Tropical diseases are diseases that are prevalent in or unique to tropical and subtropical regions. These diseases are less prevalent in temperate climates, due in part to the occurrence of a cold season, which controls the insect population by forcing hibernation during the cold season.Insects such as mosquitoes and flies are by far the most common disease carrier or "vector". These insects may carry a parasite, bacterium or virus that is infectious to humans and animals. Most often disease is transmitted by an insect "bite", which causes transmission of the infectious agent through subcutaneous blood exchange. Vaccines are not available for any of the diseases listed here.
Some of the strategies for controlling tropical diseases include:
* Draining wetlands to reduce insect populations
* The application of insecticides (or to a lesser extent, perhaps insect repellents) to strategic surfaces such as: clothing, skin, buildings, insect habitats, and bed nets.
* The use of a mosquito net over a bed (also known as a "bed net"), to reduce nighttime transmission, since tropical mosquitoes often feed only at night.
* Use of water wells, and/or water filtration, water filters, or water treatment with water tablets to produce drinking water free of parasites.
* Development and use of vaccines to promote disease immunity
* Funding and subsidizing the use of medicinal treatments to treat disease after infection
* Assisting with economic development in endemic regions. For example by providing microloans to enable investments in more efficient and productive agriculture. This in turn can help subsistence farming to become more profitable, and these profits can be used by local populations for disease prevention and treatment, with the added benefit of reducing the poverty rate.[3]
Human exploration of tropical rainforests, deforestation, raising immigration and increased international air travel and other tourism to tropical regions has led to an increased incidence of such diseases.
Relation of climate to tropical diseases
The called "exotic" diseases in the tropics has long been noted both by travelers, explorers, etc., as well as by physicians. One obvious reason is that the hot climate present during all the year and the larger volume of rains directly affect the formation of breeding grounds, the larger number and variety of natural reservoirs and animal diseases that can be transmitted to humans (zoonosis), the largest number of possible insect vectors of diseases. It is possible also that higher temperatures may favor the replication of pathogenic agents both inside and outside biological organisms. Socio-economic factors may be also in operation, since most of the poorest nations of the world are in the tropics. Tropical countries like Brazil, which have improved their socio-economic situation and invested in hygiene, public health and the combat of transmissible diseases have achieved dramatic results in relation to the elimination or decrease of many endemic tropical diseases in their territory.[citation needed]
Climate change, and global warming caused by the greenhouse effect, and the resulting increase in global temperatures, are causing tropical diseases and vectors to spread to higher altitudes in mountainous regions, and to higher latitudes that were previously spared, such as the Southern United States, the Mediterranean area, etc
Thursday, October 2, 2008
Metastatic Brain Tumors
Summary
Metastatic disease can be viewed as two simultaneously occurring diseases. Brain cancer and systemic cancer (elsewhere in the body). Each disease has quite different mortality rates. Untreated brain metastases are rapidly fatal, while systemic cancer may not be.
Metastatic brain disease is a focal disease and focal control of the tumor is paramount to patient survival. The approach in the past has been to treat metastatic brain disease as a whole brain disease, with whole brain radiation (WBR). Because of poor local control of tumor growth when treated solely by WBR, brain metastases in the past were rapidly lethal. Therefore patients with brain metastases did not benefit from many advances in cancer therapy (immuno therapy, chemo therapy, conformal radiotherapy etc.) because these therapies do no effectively reach brain metastases and individuals died quickly from neurological progression.
Now neurological progression can be effectively controlled in most patients harboring a few intracranial metastases with aggressive focal treatment (surgery or radiosurgery) in combination with WBR. WBR can be given immediately following focal treatment or at the time of recurrence. Control can be extended by frequent MR surveillance of the brain and radiosurgical treatment of new metastases months or years later. With control of intracranial disease, advances in cancer therapy will prolong survival, since most patients now succumb later to systemic, rather than intracranial disease. Aggressive, focal treatment is only beneficial in patients with controlled or no systemic disease and independent health (Karnofsky Performance Score (KPS)> 70). Age is also a determinant of outcome, with better outcomes in individuals less than 60 years old.
