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The ingrown toenail is a common problem. Improper nail trimming in combination with chronic trauma from tight shoes often causes ingrown toenails.A spicule of the nail plate lacerates the soft tissue of the lateral nailfold and leads to painful irritation, inflammation, infection, and growth of excessive granulation tissue. Many treatments have been described, such as nail edge separation, partial matrix phenolization, and the classic wedge excision. These classic treatment modalities may lead to severe damage of the nailfold or to frequent relapses.
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Our goal was to find a treatment without producing severe nail matrix damage. Therefore, based on the technique of Wallace, Milne, and Andrew, we developed a new noninvasive therapy for ingrown toenails.
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With the patient under local anesthesia, the lateral edge of the nail plate including the spicule is splinted with a lengthwise-incised small flexible plastic tube, for example, a sterile drainage tube (diameter, 2.64 mm; Sterimed) normally used after cutaneous surgery for drainage. The splint has to be pushed proximally so that the nail spicule is totally covered by the split plastic tube.

The plastic tube is then attached with wound closure strips. After this procedure, the treated toe should be washed once daily with a solution (eg, povidone-iodine) for up to 3 or 4 weeks. The splinted spicule grows out without injuring the nailfold and the granulation tissue subsides. In addition, the patients must be advised about proper nail trimming.

Since 1993, we have successfully treated 62 patients (age, 15 months to 83 years) including patients with diabetes mellitus, AIDS, leukemia, chemotherapy, drug-induced immunodeficiency, and Buerger’s disease. So far, no recurrences or complications have occurred.

The nail splinting technique is simple and easy to perform and does not require any special equipment.
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In contrast to invasive treatments, our technique does not cause permanent damage to nail matrix or nailfold. After splinting, the patients experience instant relief of pain. Moreover, with the splint in place, patients are immediately able to resume walking in their usual shoes.

1 ) Non-medical Therapy

The so-called lifestyle modifications to treat GERD are generally successful only in patients with minimal reflux disease and include elevation of the head of the bed by 4 to 6 inches, avoiding eating meals within 3 hours of recumbency, avoiding cigarettes and alcohol, avoiding chocolate, fatty foods and carminatives; and avoiding NSAIDS.

2) H2 Antagonists

For patients who fail lifestyle modifications, the classic drugs most commonly used to treat GE reflux disease are the H2 antagonists. In people with symptoms of mild reflux, these agents are often successful. However, in patients with erosive esophagitis healing is only seen in approximately 58%. As a general rule, therefore, patients with severely symptomatic heartburn, particularly associated with reflux disease, more potent agents are generally needed.

3) Prokinetic Agents

It is attractive to treat GE reflux disease by preventing the actual occurrence of reflux rather than neutralizing gastric contents. Prokinetic agents attempt to do this by increasing esophageal peristalsis, increasing LES pressure, and accelerating gastric emptying. The two prokinetic agents commonly used in this country include cisapride and metoclopramide. The development of neurologic side effects secondary to metoclopramide has made this an unpopular agent. Cisapride is now used quite frequently and has a safety profile and efficacy that parallels
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H2 blockers. In addition, it may be used with H2 blockers in a synergistic fashion. Again, patients with severe heartburn, especially when associated with erosive esophagitis do not do well with this agent. Additionally, the use of cisapride is limited by the fact that it is dosed most commonly four times daily.

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4) Proton Pump Inhibitors
Protonix – helps to control NIGHTTIME heartburn and other symptoms associated with erosive Gastroesophageal Reflux Disease (GERD).
The advent of proton pump inhibitors (omeprazole and lansoprazole) has been the major medical development in reflux disease in recent years. In essentially all patients with symptomatic reflux disease or erosive esophagitis, symptomatic relief and endoscopic healing of the esophageal mucosa can be achieved. Additionally, it was shown by Klinkenberg-Knoll (1994) that if the dose of the drug is increased to 40 mg daily, healing can be maintained in essentially all patients. The acceptance of this drug was delayed due to concerns about potential carcinogenic effects. However, despite widespread use of this drug in numerous patients in the United States and abroad, no data to support this are present and so use of these agents for indefinite periods of time is quickly gaining favor among gastroenterologists and internists.

5) Anti-Reflux Surgery

With the development of new proton pump inhibitors which provide safe and effective therapy to almost all patients, the role of surgery which had previously been limited to refractory patients came into question. Enthusiasm for surgery peaked with the development of laparoscopic techniques for performing Nissen fundoplication as well as a variety of other anti-reflux operations. Most patients with GE reflux disease will decide to remain on medical therapy rather than consider surgical therapy. However, in patients with severe symptoms who are unhappy with the prospect of lifelong medical therapy, surgery should certainly be explored as an option. Before surgery is performed, the presence of adequate peristalsis in the esophageal body must be demonstrated with esophageal motility studies and the diagnosis of GERD must be confirmed with 24 hour pH testing.

