Esophageal Cancer

Epidemiology
The epidemiology of esophageal cancer in the Western world has changed dramatically over the last two decades. Up until the 1970s most esophageal cancers were of the squamous cell type, affecting mostly elderly men drawn from the poorer social classes and influenced by smoking and alcohol consumption. Since then there has been a dramatic increase in the incidence of adenocarcinoma, which tends to affect more affluent white men, often in their most productive years of life. Squamous cell carcinoma SCC of the esophagus remains in the top ten of cancers globally and represents a major healthcare problem. The marked geographical variation in incidence suggests that environmental factors are paramount in its causation. High-incidenceregions of the world such as Southern and Eastern Africa, and a central Asian belt passing from Turkey through countries such as Iraq, Iran, and Kazakhstan and on to Northern China, are marked out by poverty and other poverty-related illnesses. The incidence in high-risk provinces can reach up to 100/10 000 per year compared to 510/10 000 per year in Western countries [2]. In the USA, SCC is more common among black people than among white people, but incidence rates have fallen by half across both groups between 1970 and 2000, with incidence rates of approximately 2/100 000 for white males and 10/100 000 for black people in 2000 [1,2,5]. These figures are probably related to increasing levels of wealth and education and reduction in exposure to causative agents. The male : female ratio is 3:1 except in high-incidence areas where the distribution is more equal and reflects an equal exposure to risk factors [6]. Regional, socioeconomic, and racial variation within a country is demonstrated by a higher incidence of SCC in low income and low socioeconomic groups [5,7,8]. Adenocarcinoma The last 30 years have seen a dramatic fall in the incidence of noncardia gastric cancer and, as mentioned earlier, a decline or stabilization in the incidence of SCC of the esophagus in Western countries [9,10,11,12,13]. Over the same period the age-standardized incidence of adenocarcinoma of the lower esophagus, previously a rare disease with incidence <1/100 000, has risen more rapidly than any other malignancy in the Western world. Since the mid 1990s its incidence has exceeded that for SCC [14,15,16]. The rise in incidence is most marked in the white male population, reaching about 5/100 000 for the white males in North America and 812/100 000 for white males in the highest incidence countries of Australia and the UK [7,13,17,18,19,20,21,22]. This represents an increase of about 400800% from the 1970s and is about four times greater than the incidence for black males in the United States. The trend is similar for other North European countries [10,23,24,25]. Not only is the incidence higher in white males, but the annual increase in incidence, _10% per year, is higher than for other racial groups and for white females, leading to an increasing sex and racial ratio [17,26,27]. The demographic

distribution shows an age peak at 5060 years and a male : female ratio between 2:1 and 12:1 [23]. Although it is possible that improved anatomic classification and histological verification might account for some of the time trends noted, the rapid changes point to a newly acquired etiological risk factor

Etiology
Squamous cell carcinoma Many of the environmental factors associated with a high incidence of SCC of the esophagus relate to poor socioeconomic circumstances. A diet rich in preserved and pickled foods and low in fresh fruit and vegetables, vitamin and mineral deficiencies, and a thermal effect of hot food and beverages have all been implicated. Alcohol intake and smoking are also strongly associated with an increased risk of SCC of the esophagus [28,29,30,31]. The risk is thought to be dose related and the genetic changes brought about by chronic exposure to causative agents lead to a progression through epithelial dysplasia and carcinoma in situ to invasive cancer [32]. After several years of cessation of exposure to irritant factors, such as smoking and alcohol, risk is substantially reduced [33]. Conditions such as caustic ingestion and achalasia of the cardia, which are associated with chronic mucosal inflammation, also predispose to SCC of the esophagus. Adenocarcinoma The recent and rapid escalation in incidence of esophageal adenocarcinoma would seem to suggest a mostly environmental rather than genetic effect. While a number of factors including race, obesity, use of esophageal sphincter-relaxing drugs, smoking, and alcohol consumption have all been incriminated as possible etiological factors in esophageal adenocarcinoma [34,35,36,37,38], many cohort studies have pointed strongly to gastroesophageal reflux and Barretts disease (Barretts esophagus) as a causative factor [39,40]. There is a strong doseresponse relationship between previous gastroesophageal reflux symptoms and esophageal adenocarcinoma, but the relationship to cardia cancer is weaker [40]. Wu et al. demonstrated a threefold increase in esophageal cancer and a doubling in cardia cancer with reflux symptoms [41]. The relationship between adenocarcinoma of the lower esophagus and adenocarcinoma of the cardia is less clear. Siewert et al. have separated adenocarcinoma occurring at or near the gastroesophageal junction into three groups depending on the anatomic relation to the gastroesophageal junction. Type 1 tumors represent cancers of the lower esophagus, mostly arising in Barretts esophagus. Type 2 and 3 tumors represent true cardia and proximal gastric cancers, respectively [42], and while their incidence has risen in recent decades, the changes are not as marked as for true lower esophageal adenocarcinoma that are associated with Barretts esophagus, Type I. The clinicalbehavior and treatment of type 2 and 3 tumors are more like those of gastric carcinoma [43,44]. Gastroesophageal reflux leads to columnar cell metaplasia in the distal esophageal epithelium, a condition known as Barretts esophagus. This increases the risk

