Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1002_Библиотеки_им_академика_М_И_Перельмана
.pdf
422
hypoproteinemia, chronic diarrhea, electrolyte and micronutrient deciencies,
hyperparathyroidism, nephrolithiasis, and gastroesophageal reux disease (GERD).
Understanding the mechanisms of malabsorption that occur in all patients undergoing DS is paramount to the successful long-term management of these patients. It is
therefore essential for patients undergoing malabsorptive operations to understand
the need for adherence with a strict follow-up plan.
D. Bahroloomi et al.
46.2 Long-Term andNutritional Complications
Intestinal bypass increases the risk of frequent bowel movements, atulence, anorectal pathology, micronutrient deciency, divalent cations, and hypoproteinemia
[6]. When assessing the true nutritional status of patients, it is essential to understand that patients with morbid obesity often have excess fat but decreased lean
muscle and vitamin stores. In fact, these patients can often present nutritionally
malnourished with lack of reserve. This state of “high-calorie malnutrition” is due
to a preoperative diet that is generally high in processed foods with limited nutritional value resulting in inadequate ability to utilize calories efciently [7].
Therefore, postoperative nutritional counseling and monitoring with long-term
blood work including total protein, iron, calcium, fat-soluble vitamins, and PTH is
essential to the success of the post-surgical patient [8]. During ofce visits, review
of systems should include assessment for new onset of numbness, weakness, lethargy, and the number and consistency of bowel movements. The vast majority of
primary BPD-DS and SADI-S patients move their bowels 2–4 times per day and
adapt to the surgical procedure with little difculty [8, 9]. Thorough physical examination should include measurement of muscle strength. One simple test is to have
the patients stand from a sitting position without assistance from the arms. As the
gluteal muscle is one of the largest in the body, it will atrophy early if intake is
poor [10].
46.2.1 Anatomic Effects onNutrition
A major concern of the DS is the consequences of shorter bowel length causing
diarrhea, perirectal complications, and protein and vitamin deciency. The nutritional effects of the DS depend on the length of the alimentary limb and the common channel. The length of the alimentary limb correlates with protein absorption,
while increased size of the common channel reduces fat malabsorption [5]. During
revision surgery, the common channel is usually elongated, allowing for a longer
segment of bowel for absorption of food. Most DS revisions report a 100cm common channel elongation, while Scopinaro recommended a 150 cm increase for
BPD [11].
46 Malabsorptive Complications
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
423
In order to further study the etiology of high revision rates after index BPD procedures, Topart etal. conducted a literature review comparing the rate of revisions
after DS and BPD [12]. This study demonstrated that the rate of revision was
0.5–4.9% for DS and 3–18.5% for BPD [12]. In their review, the chief reason for
reoperation was found to be protein malnutrition, which accounted for 43–60% of
the revision procedures [12]. Similarly, Hamoui etal. reported a series of DS requiring revision. Results of this series revealed that the most common indications for
revision were malnutrition (20/33), diarrhea (9/33), metabolic abnormalities (5/33),
abdominal pain (3/33), liver disease (2/33), and emesis (2/33) [13]. The revision
surgery was successful for those having the operation to reduce chronic diarrhea,
with the median number of daily bowel movements being reduced from 5 to 1 [13].
Almost all patients had improvement in albumin levels to >3.5g/dL except for one
patient whose albumin increased from 2.5 to 2.8g/dL [13].
This idea is further demonstrated by Lebel etal. in a study which compared the
DS with 200cm common channel vs. 100cm common channel and discovered that
the longer channel group had lower severe protein deciency (11% vs. 19%).
Furthermore, patients with the longer channel required vitamins A and D supplementation (p < 0.05). Patients also had fewer bowel movements (2.0 vs. 2.9,
p= 0.03) with no signicant decrease in weight loss [14]. This data suggests that
some of the main complications of the DS can be possibly reduced with lengthening
the common channel while still maintaining signicant weight loss [14].