Introduction
Tumors of the brain can be divided into two categories. Tumors which arise from the tissues of the brain, its blood vessels, bony and membrane coverings are termed primary brain tumors. These primary tumors may be benign or malignant. Examples of these are glioblastomas, meningiomas, pituitary tumors and acoustic neuromas. Secondary brain tumors arise from malignant sources outside the brain may invade the intracranial cavity, usually as blood- borne metastases. Common sources of these malignant tumors are carcinoma of the lungs, breast, and skin (melanoma). There are more than 1,200,000 new cases and 130,000 deaths from brain metastases each year.
Recent outcome studies of the various treatments for brain metastasis have enlarged our understanding of the management of this disorder. Untreated, patients with metastatic brain tumors may survive only a few weeks, and the addition of steroids to treat brain swelling may add a month to survival. The sensitivity of the brain to external radiation and the failure of chemotherapeutic agents to effectively penetrate the brain greatly hinders treatment.
The development of optimal treatment strategies for brain metastases has been difficult for two reasons. Virtually all studies have been retrospective reviews of various treatment paradigms. With out prospective, controlled studies no realistic comparisons of treatment can be made. Secondly there are many factors which influence the outcome of treatment, such as patient age, disability status, tumor origin, extent of disease outside the brain, tumor location and prior treatment. Controlling for these multiple risk factors has made the design of scientifically controlled studies a daunting task.
Recent Results of Common Treatments for
Brain Metastases
Whole Brain Radiation Therapy Alone:
For nearly 50 years radiologists have appreciated the fact that fractionated external beam brain radiation is effective in the treatment of brain metastases. During the 1970's the Radiation Therapy Oncology Group (RTOG) carried out a number of studies to determine an effective dose of whole brain radiation in the treatment of brain metastases. Comparing various total doses and dose fractions (radiation therapy is given in small doses each day until an effective total dose is achieved) it was determined that 30 Gy given over 10 to 15 fractions was as effective as increasingly greater doses. Total doses over 60 Gy to the brain bring higher risks of brain damage, so it is best to limit total brain radiation.
More recent RTOG studies of hyperfractionation...using 1.6 Gy doses twice a day until total doses of 48 to 70.4 Gy are reached show significant advances in intracranial control, survival and neurologic improvement. This is strong evidence that the control of intracranial disease is dose related. Also the effects of radiation on the brain are accumulative, so that further treatment at a later time adds to the possibility of injuring normally functioning brain tissue. Unfortunately whole brain radiotherapy only increases median survival from a few weeks to 15 to 20 weeks and a large number of patients die from neurologic progression of disease. A high local recurrence rate of 30 to 60%, in spite of WGR, contributes to this limited response to external, fractionated radiation therapy.
Surgery Alone:
Surgery for metastatic deposits is an appealing treatment, but only applicable in a minority of patients. Less than 1/2 of patients with metastatic disease have a single tumor and about 1/2 of these patients have surgically accessible tumors. The remainder of patients have many tumors or deeply-situated deposits which increases the surgical complexity if not the risk.
There are few studies of the utility of surgery as the only treatment for brain metastases. A retrospective study by Smally and others found a 21% intracranial relapse rate when surgery was used in conjunction with whole brain radiation (WBR), and an 85% intracranial relapse rate in patients who only had surgery only. In a important and recent prospective study, Patchell et al. compared the results of surgery alone to surgery + WBR. Ninety-five patients had their single brain metastasis removed. One half of the patients under went WBR, while the other half had no further treatment. Both groups were comparable in terms of various risk factors for treatment outcome. Similar to Smally's findings the intracranial relapse rate was 18% in the radiated group and 70% in the non-radiated group. Patients treated by surgery alone had high rates of local recurrence (46 %) and distant recurrence (37 %) and 44 % died of neurological progressions. It was clear the local control by surgery depends on the addition of WBR. Adjuvant WBR reduced the rate of recurrence of the tumor at the surgical site (46% v. 10%), and reduced the chance that additional metastases will appear in other areas of the brain (37% v. 14%). WBR reduced the potential that the patient will die from brain disease (44% v. 14%). There was no significant difference in survival or functional independence between the groups.