of developing esophageal adenocarcinoma 30- to 60-fold. The squamous cell epithelium of the normal esophagus is replaced with a mature columnar-type epithelium, with Barretts mucosa being derived from pleuripotential cells in the basal layer of the esophageal epithelium [45,46,47]. The presence of goblet and pregoblet cells is a requisite for intestinal metaplasia, which is associated with the increased risk of malignant transformation. The probable driver toward metaplasia is that the columnar epithelium is more tolerant of refluxate and the progression to columnar metaplasia is a function of the refluxate content and periodicity [34]. Metaplasia of fundic- or cardiac-type gastric mucosa not involving the presence of goblet cells is thought to carry a lower risk of malignant transformation. Most cases of distal esophageal adenocarcinomas (90%) are thought to arise in the setting of Barretts esophagus [48]. In other words, the risk of malignant transformation is greatly elevated in patients with Barretts esophagus and much less elevated in patients with reflux esophagitis or nonerosive gastroesophageal reflux without Barretts esophagus. Solaymani-Dodaran et al. reported relative risks for developing esophageal adenocarcinoma of 29.8 for Barretts esophagus, 4.5 for reflux esophagitis, and 3.1 for gastroesophageal reflux without Barretts esophagus or reflux esophagitis [39]. A patient with Barretts esophagus has a 5% lifetime risk of developing esophageal adenocarcinoma. The risk of transformation from benign intestinal epitheliumin Barretts esophagus to dysplasia and then adenocarcinoma is related to the length of Barretts epithelium lining the esophagus, duration of reflux disease, and presence of a hiatus hernia [49,50,51]. The risk of transformation may be mitigated by antireflux surgery, but the evidence is not strong enough to recommend this as a strategy for cancer prevention. Molecular markers of high risk are recognized but do not as yet form part of routine practice. Dysplasia is classified as low or high grade and is characterized by the degree of hyperchromasia, nuclear : cytoplasm ratio, and glandular atypia. High-grade dysplasia is considered as indicative of at least an intraepithelial malignancy. About one-third of patients with high-grade dysplasia at biopsy will have invasive disease evident on a resection specimen. In population terms Barretts esophagus is a common condition, occurring in 0.452.2% of all patients undergoing upper GI endoscopy, about 12% of patients undergoing endoscopy for reflux symptoms, and about 0.3% in unselected autopsy series [56]. While excess exposure to acid isdemonstrable in most patients with Barretts esophagus, progression to dysplasia is more likely in patients with alkaline or bile-containing duodenogastric reflux rather than those with pure acid reflux. Several other potential causative factors have been evaluated. The incidence of esophageal adenocarcinoma has increased since the introduction of powerful acid suppressants such as histamine-2 receptor antagonists and proton pump inhibitors, but the lead time for carcinogenesis probably precludes these agents as etiological agents and the association is likely to reflect the use of these agents to treat symptoms of reflux in patients already at increased risk of developing esophageal adenocarcinoma. Drugs that reduce the lower esophageal sphincter tone, e.g., anticholingergics, nitroglycerin, beta-adrenergic agonists, aminophylline,