46.2.2 Hypoproteinemia
Optimization of protein intake after surgery should be the primary nutritional goal
after DS.During periods of rapid weight loss, the body will need to conserve lean
body mass to support an increased metabolism and the ability to burn calories.
High-quality protein sources increase satiety as well as aid in tissue healing. It is
generally recommended that patients consume 80–100g protein/day (1.0–1.5g/kg
IBW) [15]. While this high quantity may be difcult to achieve in the rst postsurgical liquid diet phase, protein shakes and liquid supplements are important
dietary adjuncts that support this goal. Ideally, protein-rich meals should be distributed throughout the day. In one analysis of patients undergoing DS, Strain etal.
found a rate of 7.3% nutritional deciency, 5.1% of which required TPN [2]. At
9years, 30% of patients were protein decient, with 20% of patients having low
albumin levels [2].
The most concerning sequelae of hypoproteinemia is extensive peripheral edema.
When this occurs, treatment is mandatory. Peripheral and systemic edema are one
of the leading indications for revision following BPD-DS and can occur following
SADI-S [6]. In severe forms, clinical presentation can be similar to kwashiorkor
(edema, hypoproteinemia, anemia, and fatty inltration of the liver) [16]. When
assessing a patient with concern for hypoproteinemia, a physical exam can be
424
D. Bahroloomi et al.
notable for swelling in the legs, perineum, abdomen, and upper extremities [16].
These patients are best managed by the use of total parenteral nutrition (TPN)
supplementation.
46.2.3 Chronic Diarrhea
The most common theory regarding the etiology of chronic diarrhea following
SADI-S or BPD-DS is malabsorption of fat [5]. In reality, multiple synchronous
potential causes likely contribute to diarrhea. In addition to malabsorption of fat,
partial gastrectomy and increased rate of emptying can exacerbate preexisting lactose sensitivity [17]. Carbohydrates that are easily ingested by the intestinal ora
can cause bacterial overgrowth, increased fermentation, and watery diarrhea [18].
Subtle protein sensitivities such as to gluten can also become more symptomatic [17].
The key to diagnosis of factors contributing to chronic diarrhea is the detailed
assessment of the patient’s oral intake, characteristic of the stool, and the temporal
relationship of intake to bowel movements. For example, fat malabsorption or
steatorrhea has been well-documented and characterized by abundant dense stool
that oats [19]. However, post-DS patients will always have increased fecal fat in
the stool; thus, unless fecal output is monitored with 24-h collection and controlled
diet, monitoring of fecal fat is rarely helpful for management. Watery diarrhea following a bariatric procedure is more often associated with malabsorption of carbohydrates [17]. Lactose deciency presents with frequent watery diarrhea 40min
following eating [19]. Additionally, when carbohydrates are poorly absorbed, they
enter the colon where they undergo fermentation by bacteria, causing small intestinal bacterial overgrowth (SIBO). Buildup of gas (such as methane) contributes to
bloating, increased atulence, and reabsorption into the circulation [19]. SIBO can
be diagnosed by breath test for lactulose and can be treated with antibiotics
[20, 21].
A variety of treatments can help alleviate symptoms of chronic diarrhea. Initial
remedies include alteration of diet and the use of motility agents such as Imodium
and Lomotil. A histamine-2 blocker and proton pump inhibitor should be prescribed.Diet regimens should emphasize a low-fat diet which limits short-chain
carbohydrates that are poorly absorbed in the small intestine and more likely to
cause fermentation. This regimen is described as the fermentable oligosaccharides,
disaccharides, monosaccharides, and polyols (FODMAP) diet [22]. Additionally,
increased ber intake and supplementation should be encouraged.If diarrhea persists, other medications that have been utilized include clonidine, octreotide, and
GLP-1 agonists.The GLP-1 agonists delay gastric emptying and reduce motility
[23]. The GLP-2 analogue teduglutide is rarely used following bariatric surgery
[24]. Although its use leads to short-term gut hypertrophy and increased absorption, it is expensive and must be used indenitely, or the effect dissipates
46 Malabsorptive Complications
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
425
[24].Therefore, if surgical revision is practical, it is preferred, and the use of GLP-2
analogue is reserved for patients that do not have a surgical alternative [24]. If
patients continue to suffer from refractory chronic diarrhea and continued poor
nutritional parameters, consideration should be given to surgical reconstruction
following nutritional repletion. Nutritional optimization prior to surgery often
requires several weeks of parenteral nutrition and can be monitored using prealbumin levels [25].
