A comparison of the two cases is shown in Table 1. Both were equally distressed on the arrival, but the clinical course was more complicated in case 1 compared to case 2. The initial diagnoses of both cases were symptom based involving vomiting, pain in the lower thorax, and mediastinal emphysema [4].
Table 1
Comparison of the reported cases
| Case 1 | Case 2 |
Age (years) | 45 | 27 |
Physique (body mass index) | 24.4 | 18.0 |
Symptoms | Vomiting, chest pain, back pain, bilateral shoulder pain | Vomiting, chest pain, epigastralgia, hematemesis, pyrosis |
Severity | Distressed | Distressed |
Trigger | Excessive drinking from the previous day | Excessive drinking from the previous day |
Hematemesis | – | + |
Operation | + | – |
Location | On the left posterior wall of the distal esophagus | On the left wall of the distal esophagus |
First endoscopy | Day 68 | Day 9 |
Period of hospitalization | 41 days | 11 days |
Estimated time from onset to rupture | 1.2 hours | 2.5 hours |
Estimated time from rupture to operation room | 9 hours | (No operation) |
Esophagography, upright chest X-ray, and chest CT scan are useful for the correct diagnosis of Boerhaave syndrome [5, 6]. In cases similar to case 1, X-rays are more appropriate in patients with major hydropneumothorax or pneumomediastinum, but if these are minor, as in case 2, CTs are preferred owing to recent improvements in imaging quality. In case 2, conservative treatment was revealed that if the inflammation of the rupture was localized in the mediastinum, non-operative choices could be successful [3].
The mechanism of Boerhaave syndrome is caused by a lack of coordination between the upper and lower esophageal sphincters, resulting in a transmural tear of the distal esophageal wall caused by increased intragastric pressure which is transmitted to the esophagus during vomiting [7]. In both presented cases, the left wall of the distal third of the esophagus was torn, which was more likely to occur due to anatomical reasons such as the thin muscular layer, nerve and vascular entrance, and lack of support for the surrounding connective tissue [7].
Several reports have described diagnostic errors which regarded esophageal rupture as Mallory-Weiss syndrome [8–10]. Commonly, massive hematemesis with less pain indicates Mallory-Weiss syndrome and less hematemesis with more pain indicates Boerhaave syndrome, despite both disorders having an onset of vomiting after drinking. Hematemesis was observed in case 2, but the endoscopic findings showed a scar only in the esophagus, not in the stomach, namely Mallory-Weiss’s lesions were not observed at all (Fig. 5).
The etiologies of both Boerhaave and Mallory-Weiss syndromes are similar, with the result of abnormally elevated intraluminal cardio-esophageal pressures during vomiting. Some predecessors have mentioned the relationship between the two syndromes [11–17], and some of them have identified Boerhaave syndrome as an extension of Mallory-Weiss syndrome [12–17], but this may be disputed for two reasons: the differences in the common sites (left distal esophagus and gastric cardia, respectively) and scarcity of reported transitional cases. Our review of accessible “transitional cases” [14–17] shows, except for one case which might have a real transitional lesion [17], that they had both several lacerations that extended into the submucosa at the gastric cardia and a single laceration through all layers at the distal esophagus separately. Thus, the two syndromes are primarily different, and many of the “transitional cases” may be considered to have occurred independently in the same individual. Describing pathophysiology, the Mallory-Weiss’s lacerations may mainly involve the part of the gastric cardia including EGJ by repeated retching, while the Boerhaave’s lacerations may occur all at once in the weakest part of the esophageal wall based on the idea that the muscular layer initially tears before the mucosal layer when an explosive force is applied [18].
In summary, we report two cases of Boerhaave syndrome with different severities. Severity may vary greatly among the patients with this disorder. Plain CT can detect any severity of this syndrome quickly and easily, and is recommended as a preliminary test if the environment permits. Although the initial cause is the same as that of Mallory-Weiss syndrome, the nature of the two syndromes is distinctive, and correct diagnosis is essential for positive patient outcomes.