Current image guidance neurosurgical technology marries the MR or CT image with the patient's anatomy in the operating room. This advance allows the surgeon to craft a small and accurate bony opening to expose and remove brain tumors with much precision.
Surgery Plus Whole Brain Radiation Therapy:
In the 1990 study from Lexington, Kentucky group, Patchell et al. sought to compare the outcome of treatment by whole brain radiation (WBR) to WBR + surgical removal. They found recurrence at the original metastasis location was reduced in the WBR+surgical group (20%) compared to the WBR only group (52%). One would expect no difference in the rate of subsequent metastases elsewhere in the brain (20% and 13% was not significant). Importantly, the patients survived longer following surgery (median survival 40 weeks v. 15 weeks), and they had a better quality of life reflected in a longer period of functional independence. This important study first showed the value of focal treatment (surgery) in addition to WBR in improving outcome.
These results were confirmed and extended in a study from the Hague, Netherlands. Nordik and coworkers also compared the outcome in patients treated with WBR or WBR + surgery. This was a prospective study with individuals with single brain metastases randomly assigned to each treatment group after stratification for certain risk factors. Again the operated patients survived longer (median survival 40 weeks v. 24 weeks) with a better quality of life. In this study only individuals with inactive or controlled systemic disease benefited from brain surgery in addition to WBR: 52 week median survival v. 28 weeks. Those with uncontrolled disease elsewhere in the body did not benefit ( 20 week medial survival for both groups). There were 13 complications, 4 serious in the operated group.
Metastatic disease can be viewed as two simultaneously occurring diseases. Brain cancer and systemic cancer (elsewhere in the body). Each disease has quite different mortality rates. Untreated brain metastases are rapidly fatal, while systemic cancer may not be.
Metastatic brain disease is a focal disease and focal control of the tumor is paramount to patient survival. The approach in the past has been to treat metastatic brain disease as a whole brain disease, with whole brain radiation (WBR). Because of poor local control of tumor growth when treated solely by WBR, brain metastases in the past were rapidly lethal. Therefore patients with brain metastases did not benefit from many advances in cancer therapy (immuno therapy, chemo therapy, conformal radiotherapy etc.) because these therapies do no effectively reach brain metastases and individuals died quickly from neurological progression.
Now neurological progression can be effectively controlled in most patients harboring a few intracranial metastases with aggressive focal treatment (surgery or radiosurgery) in combination with WBR. WBR can be given immediately following focal treatment or at the time of recurrence. Control can be extended by frequent MR surveillance of the brain and radiosurgical treatment of new metastases months or years later. With control of intracranial disease, advances in cancer therapy will prolong survival, since most patients now succumb later to systemic, rather than intracranial disease. Aggressive, focal treatment is only beneficial in patients with controlled or no systemic disease and independent health (Karnofsky Performance Score (KPS)> 70). Age is also a determinant of outcome, with better outcomes in individuals less than 60 years old.
Introduction
Tumors of the brain can be divided into two categories. Tumors which arise from the tissues of the brain, its blood vessels, bony and membrane coverings are termed primary brain tumors. These primary tumors may be benign or malignant. Examples of these are glioblastomas, meningiomas, pituitary tumors and acoustic neuromas. Secondary brain tumors arise from malignant sources outside the brain may invade the intracranial cavity, usually as blood- borne metastases. Common sources of these malignant tumors are carcinoma of the lungs, breast, and skin (melanoma). There are more than 1,200,000 new cases and 130,000 deaths from brain metastases each year.
Recent outcome studies of the various treatments for brain metastasis have enlarged our understanding of the management of this disorder. Untreated, patients with metastatic brain tumors may survive only a few weeks, and the addition of steroids to treat brain swelling may add a month to survival. The sensitivity of the brain to external radiation and the failure of chemotherapeutic agents to effectively penetrate the brain greatly hinders treatment.
The development of optimal treatment strategies for brain metastases has been difficult for two reasons. Virtually all studies have been retrospective reviews of various treatment paradigms. With out prospective, controlled studies no realistic comparisons of treatment can be made. Secondly there are many factors which influence the outcome of treatment, such as patient age, disability status, tumor origin, extent of disease outside the brain, tumor location and prior treatment. Controlling for these multiple risk factors has made the design of scientifically controlled studies a daunting task.