46.2.4 Electrolyte Repletion andRefeeding Syndrome
Refeeding syndrome is a potentially life-threatening complication of hasty nutritional optimization that can be commonly missed in DS patients who have had signicantly decreased intake for prolonged periods of time [26]. Refeeding syndrome
develops when the reintroduction of carbohydrates leads to insulin release and an
increase in adenosine triphosphate production, for which phosphate and magnesium
are required (magnesium acts as a co-factor) [27]. As a result, potassium and phosphate are shifted into cells, leading to phosphate depletion that causes an increase in
magnesium excretion in the urine [27]. This process results in hypophosphatemia,
hypokalemia, and hypomagnesemia that leads to refeeding syndrome [27]. High
clinical suspicion should be maintained in bariatric patients, as failure to treat
refeeding syndrome can lead to serious multisystem complications, including fatal
cardiac arrhythmia, hypoglycemia, and abnormal uid shifts [28].
Treatment of refeeding syndrome begins with hospitalization and gradually
increasing calorie infusion via parenteral nutrition. Thiamine must be given prior to
administering any high dextrose solution or concentrated feeding. Placement of an
enteral feeding tube should be delayed until edema resolves and nutrition improves.
With severe hypoalbuminemia, leaky gut is common [29]. Thus, the best approach
is the slow initiation of total parenteral nutrition that has 100g of amino acids and
40g of fat and limits dextrose to 140g or less [30]. Synchronously, diuretics can be
given with albumin to maintain uid balance and improve peripheral edema [30].
Daily labs including electrolytes should be checked and repleted. When the patient
is able to tolerate a diet, calorie counts and number and consistency of bowel movements should be recorded.
Often, endoscopy and CT scan are performed to ensure no mechanical cause of
decreased intake. Colonoscopy can be considered to assure other synchronous
causes such as inammatory bowel disease are not contributing factors. Parenteral
administration should be maintained until values are normalized and PO intake
improves or there is plan for surgical revision. Whereas outtake issues are resolved
with surgery to expand surface areas, intake issues are much more difcult to solve
with surgery. Involvement with mental health providers is important. Appetite stimulants can be tried. If nutritional status cannot be maintained following resuscitation, revision with feeding tube is suggested.
426
D. Bahroloomi et al.
46.2.5 Micronutrient Considerations
Optimizing postoperative patient outcomes and nutrition status begins within the
preoperative process. Intensive preoperative nutritional counseling is crucial to
gauge patients’ motivation, predicted compliance, and ability to change habits.
Patients should be educated before and after surgery on the expected nutrient type,
dietary behaviors, and weight loss goals to support long-term outcomes. Invasive
alterations to physiology, digestion, absorption, metabolism, and excretion are
associated with higher nutrient deciencies and should be reviewed with
patients [31].
Laboratory markers are imperative for completing the initial nutrition assessment and continued in follow-up care. Baseline values help distinguish between
postoperative complications, deciencies related to surgery, and noncompliance
with recommended supplementation. Any nutrient deciencies identied presurgery should be repleted following the RDA in addition to any individualized
recommendations. Common deciencies include the following.