and benzodiazepines, have all been implicated through increasing the potential for reflux [36]. Reduction in intragastric acidity through gastric mucosal atrophy-induced hypochlorhydria from Helicobacter pylori infection may be another factor in the promotion of distal esophageal SCC, while its carcinogenic effect in noncardia gastric cancer is well recognized. By contrast, Helicobacter pylori infection, especially of the cagA strain, may have a protective effect against esophageal adenocarcinoma . The role of diet is controversial, and while there appears to be an association with noncardia gastric cancer, the link to esophageal cancer is not so clear . The relationship to smoking is less clear than that for SCC. Increased abdominal pressure brought about by central obesity, sedentary posture, and tight belts has also been implicated , although a high body mass index appears to be an independent risk factor for adenocarcinoma but not SCC. Familial clustering has been demonstrated in Barretts esophagus and adenocarcinoma of the esophagus, but no Barrett gene has been identified, and it is not clear whether the familial tendency represents a genetic predisposition or merely the effect of similar lifestyle factors among family members . The carcinogenic pathway from Barretts mucosa involves a multistep alteration in the genotype, loss of regulatory function, induction of proinflammatory enzymes such as cyclooxygenase-2, and angiogenesis. Consequently, chemoprevention and treatment through the use of therapies directed at specific molecular targets has been postulated. Clinical

Risk factors
Risk factors Tobacco smoking Excess alcohol consumption Barrett's esophagus Reflux (GERD) symptoms Obesity Excess energy consumption Excess fat consumption Poverty Low education level Excess intake of hot beverage (thermal injury) H. pylori infection* ESCC +++ ++ NS NS NS NS NS ++ + + Protective3 EAC ++ ++ +++ +++ ++ + ++ NS NS NS Protective

+++, Very strong effect; ++ moderate effect; +, some effect. EAC, esophageal adenocarcinoma; ESCC, esophageal squamous cell carcinoma; GERD, gastroesophageal reflux disease; NS, not significant. *Role of Helicobacter pylori infection as a risk factor affecting esophageal carcinoma was cited from sources other than 2.

Prevention

Reducing use of tobacco and alcohol can reduce the frequency of squamous cell carcinoma of the esophagus. At least 90% of cases of this cancer in North America may be attributable to alcohol and tobacco.

Adenocarcinoma of the esophagus is a frequent complication in Barrett's esophagus, which may be found in up to 20% of people with symptoms of gastroesophageal reflux disease (GERD).
o

People with frequent symptoms of reflux (heartburn or regurgitation) should undergo screening with endoscopy.

People with Barrett's esophagus should have regular endoscopic tests to detect precancerous changes of the esophageal lining.

They also require tight control of the symptoms of gastroesophageal reflux, which may include dietary and lifestyle changes as well as medications and possible surgery, to prevent progression of Barrett;s esophagus.

Clinical Manifestations
Trouble swallowing The most common symptom of esophageal cancer is a problem swallowing, with the feeling like the food is stuck in the throat or chest. The medical term for this is dysphagia. This is often mild when it starts, and then gets worse over time as the opening inside the esophagus gets narrower. Dysphagia is commonly a late symptom caused by a large cancer. When swallowing becomes difficult, people often change their diet and eating habits without realizing it. They take smaller bites and chew their food more carefully and slowly. As the cancer grows larger, the problem gets worse. People then may start eating softer foods that

can pass through the esophagus more easily. They may avoid bread and meat, since these foods typically get stuck. The swallowing problem may even get bad enough that some people stop eating solid food completely and switch to a liquid diet. To help pass food through the esophagus, the body makes more saliva. This causes some people to complain of bringing up lots of thick mucus or saliva. If the cancer keeps growing, at some point even liquids will not be able to pass. Chest pain Sometimes, people complain of pain or discomfort in the middle part of their chest. Some people describe a feeling of pressure or burning in the chest. These symptoms are more often caused by problems other than cancer, such as heartburn, and so they are rarely seen as a signal that a person may have cancer. Swallowing may become painful when the cancer is large enough to limit the passage of food through the esophagus. Pain may be felt a few seconds after swallowing, as food or liquid reaches the tumor and has trouble getting past it. Weight loss About half of patients with esophageal cancer lose weight (without trying to). This happens because their swallowing problems keep them from eating enough to maintain their weight. Other factors include a decreased appetite and an increase in metabolism from the cancer. Other symptoms Other possible symptoms with cancer of the esophagus can include:

Hoarseness Constant cough Hiccups Pneumonia Bone pain Bleeding into the esophagus. This blood then passes through the digestive tract, which may turn stools black. Over time, this blood loss can lead to anemia (low red blood cell levels), which may make a person feel tired.