Recent Results of Common Treatments for
Brain Metastases
Whole Brain Radiation Therapy Alone:
For nearly 50 years radiologists have appreciated the fact that fractionated external beam brain radiation is effective in the treatment of brain metastases. During the 1970's the Radiation Therapy Oncology Group (RTOG) carried out a number of studies to determine an effective dose of whole brain radiation in the treatment of brain metastases. Comparing various total doses and dose fractions (radiation therapy is given in small doses each day until an effective total dose is achieved) it was determined that 30 Gy given over 10 to 15 fractions was as effective as increasingly greater doses. Total doses over 60 Gy to the brain bring higher risks of brain damage, so it is best to limit total brain radiation.
More recent RTOG studies of hyperfractionation...using 1.6 Gy doses twice a day until total doses of 48 to 70.4 Gy are reached show significant advances in intracranial control, survival and neurologic improvement. This is strong evidence that the control of intracranial disease is dose related. Also the effects of radiation on the brain are accumulative, so that further treatment at a later time adds to the possibility of injuring normally functioning brain tissue. Unfortunately whole brain radiotherapy only increases median survival from a few weeks to 15 to 20 weeks and a large number of patients die from neurologic progression of disease. A high local recurrence rate of 30 to 60%, in spite of WGR, contributes to this limited response to external, fractionated radiation therapy.
Surgery Alone:
Surgery for metastatic deposits is an appealing treatment, but only applicable in a minority of patients. Less than 1/2 of patients with metastatic disease have a single tumor and about 1/2 of these patients have surgically accessible tumors. The remainder of patients have many tumors or deeply-situated deposits which increases the surgical complexity if not the risk.
There are few studies of the utility of surgery as the only treatment for brain metastases. A retrospective study by Smally and others found a 21% intracranial relapse rate when surgery was used in conjunction with whole brain radiation (WBR), and an 85% intracranial relapse rate in patients who only had surgery only. In a important and recent prospective study, Patchell et al. compared the results of surgery alone to surgery + WBR. Ninety-five patients had their single brain metastasis removed. One half of the patients under went WBR, while the other half had no further treatment. Both groups were comparable in terms of various risk factors for treatment outcome. Similar to Smally's findings the intracranial relapse rate was 18% in the radiated group and 70% in the non-radiated group. Patients treated by surgery alone had high rates of local recurrence (46 %) and distant recurrence (37 %) and 44 % died of neurological progressions. It was clear the local control by surgery depends on the addition of WBR. Adjuvant WBR reduced the rate of recurrence of the tumor at the surgical site (46% v. 10%), and reduced the chance that additional metastases will appear in other areas of the brain (37% v. 14%). WBR reduced the potential that the patient will die from brain disease (44% v. 14%). There was no significant difference in survival or functional independence between the groups.
Current image guidance neurosurgical technology marries the MR or CT image with the patient's anatomy in the operating room. This advance allows the surgeon to craft a small and accurate bony opening to expose and remove brain tumors with much precision.
Surgery Plus Whole Brain Radiation Therapy:
In the 1990 study from Lexington, Kentucky group, Patchell et al. sought to compare the outcome of treatment by whole brain radiation (WBR) to WBR + surgical removal. They found recurrence at the original metastasis location was reduced in the WBR+surgical group (20%) compared to the WBR only group (52%). One would expect no difference in the rate of subsequent metastases elsewhere in the brain (20% and 13% was not significant). Importantly, the patients survived longer following surgery (median survival 40 weeks v. 15 weeks), and they had a better quality of life reflected in a longer period of functional independence. This important study first showed the value of focal treatment (surgery) in addition to WBR in improving outcome.
These results were confirmed and extended in a study from the Hague, Netherlands. Nordik and coworkers also compared the outcome in patients treated with WBR or WBR + surgery. This was a prospective study with individuals with single brain metastases randomly assigned to each treatment group after stratification for certain risk factors. Again the operated patients survived longer (median survival 40 weeks v. 24 weeks) with a better quality of life. In this study only individuals with inactive or controlled systemic disease benefited from brain surgery in addition to WBR: 52 week median survival v. 28 weeks. Those with uncontrolled disease elsewhere in the body did not benefit ( 20 week medial survival for both groups). There were 13 complications, 4 serious in the operated group.