46.2.5.1 Vitamin A
Vitamin A deciency has been reported to be at 52% at 1year and 69% at 4years
after DS [32]. Early symptoms of vitamin A deciency are night blindness and
changes in conjunctiva of the eyes [32]. Treatment includes 10,000IU PO. Iron,
zinc, and protein levels need to be corrected to normalize vitamin A levels [32].
Vitamin A deciency has been found to be associated with low serum prealbumin.
Vitamin A levels should especially be monitored in postoperative pregnant patients,
and beta-carotene should be used for repletion in this population [33].
46.2.5.2 Calcium andVitamin D
Calcium and vitamin D are important for bone formation, blood coagulation, muscle contraction, and myocardial conduction. An acidic environment and adequate
levels of vitamin D are needed for proper absorption of calcium and other minerals.
Limited intake and/or decreased absorption of one or both can lead to osteopenia,
osteoporosis, and/or osteomalacia. While calcium and vitamin D deciencies have
higher incidences after malabsorptive procedures, bone mineral depletion directly
correlates with the amount of weight lost in an individual, regardless of the cause of
weight loss [34]. Calcium citrate supplementation is preferred as it requires minimal acid for absorption, and a supplement including magnesium and vitamin D
enhances absorption. DS patients require higher calcium doses than other bariatric
surgery patients, typically 1800–2400mg divided into doses of 500mg per dose.
Vitamin D deciency is prevalent even before weight loss surgery with reports of
46 Malabsorptive Complications
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
427
16–57% [34, 35]. Vitamin D supplementation may consist of up to 50,000 IU
weekly for up to 9weeks and 5000IU daily thereafter [36]. Parathyroid (PTH) is
the best indicator of calcium status; when PTH increases, bone resorption of calcium increases in order to maintain normal blood levels of calcium. It is generally
recommended that the PTH level be kept below 100pg/mL to reduce the risk of
metabolic bone disease [36]. Bone density should be tracked serially. Blood work
should include a minimum of annual albumin, calcium, PTH, and 25-OHD levels to
assess bone health. It is important to note that elevated PTH values are commonly
found in patients who have had DS or RYGB even with normal vitamin D levels and
no change on bone density scans. The signicance is not yet known.
46.2.5.3 Folic Acid
Typically 100mcg of folate is excreted in bile daily; most is reabsorbed in the upper
third portion of the unaltered small intestine but may be absorbed throughout the
entire small bowel [37]. Since much of the small bowel is bypassed, daily excretion
of folate is greater, and deciency may occur rapidly without adequate supplementation of minimum 400mcg daily which can be found in multivitamins [38]. Folate
and vitamin B12 are codependent, and deciency of either can contribute to macrocytic anemia [39].
46.2.5.4 Zinc
Zinc deciency can be suspected with hair loss, poor wound healing, diarrhea, glossitis, dermatitis, and hypogeusia [40]. Zinc deciency may arise due to lack of
absorption in the proximal jejunum, intolerance to zinc-rich foods such as meat, and
fat malabsorption. Supplementing with elemental zinc of 30–50mg daily or every
other day may be suggested [40].
46.2.5.5 Iron
Iron deciency anemia is the most common micronutrient deciency following DS
[12]. Iron absorption is compromised due to reduced stomach size and less exposure
to hydrochloric acid. Furthermore, the principal sites of iron absorption (duodenum
and proximal jejunum) are bypassed in the DS [41]. It is important to rule out other
causes of anemia, such as deciency of protein, vitamin B12, folate, selenium, zinc,
and copper [42]. The 2016 ASMBS Nutritional Guidelines recommend 150–200mg
of elemental iron in the form of ferrous fumarate, sulfate, or gluconate for treatment
in iron deciency through repletion [43]. If oral supplementation is not effective,
intravenous iron infusions containing ferric gluconate may be necessary.
