In case of iatrogenic perforation common site is cervical esophagus just above the upper sphincter whereas spontaneous rupture as seen in Boerhaaves syndrome perforation commonly occurs in the lower one-third of esophagus. Signs and symptoms
The classic history of esophageal rupture is one of severe retching and vomiting followed by excruciating retrosternal chest and upper abdominal pain. Odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock develop rapidly thereafter.Physical examination is usually not helpful, particularly early in the course. Subcutaneous emphysema (crepitation) is an important diagnostic finding but is not very sensitive, being present in only 9 of 34 patients (27 percent) in one series. A pleural effusion may be detected.Macklers triad includes chest pain, vomiting, and subcutaneous emphysema, and while it is a classical presentation, it is only present in 14% of people.Pain can occasionally radiate to the left shoulder, causing physicians to confuse an esophageal perforation with a myocardial infarction.It may also be audibly recognized as Hammans sign. Pathophysiology
Esophageal rupture,  in Boerhaave syndrome, is thought to be the result of a sudden rise in internal esophageal pressure produced during vomiting, as a result of neuromuscular incoordination causing failure of the cricopharyngeus muscle (a sphincter within the pharynx) to relax. As the intra-oesophageal pressure increases, the bolus within the oesophagus has nowhere to go superiorly (as the cricopharyngeus fails to relax) which causes the oesophagus to rupture.
To him, he felt that he had just come to consciousness for the first time every time he was unable to hold on to information. This case also can be used as evidence that there are different memory systems for declarative and non-declarative memory. This case was more evidence that the hippocampus is an important part of the brain in remembering past events and that declarative and non-declarative memories have different processes in different parts of the brain. Patient R.B. Patient R.B. was a normally functioning man until the age of 52. At age 50, he had been diagnosed with angina and had surgery for heart problems on two occasions. After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. demonstrated a loss of anterograde memory, but almost no loss of retrograde memory, with the exception of a couple of years before his surgery, and presented no sign of any other cognitive impairment. It wasnt until after his death that researchers had the chance to examine his brain, when they found his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory. Patient G.D. Patient G.D. was a white male born in 1940 who served in the Navy. He was diagnosed with chronic kidney failure and received hemodialysis treatment for the rest of his life. In 1983, he went to the hospital for elective parathyroidectomy.