Achalasia
Achalasia, also known as esophageal achalasia, achalasia cardiae, cardiospasm, dyssynergia esophagus, and esophageal aperistalsis, is an esophageal motility disorder: The smooth muscle layer of the esophagus loses normal peristalsis (muscular ability to move food down the esophagus), and the lower esophageal sphincter (LES) fails to relax properly in response to swallowing.[1]
Achalasia is characterized by difficulty swallowing, regurgitation, and sometimes chest pain. Diagnosis is reached with esophageal manometry and barium swallow X-ray studies. Various treatments are available, although none cure the condition completely. Certain medications or Botox may be used in some cases, but more permanent relief is brought by esophageal dilatation and surgical cleaving of the muscle (Heller myotomy).
The most common form is primary achalasia, which has no known underlying cause. However, a small proportion occurs as a secondary result of other conditions, such as esophageal cancer or Chagas disease (an infectious disease common in South America).[2] Achalasia affects about one person in 100,000 per year.
Signs and symptoms
* Dysphagia (difficulty in swallowing) which becomes worse over time, generally involving both liquids and solids.
* Regurgitation of undigested food.
* Coughing, especially when lying in a horizontal position. Food and liquid, including saliva, are retained in the esophagus and may be inhaled into the lungs (aspiration),[2] potentially leading to aspiration pneumonia.
* Some patients experience chest pains resembling heartburn or pressure on the sternum.
* Most patients, but not all, have weight loss due to inadequate nutrient intake.
Diagnosis
Due to the similarity of symptoms, achalasia can be mistaken for more common disorders such as gastroesophageal reflux disease (GERD), hiatus hernia, and even psychosomatic disorders.
Specific tests for achalasia are barium swallow and esophageal manometry. In addition, a CT scan of the chest and endoscopy of the esophagus, stomach and duodenum (esophagogastroduodenoscopy or EGD), with or without endoscopic ultrasound, are typically performed to rule out the possibility of cancer.[2] The internal tissue of the esophagus generally appears normal in endoscopy, although a "pop" may be observed as the scope is passed through the non-relaxing lower esophageal sphincter with some difficulty.
Barium Swallow
The patient swallows a barium solution, with continuous fluoroscopy (X-ray recording) to observe the flow of the fluid through the esophagus. Normal peristaltic movement of the esophagus is not seen. There is acute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a "bird's beak" or "rat's tail" appearance. The esophagus above the narrowing is often dilated (enlarged) to varying degrees as the esophagus is gradually stretched, and it may contain food debris.[2] An air-fluid margin is often seen over the barium column due to the lack of peristalsis. A five-minute timed barium swallow can provide a useful benchmark to measure the effectiveness of treatment.
Esophageal manometry
Because of its sensitivity, manometry (esophageal motility study) is considered the key test for establishing the diagnosis. A thin tube is inserted through the nose, and the patient is instructed to swallow several times. The probe measures muscle contractions in different parts of the esophagus during the act of swallowing.
[edit] Biopsy
Biopsy, the removal of a tissue sample during endoscopy, is not typically necessary in achalasia, but if performed shows hypertrophied musculature and absence of certain nerve cells of the myenteric plexus, a network of nerve fibers that controls esophageal peristalsis.
Treatment
Medication
Drugs that reduce LES pressure may be useful, especially as a way to buy time while waiting for surgical treatment. These include calcium channel blockers such as nifedipine, and nitrates such as isosorbide dinitrate and nitroglycerin. However, many patients experience unpleasant side effects such as headache and swollen feet, and these drugs often stop helping after several months.