Diagnosis
When you come to Hopkins for diagnosis and staging, you may receive one or several of these procedures. The most commonly used is the endoscopy with biopsy.

Barium swallow X-ray, or esophogram: This procedure may be used to diagnose cancer and also in staging the extent of the cancer. CT scan, or computed tomography: A CT scan is used after the cancer is diagnosed to see how locally advanced the cancer is or if it has spread to areas near the esophagus or to distant sites. Endoscopic ultrasonography (EUS): EUS combines endoscopy with high-frequency ultrasound to provide high-resolution, detailed images of the tumor, the esophageal wall, and adjacent structures. It is used in some cases to diagnose and more often to stage the cancer locallyto see if it has spread beyond the initial tumor to other places around the esophagus. Endoscopic confocal microscopy: This technology allows doctors to obtain smart biopsies (which use laser technology to provide immediate results) and produce detailed cross-sectional images of the esophagus during endoscopy, allowing the endoscopist to make a tissue diagnosis during endoscopy without a biopsy or pathology. Endoscopy with biopsy (sometimes called a esophagogastroduodenoscopy): This is the most common test an endoscopist will do. With this technique, the endoscopist can use the endoscope to target abnormal areas to biopsy. PET scan (positron emission topography): In cases of esophageal cancer, a PET scan is used to determine if the cancer has spread to areas beyond the esophagus

Staging Staging of squamous cell carcinoma of the esophagus

In addition to the TNM classifications, for squamous cell carcinoma, the stages may be subdivided based on the location of the original tumor (the upper, middle, or lower section of the esophagus), as well as the grade (G) of the tumor cells. Stage 0: This is the same as Tis cancer, in which cancer is found in only the top lining of the esophagus (Tis, N0, M0, G1). Stage IA: This is the same as T1 cancer, in which the cancer is located in only the two inside layers of the esophagus (T1, N0, M0, G1). Stage IB: Either of these two conditions:

The cancer is located in only the two inside layers of the esophagus, but the tumor cells are less differentiated (T1, N0, M0, G2 or G3). The tumor is located in the lower part of the esophagus, and the cancer has spread to either of the two outer layers of the esophagus, but not to the lymph nodes or other parts of the body (T2 or T3, N0, M0, G1).

Stage IIA: Either of these two conditions:

The tumor is located in the upper or middle part of the esophagus, and the cancer is in either of the two outer layers of the esophagus (T2 or T3, N0, M0, G1). The tumor is located in the lower part of the esophagus, and the cancer is in either of the two outer layers of the esophagus. The tumor cells are less differentiated (T2 or T3, N0, M0, G2 or G3).

Stage IIB: Either of these two conditions:

The tumor is located in the upper or middle part of the esophagus, and cancer is in either of the two outer layers of the esophagus. The tumor cells are less differentiated (T2 or T3, N0, M0, G2 or G3). Cancer is in the inner layers of the esophagus and has spread to one or two lymph nodes near the tumor (T1 or T2, N1, M0, any G).

Stage IIIA: Any of these three conditions:

Cancer is in the inner layers of the esophagus and has spread to three to six lymph nodes near the tumor (T1 or T2, N2, M0, any G). Cancer is in the outside layer of the esophagus and has spread to one or two lymph nodes (T3, N1, M0, any G). Cancer has spread beyond the esophagus to nearby tissue but not to lymph nodes or other areas of the body (T4a, N0, M0, any G).