428
D. Bahroloomi et al.
46.2.6 Metabolic Bone Disease
All bariatric procedures that bypass the duodenum and proximal intestine can
increase the incidenceof osteomalacia, osteoporosis, osteopenia, and secondary
hyperparathyroidism [40]. Calcium absorption is compromised as it is preferentially absorbed in the duodenum and proximal jejunum. Vitamin D absorption is
hindered by bile diversion.In general, supplements are effective in mitigating damage and helping achieve. However, if there is increased malabsorption, then calcium will bind to fatty acids increasing the rate of depletion [44]. To normalize,
parathyroid hormone will increase recruiting calcium from your bones. Rising
PTH reduces phosphate.To minimize the risk of hungry bones, it is essential to
optimize calcium and vitamin D [44]. Routine monitoring and serial bone density
are suggested.
46.2.7 Nephrolithiasis
Another risk of surgically induced malabsorption is nephrolithiasis.This condition
is exacerbated by increases in oxalate circulation postoperatively. In cases of fat
malabsorption, calcium will bind to free fatty acids creating a soap-like consistency.This environment leaves oxalate free, allowing it to be more freely absorbed
by the colon. Oxalate then enters the bloodstream, is ltered by the kidney, and
binds to calcium inside the urinary tract.This process can result in stones or calcinosis of the kidney [31]. Prevention includes a low oxalate diet with appropriate
protein intake. Additionally, calcium supplementation is prescribed to improve calcium binding to oxalate.Finally, brisk hydration to prevent hypovolemia is essential
[31]. Early detection is necessary, as poorly controlled or recurrent nephrolithiasis
can progress overlying urosepsis to renal failure.
46.3 Conclusion
The DS is an effective modality for the promotion of weight loss in patients
with morbid obesity. The DS has the highest rate of weight loss while bariatric
surgeries are performed today but is also associated with the most significant
malabsorption and nutrition abnormalities. Important factors to consider in DS
patients include chronic diarrhea, electrolyte and micronutrient deficiencies,
hyperparathyroidism, nephrolithiasis, and GERD.Understanding the mechanisms of malabsorption that occur in all patients undergoing DS is paramount
to the successful long-term management of these patients. It is essential for
patients undergoing malabsorptive operations to understand the need for adherence with a strict follow-up plan.
46 Malabsorptive Complications
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
429
References
1. Moshiri M, Osman S, Robinson TJ, Khandelwal S, Bhargava B, Rohrmann CA.Evolution of
bariatric surgery: a historical perspective. Am J Roentgenol. 2013;201(1):W40–8.
2. Strain GW, Ebel F, Honohan J, Gagner M, Dakin G, Pomp A, etal. Comparison of weight
loss and body composition changes with four surgical procedures. Surg Obes Relat Dis.
2009;5:582–7.
3. Hess DS, Hess DW, Oakley RS. The biliopancreatic diversion with the duodenal switch:
results beyond 10 years. Obes Surg. 2005;15(3):408–16.
4. Buchwald H, Avidor Y, Baunwald E, Jensen M, Pories W, Fahrbach K, etal. Bariatric surgery:
a systematic review and meta-analysis. JAMA. 2004;292(14):1724–37.
5. Billeter AT, Fischer L, Wekerle AL, Senft J, Müller-Stich B.Malabsorption as a therapeutic
approach in bariatric surgery. Viszeralmedizin. 2014;30(3):198–204.
6. Dorman RB, Rasmus N, al-Haddad B, Serrot FJ, Slusarek B, Sampson B, Buchwald H, etal.
Benets and complications of the duodenal switch/biliopancreatic diversion compared to the
Roux-en-Y gastric bypass. Surgery. 2012;152(4):758–65.
7. Lonsdale D.Crime and violence: a hypothetical explanation of its relationship with high calorie malnutrition. J Adv Med. 1994;7(3):171–80.
8. Marceau P, Hould FS, Simard S, Lebel S, Bourque RA, Potvin M, etal. Biliopancreatic diversion with duodenal switch. World J Surg. 1998;22(9):947–54.