Botulinum toxin (Botox) may be injected into the lower esophageal sphincter to paralyze the muscles holding it shut. As in the case of cosmetic Botox, the effect is only temporary, and symptoms return relatively quickly in most patients. Botox injections cause scarring in the sphincter which may increase the difficulty of later Heller myotomy. This therapy is only recommended for patients who cannot risk surgery, such as elderly persons in poor health.[2]
Pneumatic dilatation
In balloon (pneumatic) dilation, also called dilatation, the muscle fibers are stretched and slightly torn by forceful inflation of a balloon placed inside the lower esophageal sphincter. Gastroenterologists who specialize in achalasia and have performed many of these forceful balloon dilations achieve better results and fewer perforations. There is always a small risk of a perforation which must be fixed by surgery right away. This treatment causes some scarring which may increase the difficulty of Heller myotomy if this surgery is needed later. Gastroesophageal reflux (GERD) occurs after pneumatic dilation in some patients. Pneumatic dilation is most effective on the long term in patients over the age of 40; the benefits tend to be shorter-lived in younger patients. It may need to be repeated with larger balloons for maximum effectiveness.[3]
Surgery
Heller myotomy helps 90% of achalasia patients. It can usually be performed by a keyhole approach, or laparoscopically.The myotomy is a lengthwise cut along the esophagus, starting above the LES and extending down onto the stomach a little way. The esophagus is made of several layers, and the myotomy only cuts through the outside muscle layers which are squeezing it shut, leaving the inner muscosal layer intact. A partial fundoplication or "wrap" is generally added in order to prevent excessive reflux, which can cause serious damage to the esophagus over time. After surgery, patients should keep to a soft diet for several weeks to a month, avoiding foods that can aggravate reflux.
Alternative medicine
Temporary improvement of achalasia symptoms in some cases has been reported with acupuncture, traditional Chinese herbal medicine, and relaxation techniques.[citation needed]
Lifestyle changes
Both before and after successful treatment, achalasia patients may need to eat slowly, chew very well, drink plenty of water with meals, and avoid eating near bedtime. Raising the head of the bed or sleeping with a wedge pillow promotes emptying of the esophagus by gravity. After surgery or pneumatic dilatation, proton pump inhibitors can help prevent reflux damage by inhibiting gastric acid secretion; and foods that can aggravate reflux, including ketchup, citrus, chocolate, mint, alcohol, and caffeine, may need to be avoided.
Follow-up
Follow-up monitoring: Even after successful treatment of achalasia, swallowing may still deteriorate over time. The esophagus should be checked every year or two with a timed barium swallow because some may need pneumatic dilations, a repeat myotomy, or even esophagectomy after many years. In addition, some physicians recommend pH testing and endoscopy to check for reflux damage, which may lead to a premalignant condition known as Barrett's esophagus or a stricture if untreated.
Achalasia is characterized by difficulty swallowing, regurgitation, and sometimes chest pain. Diagnosis is reached with esophageal manometry and barium swallow X-ray studies. Various treatments are available, although none cure the condition completely. Certain medications or Botox may be used in some cases, but more permanent relief is brought by esophageal dilatation and surgical cleaving of the muscle (Heller myotomy).
The most common form is primary achalasia, which has no known underlying cause. However, a small proportion occurs as a secondary result of other conditions, such as esophageal cancer or Chagas disease (an infectious disease common in South America).[2] Achalasia affects about one person in 100,000 per year.
Signs and symptoms
* Dysphagia (difficulty in swallowing) which becomes worse over time, generally involving both liquids and solids.
* Regurgitation of undigested food.
* Coughing, especially when lying in a horizontal position. Food and liquid, including saliva, are retained in the esophagus and may be inhaled into the lungs (aspiration),[2] potentially leading to aspiration pneumonia.
* Some patients experience chest pains resembling heartburn or pressure on the sternum.
* Most patients, but not all, have weight loss due to inadequate nutrient intake.
Diagnosis
Due to the similarity of symptoms, achalasia can be mistaken for more common disorders such as gastroesophageal reflux disease (GERD), hiatus hernia, and even psychosomatic disorders.
Specific tests for achalasia are barium swallow and esophageal manometry. In addition, a CT scan of the chest and endoscopy of the esophagus, stomach and duodenum (esophagogastroduodenoscopy or EGD), with or without endoscopic ultrasound, are typically performed to rule out the possibility of cancer.[2] The internal tissue of the esophagus generally appears normal in endoscopy, although a "pop" may be observed as the scope is passed through the non-relaxing lower esophageal sphincter with some difficulty.
