Month: November 2015
There are a a number of skin conditions that are associated with the disease of obesity. Acanthosis Nigricans is characterized as areas of thickened, dark, velvety discoloration in body folds and creases. Usually seen in the armpits, neck, under the breasts, in the skin folds of the abdomen and groin. The exact cause of it at the molecular level is not clear other than seen frequently with insulin excess in the case of benign conditions. This symptom can give a warning about health conditions that require further investigation.
Patients may assume excessive sweating and poor hygiene are the causes of this condition- both of which are incorrect.
Acanthuses Nigerians is caused by acanthosis and papillomatosis of the epidermis (the outer most layer of the skin) pigmentation is usually not in this area, rather than pigment-producing cells. The skin proliferation abnormalities in acanthosis nigrcans are frequently associated with hyperinsulinemia and insulin resistance. This probably presents the best understanding of the pathology behind it. It suggests that the layer of skin gets thicker probably caused by some stimuli- as indicated above seen with insulin excess.
There are two forms of this condition: Benign and Malignant.
Benign forms are associated with obesity, insulin resistance, and type II diabetes.
Insulin resistance: Insulin is a hormone secreted by the pancreas that allows your body to process sugar. Resistance predisposes to type II diabetes.
Hormonal disorders: Hypothyroidism, Polycystic Ovarian Disease, and other endocrine disorders of adrenal glands are ovaries
Drugs: Certain drugs and supplements such as high-dose niacin, birth control pills, steroids, may cause acanthosis nigricans.
Malignant forms may be an indication of Gastro-intestinal cancer such as stomach, colon, or liver cancer.
Treatment: No specific treatment is available for acanthosis nigricans. Treating the underlying conditions may restore some of the normal color and texture to affected areas of skin.
Achalasia is a motility disorder of the esophagus. The neuro-muscular mechanisms which is suppose to propel food down the esophagus after the initiation of swallowing does not work and this results is a narrowing of a segment of the esophagus, with significant dilation of the esophagus above.
The weight loss with achalasia is the result of dysphagia (inability to swallow) both solids and liquids. Patient with other esophageal motility disorders have primarily solid intolerance, but with proper positioning tolerate liquids well. This is because unlike other esophageal motility disorders (where the esophagus fails to push the food down after swallowing is initiated) in achalasia, the food is carried down to a certain level, but it gets stuck, because of non relaxation of muscles that form the lower esophageal. The key would be to make the proper diagnosis by manometry, endoscopy, and radiologic studies. The treatment for achalasia is very different-than that of an esophageal motility disorders.
In Achalasia, at the treatment includes nutritional support, and laparoscopic division of the muscle fiber that are wrapped around the esophagus to allow for gravity to help with the passage of the food down to the stomach. Additionally this operation should include steps and components to prevent reflux. This video shows segments of the operation.
The 2015 ASMBS meeting was held November 2-6, 2015. It was combined with TOS (The Obesity Society) and had more than 5,600 attendees from all over the world in every aspect of obesity treatment. There were some interesting additions and deletions from this meeting compared to the past.
The one sentence that comes to my mind is “I told you so”.
One important addition was a DS course for Surgeons and Allied Health. This was very exciting, except the content and questions seemed to gravitate to SADI/SIPS/Loop rather than DS. Dr. Cottam was one of the moderators of the course. It seems that they have found the value in preserving the pyloric valve. It was clear that the discussion was driven by the need to come legitimize the single anastomosis procedures at this early stage with almost no data to prove long term outcome. With many of the Vertical Sleeve Gastrectomies having re-gain and the they are looking for a surgery that the “masses” can perform. This was actually the term used by one of the presenters, implying that the duodenal switch needed to be simplified so that all surgeons, those who have pushed all other procedures can not offer Duodenal Switch to their patients with less than desirable outcome. Several surgeons also voiced their concern and dissatisfaction with the issues and complication of the RNY and want an alternative. There was much discussion regarding SADI/SIPS/Loop being investigational and that it shouldn’t be as it is a Sleeve Gastrectomy with a Billroth II. Dr. Roslin and Dr. Cottam discussed their SIPS nomenclature saying they wanted to stay away from something that had Ileostomy, suggesting bowel issues, or the word “SAD”i due to negative connotations. The point to be made is that the SADI and SIPS and the loop are all the same. I have also noticed other surgeons using SADS (Single Anastomosis Duodenal Switch). There is a great deal of industry behind these procedures and many surgeons being trained in courses funded by industry. One surgeon stood up and informed the entire course that they need to be clear with their patients about the surgery they are performing, as he had been in Bariatric chat rooms and there is upset within the community about SADI/SIPS/Loop being toted as “the same or similar to Duodenal Switch”.