Stage IIIB: Cancer is in the outside layer of the esophagus and in three to six lymph nodes (T3, N2, M0, any G). Stage IIIC: Any of these three conditions:

Cancer has spread beyond the esophagus into nearby tissue. Cancer is also in six or less lymph nodes (T4a, N1 or N2, M0, any G). Cancer has spread beyond the esophagus into nearby tissue and cannot be removed by surgery (T4b, any N, M0, any G). Cancer has spread to seven or more lymph nodes but not to distant parts of the body (any T, N3, M0, any G).

Stage IV: Cancer has spread to another part of the body (any T, any N, M1, any G). Staging of adenocarcinoma of the esophagus

For adenocarcinoma, doctors use the T, N, and M classifications, as well as the grade (G). Stage 0: This is the same as Tis cancer, in which cancer is found in only the top lining of the esophagus (Tis, N0, M0, G1). Stage IA: This is the same as T1 cancer, in which the cancer is located in either of the two inside layers of the esophagus only (T1, N0, M0, G1 or G2). Stage IB: Either of these two conditions:

The cancer is located in either of the two inside layers of the esophagus only, and the tumor cells are poorly differentiated (T1, N0, M0, G3). The cancer has spread to an outer layer of the esophagus but not to the lymph nodes or other parts of the body (T2, N0, M0, G1 or G2).

Stage IIA: Cancer is in an outer layer of the esophagus, and the cells are poorly differentiated (T2, N0, M0, G3). Stage IIB: Either of these two conditions:

Cancer is in the outside layer of the esophagus but not beyond (T3, N0, M0, any G). Cancer is in an inner layer or the muscularis propria of the esophagus and has spread to one or two lymph nodes (T1 or T2, N1, M0, any G).

Stage IIIA: Any of these three conditions:

Cancer is in the inner layers of the esophagus and has spread to three to six lymph nodes near the tumor (T1 or T2, N2, M0, any G). Cancer is in the outside layer of the esophagus and has spread to one or two lymph nodes (T3, N1, M0, any G). Cancer has spread beyond the esophagus to nearby tissue but not to lymph nodes or other areas of the body (T4a, N0, M0, any G).

Stage IIIB: Cancer is in the outside layer of the esophagus and in three to six lymph nodes (T3, N2, M0, any G). Stage IIIC: Any of these three conditions:

Cancer has spread beyond the esophagus into nearby tissue. Cancer is also in six or less lymph nodes (T4a, N1 or N2, M0, any G). Cancer has spread beyond the esophagus into nearby tissue and cannot be removed by surgery (T4b, any N, M0, any G).

Cancer has spread to seven or more lymph nodes but not to distant parts of the body (any T, N3, M0, any G).

Stage IV: Cancer has spread to another part of the body (any T, any N, M1, any G)

Prognosis
Despite the widespread use of endoscopy, significant advances in surgical techniques and neoadjuvant chemoradiation therapy, and improvements in postoperative care, the prognosis for patients with esophageal cancer remains poor. The reported overall 5-year survival rates are at best 10-15%. Delayed clinical manifestations and rapid intramural invasion and distant metastases account for the poor prognosis of this GI malignancy. Patients with an early stage of disease carry a better prognosis. For patients with T1 or T2 disease and no nodal involvement, the 5-year survival rate is greater than 40%. On the other hand, patients with T3 or T4 lesions have a 5-year survival of less than 25%. Stage 0, I, and II tumors are considered resectable for cure. The 5-year survival for such patients who are sufficiently fit to undergo surgery ranges from greater than 85% for stage 0, to 50% for stage I, to 40% for stage II. On the other hand, stage III tumors are rarely resectable for cure, and stage IV cancers are considered incurable and nonresectable by most clinicians. The presence or absence of nodal involvement also has a significant prognostic impact. The 5year survival for N0 disease is over 70%, whereas N1 disease is associated with a survival near 40%, independent of the T classification.

Medical treatment
Chemotherapy Chemotherapy is drug treatment that uses chemicals to kill cancer cells. Chemotherapy drugs are typically used before (neoadjuvant) or after (adjuvant) surgery in people with esophageal cancer. Chemotherapy can also be combined with radiation therapy. In people with advanced cancer that has spread beyond the esophagus, chemotherapy may be used alone to help relieve signs and symptoms caused by the cancer.