Barium Swallow
The patient swallows a barium solution, with continuous fluoroscopy (X-ray recording) to observe the flow of the fluid through the esophagus. Normal peristaltic movement of the esophagus is not seen. There is acute tapering at the lower esophageal sphincter and narrowing at the gastro-esophageal junction, producing a "bird's beak" or "rat's tail" appearance. The esophagus above the narrowing is often dilated (enlarged) to varying degrees as the esophagus is gradually stretched, and it may contain food debris.[2] An air-fluid margin is often seen over the barium column due to the lack of peristalsis. A five-minute timed barium swallow can provide a useful benchmark to measure the effectiveness of treatment.
Esophageal manometry
Because of its sensitivity, manometry (esophageal motility study) is considered the key test for establishing the diagnosis. A thin tube is inserted through the nose, and the patient is instructed to swallow several times. The probe measures muscle contractions in different parts of the esophagus during the act of swallowing.
[edit] Biopsy
Biopsy, the removal of a tissue sample during endoscopy, is not typically necessary in achalasia, but if performed shows hypertrophied musculature and absence of certain nerve cells of the myenteric plexus, a network of nerve fibers that controls esophageal peristalsis.
Treatment
Medication
Drugs that reduce LES pressure may be useful, especially as a way to buy time while waiting for surgical treatment. These include calcium channel blockers such as nifedipine, and nitrates such as isosorbide dinitrate and nitroglycerin. However, many patients experience unpleasant side effects such as headache and swollen feet, and these drugs often stop helping after several months.
Botulinum toxin (Botox) may be injected into the lower esophageal sphincter to paralyze the muscles holding it shut. As in the case of cosmetic Botox, the effect is only temporary, and symptoms return relatively quickly in most patients. Botox injections cause scarring in the sphincter which may increase the difficulty of later Heller myotomy. This therapy is only recommended for patients who cannot risk surgery, such as elderly persons in poor health.[2]
Pneumatic dilatation
In balloon (pneumatic) dilation, also called dilatation, the muscle fibers are stretched and slightly torn by forceful inflation of a balloon placed inside the lower esophageal sphincter. Gastroenterologists who specialize in achalasia and have performed many of these forceful balloon dilations achieve better results and fewer perforations. There is always a small risk of a perforation which must be fixed by surgery right away. This treatment causes some scarring which may increase the difficulty of Heller myotomy if this surgery is needed later. Gastroesophageal reflux (GERD) occurs after pneumatic dilation in some patients. Pneumatic dilation is most effective on the long term in patients over the age of 40; the benefits tend to be shorter-lived in younger patients. It may need to be repeated with larger balloons for maximum effectiveness.[3]
Surgery
Heller myotomy helps 90% of achalasia patients. It can usually be performed by a keyhole approach, or laparoscopically.The myotomy is a lengthwise cut along the esophagus, starting above the LES and extending down onto the stomach a little way. The esophagus is made of several layers, and the myotomy only cuts through the outside muscle layers which are squeezing it shut, leaving the inner muscosal layer intact. A partial fundoplication or "wrap" is generally added in order to prevent excessive reflux, which can cause serious damage to the esophagus over time. After surgery, patients should keep to a soft diet for several weeks to a month, avoiding foods that can aggravate reflux.
Alternative medicine
Temporary improvement of achalasia symptoms in some cases has been reported with acupuncture, traditional Chinese herbal medicine, and relaxation techniques.[citation needed]
Lifestyle changes
Both before and after successful treatment, achalasia patients may need to eat slowly, chew very well, drink plenty of water with meals, and avoid eating near bedtime. Raising the head of the bed or sleeping with a wedge pillow promotes emptying of the esophagus by gravity. After surgery or pneumatic dilatation, proton pump inhibitors can help prevent reflux damage by inhibiting gastric acid secretion; and foods that can aggravate reflux, including ketchup, citrus, chocolate, mint, alcohol, and caffeine, may need to be avoided.