There was also presenter who said “We are doing something new about every five years.” No, “we” are not. Some of us have stood by the surgery and techniques with the best long term outcomes and not gone with every “new” thing out there. The process of Duodenal Switch may have changes, open Vs. Lap, drains, location of incisions, post operative care and stay, but the tested procedure with the best outcome has been the duodenal switch operation and not the shortcut versions. Although, those of us that are standing by long term results seems to be in the minority. Why do I stand by Duodenal Switch? Because it works, when done correctly by making the length of the bowel proportional to the patient total bowel length, and height, and not just cookie cutter length for all patients, with the right follow-up, patient education, vitamin and mineral regime and eating habits.
A new addition was the Gastric Balloon, which in the research presented had a 60-70% re-gain rate and a no more than 10-15% weight loss one year only. This data represents more than 70% weight regain when the balloon is taken out. The Gastric Balloons can be left in between 4-6 months depending on the brand or type of balloon. The Gastric Balloon is not new to the Bariatrics and was first introduced in 1985. After 20 years and 3,608 patients the results were and average of 17.6% excess weight loss. It seems that we are re-gurgiating old procedures. There are many new medications that were front and center in this meeting.
The Adjustable Gastric Bands were missing from the exhibit hall this year. It is my hope and feeling from the other attendees that we may be seeing the era of the Adjustable Gastric Band being placed in patients come to an end. Although there are some still holding out that there are some patients that can do well with the Band.
Attending the 2015 ASMBS meeting this year, as it has every year, only reemphasized the importance of avoiding what has become the norm of chasing a simple solution that is fashionable and easy now. We stay convinced that the duodenal switch operation with the common channel and the alimentary length measured as a percentage of the total length is by far the best procedure with the proven track record. The patient should avoid the temptation of settling for an unproven procedure or device, because if history holds true, there will be a need for revision surgeries in the future.
Malnutrition is one of the most feared complication of the duodenal switch operation. It may present years after surgery. What is common is a mix of nutritional deficiencies which include fat soluble vitamins, and protein calorie malnutrition. These all point to possible excessive shortening of the common channel. In my practice we have seen patients that have had lengthening of their common channel to improve their metabolic picture. What is very obvious to us, is that we see disproportionately higher number of cases coming to us for revision from practices where the common and alimentary lengths are done as a “standard” numbers with no specific adjustments made for the patient, their anatomy and situation. I have said for years, that the length of the bowel that is measured to be become the common and the alimentary limb should be a percentage of the total length of small bowel, rather than a pre-determined measurement. Here is a visual description of how this works.
If a common channel and the alimentary limb is measured to be a percent of the total length then the chance of protein calorie malnutrition is minimized since this will take into account the bowels absorptive capacity which is being reduced. This decrease in the absorption is done as a fraction of the total length.
Raines et al. published a study in 2014, that showed how small bowel length is related more closely to a patient’s height and not weight. And yet, some surgeons totally based the length of the common channel and the alimentary limb arbitrarily based on the patient pre operative BMI and nothing else. Could this be the cause of why I see some patients coming to us for revision of their duodenal switch for malnutrition?