Nursing considerations
Pre-operative teaching Preoperative teaching is, as always, essential. The patient and family members must be included in all aspects of this. It is the physicians responsibility to explain the surgical procedure. Patients with esophageal cancer need general pre-op instructions with additional information related to the specific surgical procedure to be performed. As the nurse caring for the patient and family, you will be reinforcing this information. The pre-op assessment includes careful evaluation of pulmonary, cardiovascular, andnutritional status.3 A nutritional assessment should be done prior to chemotherapy and/or radiation therapy, and a registered dietitian should be consulted about nutritional supplements. Oral supplements or tube feeding

might be needed during this time. Patients and their families need to know that an NG tube will be in place, as will Foley catheter, intravenous access, jejunostomy tube for tube feedings, chest tube, and possibly a tracheaostomy tube, if the larynx is removed.5 The patient must be instructed about the importance of early ambulation to prevent pulmonary complications and thrombus. Pain control can be achieved through intramuscular, intravenous, or epidural methods. Adequate pain control is essential to recovery and to decreasing the possibility of postoperative complications. Postoperative care Immediately postop, the patient might be transferred to the ICU for 24 to 48 hours.3 Along with the usual hemodynamic monitoring done during the post-op period, the patient is also monitored for signs of potential l Life-threatening complications A chest tube will have been inserted, if a thoracotomy was performed. The tube might be connected to suction or left to gravity drainage. It is important to assess the dressing for drainage and to replace loose tape. The tubing should remain free of kinks and dependent loops. The area around the chest tube should be palpated for subcutaneous emphysema. The patient must be assessed for any signs of respiratory distress, and distress or subcutaneous emphysema should be reported to the surgeon as soon as possible. The drainage from the chest tube might be bloody initially, but it should becomes sevosanguineous within a few hours postoperatively. During the first postoperative day, expect drainage amounts of 100200mL/hr. This amount should decrease over the next several days.3 Any increase in bloody, purulent, salivary or excessive drainage might indicate a complication and should be reported at once to the surgeon.5 The tube may be left in place until an astomotic patency is demonstrated, regardless of whether there is any drainage.3 Patients are at risk for developing anastomotic leaks and fistulas. Monitoring patients for anastomic leaks requires knowing the type of surgical procedure performed, so that the anastomosis sites are identified. General signs of ananastomotic leak are pain, fever, and pleural effusion. A leak of a thoracic anastomosis is indicated by excessive bloody or purulent drainage from the chest tube. A pneumothorax or hydrothorax canal also indicate a thoracic leak.4 Indications of an intestinal leak are diffuse abdominal pain, which is worse with movement, distention, nausea, vomiting, and decreasedor absent bowel sounds.6 Maintaining patency of nasogastric tubes and/or gastrostomy tubes will help to prevent the build-up of tension and pressure at the anastomotic site.3 The tubes should never be manipulated except by a physician.1 The use of a gastrostomy tube holder willreduce liklihood of patient tampering. Thepatient is maintained on strict NPO status until the seventh postop day, when a Gastografin swallow is performed. The Gastrografin will reveal an anastomotic leak, if one is present. If there is no leak, then the tube will be removed and oral feedings will be started. The chest tube will be removed when drainage has decreased and no evidence of a leak is found.1 A fistula canal so occur during the postop period. Indications of fistula formation are fever, tachycardia, tachypnea, and malaise. Tracheoesophageal fistula formation may be indicated by pneumonia or respiratory difficulty. Signs of a cutaneous fistula include a suture-line inflammation, drainage, edema, and necrosis.4 Prevention of fistula formation is the same as for anastomic leaks. Respiratory complications can be reduced or prevented with early ambulation,