Follow-up
Follow-up monitoring: Even after successful treatment of achalasia, swallowing may still deteriorate over time. The esophagus should be checked every year or two with a timed barium swallow because some may need pneumatic dilations, a repeat myotomy, or even esophagectomy after many years. In addition, some physicians recommend pH testing and endoscopy to check for reflux damage, which may lead to a premalignant condition known as Barrett's esophagus or a stricture if untreated.
Schatzki ring
A Schatzki ring or Schatzki-Gary ring is a ring found in the lower part of the esophagus that can cause difficulty swallowing. The ring is made up of mucosal tissue (which lines the esophagus) or muscular tissue.Patients with Schatzki rings can develop intermittent dysphagia (difficulty swallowing), or, more seriously, a completely blocked esophagus. The ring is named after the American physician Richard Schatzki.
The term "esophageal ring" is a more general term. A "Schatzki ring" is equivalent to an esophageal "B ring".An "A ring" refers to a ring at the esophagus/stomach junction.
Clinical presentation
Not all patients with Schatzki rings have symptoms; indeed, barium swallow tests of the esophagus will sometimes show Schatzki rings in patients who have no symptoms. When Schatzki rings cause symptoms, they usually result in episodic dysphagia with solid foods, or a sensation that the food "sticks" while swallowing. This particularly occurs if the food is not chewed thoroughly. Cases of complete obstruction have been called steakhouse syndrome: during a meal, there is a bolus obstruction of the esophagus with the foodstuff, resulting in acute crushing chest pain and dysphagia. Patients usually are able to regurgitate or force through the food material, but may need immediate treatment with endoscopy, which is the use of a specialized fibre-optic camera in order to remove the lodged food.This involves urgent endoscopy to locate the obstruction, followed by the insertion of devices to either pull the food out of the esophagus, or to push it into the stomach. The latter is usually done only with caution, or if the anatomy of the structures where the obstruction occurred is already known. Snares and forceps passed through the endoscope can be used for these purposes.
Diagnosis
When a patient has a suspect Schatzki ring, the physician can make the diagnosis by doing one of two tests: either an esophagogastroduodenoscopy or barium swallow. The endoscopy typically shows a ring within the lumen of the esophagus which can be of variable size. The ring is typically located a few centimetres above the gastro-esophageal junction, which joins the stomach and the esophagus. Schatzki rings can often resemble a related entity, called an esophageal web. Esophageal webs are similar in that they also contain extra mucosal tissue, but they do not completely encircle the esophagus.
Endoscopies and barium swallows done for other reasons often show evidence of Schatzki rings,meaning that many Schatzki rings are asymptomatic.
Two varieties of Schatzki rings have been described. The original description by Schatzki and Gary was of a ring of fibrous tissue seen on autopsy; this is the far less common type of Schatzki ring.[1] More commonly, the ring consists of the same mucosal tissue that lines the entire esophagus. Many hypotheses have been raised as to the cause of the Schatzki rings, but the cause is uncertain, and may be related to both congenital and acquired factors.
Treatment
If asymptomatic, there is evidence that Schatzki rings do not progress to cause symptoms, and no treatment is suggested.
Symptomatic Schatzki rings may be treated with esophageal dilatation, either using bougie or balloon dilators. These have been found to be equally effective.Bougie dilatation involves the passage of long dilating tubes of increasing size down the esophagus to stretch the area of narrowing. This is either done over a guidewire passed into the stomach by endoscopy (the Savary-Gillard system) or using mercury-weighted dilators (the Maloney system). This is usually done with intravenous sedation to ensure comfort. The duration of the effect of dilation varies between individuals, but may be from months to years. Dilation may need to be repeated if further narrowing at the site of the ring occurs over time.
After treatment with dilatation or endoscopic management of a bolus obstruction, there is often some trauma associated with the procedure. A short course of proton pump inhibitor therapy may be given to decrease stomach acid reflux into the esophagus, which may aggravate the area of trauma.
Disease
This is a blog dedicated to diseases.So far i have created three to four blogs on diseases.I suppose this is my fourth or fifth.Hope those who visit my blog get enough information on the diseases I post. Peace !!!
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