9. Elias K, Bekhali Z, Hedberg J, Graf W, Sundbom M. Changes in bowel habits and patientscored symptoms after Roux-en-Y gastric bypass and biliopancreatic diversion with duodenal
switch. Surg Obes Relat Dis. 2018;14(2):144–9.
10. Fischer M, JeVenn A, Hipskind P.Evaluation of muscle and fat loss as diagnostic criteria for
malnutrition. Nutr Clin Pract. 2015;30(2):239–48.
11. Scopinaro N, Gianetta E, Civalleri D, Bonalumi U, Lombezzi R, Friedman D, et al.
The bilio-pancreatic bypass for functional surgical treatment of obesity. Minerva Med.
1979;70(52):3537–47.
12. Topart PA, Becouarn G.Revision and reversal after biliopancreatic diversion for excessive side
effects or ineffective weight loss: a review of the current literature on indications and procedures. Surg Obes Relat Dis. 2015;11(4):965–72.
13. Hamoui N, Chock B, Anthone GJ, Crookes PF.Revision of the duodenal switch: indications,
technique, and outcomes. J Am Coll Surg. 2007;204(4):603–8.
14. Lebel S, Dion G, Marceau S, Biron S, Robert M, Biertho L.Clinical outcomes of duodenal
switch with a 200-cm common channel: a matched, controlled trial. Surg Obes Relat Dis.
2016;12(5):1014–20.
15. Campbell B, Kreider R, Ziegenfuss T, La Bounty P, Roberts M, Burke D, etal. International
Society of Sports Nutrition position stand: protein and exercise. J Int Soc Sports Nutr. 2007;4:8.
16. Kushner R.Managing the obese patient after bariatric surgery: a case report of severe malnutrition and review of the literature. JPEN J Parenter Enteral Nutr. 2000;24(2):126–32.
17. Hammer HF, Hammer J.Diarrhea caused by carbohydrate malabsorption. Gastroenterol Clin
North Am. 2012;41(3):611–27.
18. Jammah AA. Endocrine and metabolic complications after bariatric surgery. Saudi J
Gastroenterol. 2015;21(5):269–77.
19. Juckett G, Trivedi R.Evaluation of chronic diarrhea. Am Fam Physician. 2011;84(10):1119–26.
20. Pimentel M, Mayer AG, Park S, Chow EJ, Hasan A, Kong Y. Methane production during
lactulose breath test is associated with gastrointestinal disease presentation. Dig Dis Sci.
2003;48(1):86–92.
21. Shah SC, Day LW, Somsouk M, Sewell JL.Meta-analysis: antibiotic therapy for small intestinal bacterial overgrowth. Aliment Pharmacol Ther. 2013;38(8):925–34.
22. Whelan K, Martin LD, Satudacher HM, Lomer MCE.The low FODMAP diet in the management of irritable bowel syndrome: an evidence-based review of FODMAP restriction, reintroduction and personalisation in clinical practice. J Hum Nutr Diet. 2018;31(2):239–55.
430
23. Parhofer KG.Glucagon-like peptide 1 (GLP-1). MMW Fortschr Med. 2007;149(25):41–3.
24. Jeppesen PB.Teduglutide, a novel glucagon-like peptide 2 analog, in the treatment of patients
with short bowel syndrome. Ther Adv Gastroenterol. 2012;5(3):159–71.
25. Beck FK, Rosenthal TC.Prealbumin: a marker for nutritional evaluation. Am Fam Physician.
2002;65(8):1575–8.
26. National Collaborating Centre for Acute Care. National Institute for Health and Clinical
Excellence: guidance, in nutrition support for adults: oral nutrition support, enteral tube feeding and parenteral nutrition. National Collaborating Centre for Acute Care, UK. 2006.
27. Crook MA, Hally V, Panteli JV. The importance of the refeeding syndrome. Nutrition.
2001;17(7):632–7.