aggressive pulmonary care, and antibiotic therapy. Patients with esophageal cancer typically enter surgery in a poor nutritional state. Enteral feedings via the jejunostomy tube should be started as soon as possible postop. Enteral feedings are preferable, since they maintain gastrointestinal integrity and reduce translocation of bacteria.1 Because of their poor nutritional status, patients are more susceptible to infections and should be monitored closely.Nursing assessment includes pulmonary auscultation and monitoring vital signs, edema, redness, or drainage from the suture line. The ability to inspect the wound site without causing additional trauma can be achieved by using a tape-free method to secure thewound, such as a secondary wound dressing and a holder with Velcro closures. If a segment of the colon is used to reconstruct or to bypass the esophagus, pulmonary hygiene, prevention of infection, reflux, control of odor, and nutrition are nursing priorities. Postoperative nursing care of the patient with esophagogastrectomy includes anticipation and prevention of reflux aspiration.5 The head of the bed should be elevated at all times. The patient should be upright when ingesting any foods and liquids and for 20-30 minutes after eating. Small, frequent meals are better tolerated than large meals. Patients should be taught to avoid bending at the waist or any activity that would increase intra-abdominal pressure.

Complications
Esophageal cancer readily extends through the thin esophageal wall due to the absence of a serosa to invade adjacent structures. The vital mediastinal structures adjacent to the esophagus include the trachea, the right and left bronchi, the aortic arch and descending aorta, the pericardium, the pleura, and the spine. Tumor infiltration into these structures accounts for the most serious and, sometimes, life-threatening complications of esophageal cancer. Most complications due to esophageal cancer are attributed to luminal obstruction and local tumor invasion. Patients often subconsciously adjust their diets to soft or liquid foods to avoid solid food dysphagia. The progressive inability to swallow solids leads to weight loss and nutritional deficiencies. Solid food impaction can result when there is severe stenosis, requiring endoscopic intervention for disimpaction. Regurgitation of food or oral secretions may also occur in the setting of significant luminal obstruction. Halitosis may be present due to food stasis and regurgitation. Pulmonary complications from aspiration include pneumonia and pulmonary abscess. The tumor mass may cause compression and obstruction of the tracheobronchial tree, leading to dyspnea, chronic cough, and at times postobstructive pneumonia. Esophago airway fistula may develop with tumor invasion of the trachea or bronchus. Airway fistulas are severely debilitating and are associated with significant mortality owing to the high risk of pulmonary complications such as pneumonia and abscess.

Although the aortic arch and descending aorta lie adjacent to the esophagus, extension into these structures is less frequent than airway invasion. Erosion through the aortic wall can result in severe hemorrhage and is often fatal. Tumor ingrowth of the pericardium has been reported as an infrequent cause of arrhythmias and conduction abnormalities. Pleural effusions are usually small, but may signify pleural invasion when large effusions are present.

Consideration for older adults

Chemoradiotherapy (CRT) is an effective treatment and does not present major toxicity for elderly patients with esophageal cancer, according to the results of a study released in an early online publication of the November issue of the British Journal of Cancer.[1] The esophagus is a tube that carries food from the mouth to the stomach. Esophageal cancer is relatively uncommon, but is one of the most aggressive and deadly forms of cancer. It is the eighth most common cancer, but the sixth cause of cancer death worldwide. Standard treatment for esophageal cancer may include chemotherapy, radiation therapy, and/or surgery. Historically, treatment of elderly patients with esophageal cancer has been challenging because it is believed that the elderly cannot tolerate the side effects associated with treatment. However, there is very little data regarding the outcomes and side effects associated with CRT in elderly patients with locally advanced esophageal cancer. Researchers in the UK conducted a study in 109 patients over the age of 70 with locally advanced esophageal cancer. The patients received CRT, consisting of radiation plus cisplatinbased chemotherapy. In this study, 38.5% of patients received the planned treatment, while 53.2% required a dose adjustment. Severe side effects (grade 3) occurred in 23.8% of patients, with 16.5% of patients being hospitalized. Six to eight weeks after completing CRT, patients underwent endoscopy (examination of the esophagus through a long, lighted tube) and computed tomography scan (a series of detailed pictures of areas inside the body taken from different angles). The results indicated that 57.8% of patients experienced a complete response (total disappearance of cancer in response to treatment) and the two-year survival was 35.5% The researchers concluded that CRT was an effective treatment for elderly patients, with no major side effects. In addition, they noted that their results showed that CRT in elderly patients produced similar response rates and overall survival as typically reported in younger patients treated with the same regimen.