Angina-like non-cardiac chest pain of esophageal origin was proposed by Hippocrates. For many years the concept of “esophageal spasm” has held its place in the medical literature although documenting consistent esophageal motility disorders in these patients has been difficult. Recent work by Richter et al has demonstrated that up to 50% of patients with anginal-like chest pain and negative cardiac catheterizations in fact have GE reflux disease, and certainly a trial of proton pump inhibitor therapy is warranted in patients with anginal-like pain and negative cardiac workups.

The extra-esophageal manifestations of GE reflux disease are now being more frequently recognized and treated. These manifestations include ENT manifestations including reflux laryngitis, laryngeal stenosis, laryngeal carcinoma, chronic hoarseness, chronic cough and globus sensation.

Pulmonary manifestations include asthma, chronic cough, aspiration pneumonia and pulmonary fibrosis.

The association between GE reflux disease and chronic pulmonary disease has been speculated upon for many years. The pathophysiology for this connection remains poorly understood and is complicated by the fact that many of the treatments for patients with chronic lung disease and the lung disease itself can exacerbate GE reflux disease.

The two most commonly proposed theories include a neural reflex caused by acid reflux into the distal esophagus versus micro-aspiration of tiny amounts of acid into the tracheobronchial tree with resultant bronchospasm and/or pulmonary parenchymal damage. At present, there is more evidence supporting the micro-aspiration theory. Treatment of pulmonary complications of GERD remains the same as for other forms of GERD.

As commonly used, Barrett’s esophagus now refers to the presence of specialized intestinal metaplasia in the distal esophagus. It is only when intestinal type mucosa associated with goblet cells is seen that we use the term Barrett’s esophagus. There has been an enormous surge in interest in Barrett’s esophagus due to the marked increase in incidence in adenocarcinoma of the GE junction of which Barrett’s esophagus is felt to be the predisposing condition. The risk of developing esophageal carcinoma in a patient with Barrett’s esophagus remains a subject of great controversy. Depending on the series, the prevalence of carcinoma has ranged between 4% and 45%. Recent studies demonstrate that carcinoma will develop in patients with established Barrett’s esophagus in one patient out of 80 to one patient out of 450 per year. Therefore, although the risk of esophageal adenocarcinoma is about 35 times that of the general population in patients with Barrett’s, it is still a relatively low lesion.
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The treatment of patients with Barrett’s esophagus is as well controversial. Therapy is generally aimed at the symptoms of GE reflux disease rather than the Barrett’s mucosa. A number of studies have attempted to show regression of Barrett’s mucosa with proton pump inhibitors, however, it has not been shown that the overall malignant potential of the Barrett’s mucosa is altered by this approach. Additionally, treatment with YAG laser, and more recently, photodynamic therapy (using argon dye laser with Photofrin pretreatment) to ablate the Barrett’s mucosa in patients with dysplasia has been tried. The long-term risk and efficacy of this approach remain to be proved, and it is not yet considered generally accepted treatment.

There is consensus that patients with Barrett’s esophagus require regular endoscopic surveillance. Typically, patients with Barrett’s esophagus in the absence of dysplasia undergo endoscopy every one to two years with numerous surveillance biopsies. If the biopsies show no dysplasia this program is continued. If low-grade dysplasia is detected and confirmed by a second pathologist, this examination should be performed every six months until either the dysplasia is no longer documented or high-grade dysplasia is identified. Once high-grade dysplasia is identified ancompression fractured confirmed by another pathologist, surgery (total esophagectomy) is recommended. By the time high-grade dysplasia is detected on biopsy approximately one-third of patients will already have foci of invasive carcinoma found in the resected specimen. If surveillance is continued to the point where gross esophageal cancer is detected by endoscopy or biopsy, most patients will no longer have resectable lesions and therefore this approach is not advocated.

Complications of GE Reflux Disease
Sequelae of GERD are typically broken down into the esophageal complications and the extra-esophageal manifestations.
-Esophageal Complications:
—Peptic Strictures: These can develop in patients with symptomatic heartburn or in patients with clinically silent heartburn. They generally present as solid food dysphagia unattended by weight loss. These are generally treated with anti-reflux medications and with endoscopically guided dilation.

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-Barrett’s Esophagus: With the advent of high resolution video endoscopy Barrett’s esophagus, particularly short segment Barrett’s esophagus (less than 3 cm in length) is being seen in up to 10-15% of patients having endoscopy for GE reflux. Of interest, many of the patients with Barrett’s esophagus do not have symptoms of severe heartburn and do not therefore seek medical attention. This may be because the Barrett’s mucosa is protective and prevents esophageal erosion and complaints of symptomatic heartburn. Additionally, many patients with well-developed Barrett’s esophagus do not have abnormal 24 hour pH probe studies which suggests that the damage which resulted in the development of the Barrett’s esophagus occurred in the past and that the patient no longer has ongoing reflux disease, however, does have persistent Barrett’s esophagus.