28. Silk Z, Jones L, Heath D.Refeeding syndrome: an important complication after bariatric surgery. Surg Obes Relat Dis. 2011;7(5):21–3.
29. Ballinger AB, Farthing MJ.Octreotide in the treatment of intestinal lymphangiectasia. Eur J
Gastroenterol Hepatol. 1998;10(8):699–702.
30. Stanga Z, Brunner A, Leuenberger M, Grimble RF, Shenkin A, Allison SP, etal. Nutrition in
clinical practice—the refeeding syndrome: illustrative cases and guidelines for prevention and
treatment. Eur J Clin Nutr. 2008;62(6):687–94.
31. Cummings S, Pratt J.Metabolic and bariatric surgery: nutrition and dental considerations. J
Am Dent Assoc. 2015;146(10):767–72.
32. Slater GH, Ren CJ, Siegel N, Williams T, Barr D, Wolfe B, et al. Serum fat-soluble vitamin deciency and abnormal calcium metabolism after malabsorptive bariatric surgery. J
Gastrointest Surg. 2004;8(1):48–55.
33. Slater C, Morris L, Ellison J, Syed AA.Nutrition in pregnancy following bariatric surgery.
Nutrients. 2017;9(12):1338.
34. Guney E, Kisakol G, Ozgen G, Yilmaz C, Yilmaz R, Kabalak T.Effect of weight loss on bone
metabolism: comparison of vertical banded gastroplasty and medical intervention. Obes Surg.
2003;13(3):383–8.
35. Toh SY, Zarshenas N, Jorgensen J. Prevalence of nutrient deciencies in bariatric patients.
Nutrition. 2009;25(11):1150–6.
36. Hamoui N, Anthone G, Crookes PF.Calcium metabolism in the morbidly obese. Obes Surg.
2004;14(1):9–12.
37. Ziegler O, Sirveaux MA, Brunaud L, Reibel N, Quilliot D.Medical follow up after bariatric
surgery: nutritional and drug issues. General recommendations for the prevention and treatment of nutritional deciencies. Diabetes Metab. 2009;35(6):544–57.
38. Reynolds E.Vitamin B12, folic acid, and the nervous system. Lancet Neurol. 2006;5(1):949–60.
39. Dimopoulos N, Piperi C, Salonicioti A, Vassiliki P, Gazi F, Nounopoulos C, etal. Association
of cognitive impairment with plasma levels of folate, vitamin B12 and homocysteine in the
elderly. In Vivo. 2006;20(6B):895–9.
40. Bal BS, Finelli FC, Shope TR, Koch TR.Nutritional deciencies after bariatric surgery. Nat
Rev Endocrinol. 2012;8:544–56.
41. Herron DM, Roohipour R.Bariatric surgical anatomy and mechanisms of action. Gastrointest
Endosc Clin N Am. 2011;21(2):213–28.
42. Mechanick JI, Youdim A, Jones DB, Garvey WT, Hurley DL, McMahon M, et al. Clinical
practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of
the bariatric surgery patient—2013 update: cosponsored by American Association of Clinical
Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric
Surgery. Obesity. 2013;21:S1–S27.
43. Parrott J, Frank L, Rabena R, Craggs-Dino L, Isom KA, Greiman L.American Society for
Metabolic and Bariatric Surgery Integrated Health Nutritional Guidelines for the surgical
weight loss patient 2016 update: micronutrients. Surg Obes Relat Dis. 2017;13(5):727–41.
44. Kaidar-Person O, Person B, Szomstein S, Rosenthal RJ.Nutritional deciencies in morbidly
obese patients: a new form of malnutrition? Part A: vitamins. Obes Surg. 2008;18(7):870–6.
D. Bahroloomi et al.
Chapter 47
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Postoperative Psychological Assistance
HélioTonelli andAndréiaMinski
47.1 Introduction
Obesity is an important public health problem for which pharmacological, behavioral, and surgical treatments are currently available [1]. