerhaave syndrome is a relatively rare but highly dangerous condition. Delayed diagnosis or lack of treatment can lead to severe complications, including:20

Dehydration and Electrolyte Imbalance: Due to vomiting, NPO status, and systemic illness.
Mediastinitis: Inflammation of the mediastinum, a severe and potentially life-threatening infection.
Sepsis: Systemic inflammatory response to infection, leading to organ dysfunction.
Acute Respiratory Distress Syndrome (ARDS): Severe lung injury causing respiratory failure.
Massive Pleural Effusion and Empyema: Accumulation of fluid or pus in the pleural space, compromising lung function.
Esophageal Fistula: Abnormal connection between the esophagus and other structures, such as the trachea or pleura.
Shock (Septic or Hypovolemic): Life-threatening condition due to infection or fluid loss.
Death: The most severe outcome if Boerhaave syndrome is not promptly and effectively managed.

Postoperative and Rehabilitation Care

Recovery from Boerhaave syndrome, particularly after surgical intervention for transmural esophageal rupture, is a comprehensive process. Rehabilitation is tailored to the severity of the tear, the type of intervention performed, and the degree of systemic impact on the patient. Key aspects of postoperative and rehabilitation care include:

Gradual Reintroduction of Oral Feeding: Starting with clear liquids and progressing to a soft diet as tolerated, under the guidance of a dietitian and speech therapist if swallowing difficulties are present.
Normalization of Organ Systems: Monitoring and supporting cardiovascular, respiratory, and renal function, especially in patients who experienced sepsis or ARDS.
Weaning from Intensive Measures: Gradually discontinuing mechanical ventilation, invasive monitoring lines, and intravenous medications as the patient stabilizes.
Physical Therapy and Rehabilitation: Regaining strength, endurance, and mobility to facilitate a return to independent activities of daily living. This may involve muscle strengthening, respiratory exercises, and occupational therapy.
Pain Management: Effective control of postoperative pain to promote comfort and facilitate participation in rehabilitation.
Psychological Support: Addressing the psychological impact of a critical illness and prolonged hospitalization, providing counseling or support groups as needed.

Consultations in Boerhaave Syndrome Management

Early consultation with thoracic and general surgeons is paramount in suspected cases of Boerhaave syndrome. Additional consultations that may be beneficial include infectious disease specialists to guide antibiotic therapy, critical care specialists for management in the intensive care unit, radiologists for diagnostic imaging interpretation, and gastroenterologists for long-term esophageal health follow-up.

Deterrence and Patient Education

Boerhaave syndrome is a rare condition, and there are no definitive predictive models to identify at-risk individuals. However, patient education plays a crucial role in awareness, particularly for individuals with known risk factors such as excessive alcohol consumption and binge eating. These individuals should be counseled about the potential risks associated with forceful vomiting and advised to seek immediate medical attention if they experience sudden onset chest, neck, or abdominal pain following forceful emesis. Patients who have been treated for Boerhaave syndrome require close follow-up with gastroenterology and their primary care provider to monitor for any long-term esophageal issues and manage underlying risk factors.

Key Clinical Pearls for Boerhaave Syndrome

Key points to remember in the diagnosis and management of Boerhaave syndrome are:

High Index of Suspicion: Boerhaave syndrome diagnosis requires a high degree of clinical suspicion, particularly in patients presenting with chest or abdominal pain after vomiting.
Time is Critical: Delay in diagnosis significantly worsens outcomes and can be fatal. Prompt recognition and intervention are essential.
Water-Soluble Contrast Imaging: When performing contrast esophagography, water-soluble contrast agents are preferred initially to minimize mediastinal irritation in case of extravasation.
Conservative vs. Surgical Management: Conservative management may be considered in highly selected, stable patients with contained leaks, but surgical intervention is the mainstay for frank extravasation and clinical deterioration.
VATS and Endoscopic Repair: VATS with fundic reinforcement is a gold standard surgical approach, and endoscopic repair techniques are increasingly utilized as minimally invasive alternatives.
Multidisciplinary Approach: Optimal management requires a collaborative interprofessional team including surgeons, radiologists, gastroenterologists, intensivists, pharmacists, and nurses.

Enhancing Healthcare Team Outcomes

Given the diagnostic challenges and high mortality associated with Boerhaave syndrome, a collaborative, interprofessional team approach is crucial for improving patient outcomes. Effective communication and coordination among all team members—including surgeons, radiologists, gastroenterologists, intensivists, pharmacists, and nursing staff—are essential. Each team member brings unique expertise to the management process. Radiologists provide critical diagnostic imaging interpretation, gastroenterologists offer endoscopic expertise, intensivists manage critical care aspects, pharmacists optimize medication regimens, and nurses provide continuous patient monitoring and care, as well as crucial patient and family education. Timely and coordinated involvement of all team members is paramount in the successful management of this life-threatening condition, ensuring the most comprehensive and attentive care possible.

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References

(References are identical to the original article and are included for completeness.)

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Disclosures:

Disclosure: Anisha Turner declares no relevant financial relationships with ineligible companies.

Disclosure: Sara Collier declares no relevant financial relationships with ineligible companies.

Disclosure: Sherry Turner declares no relevant financial relationships with ineligible companies.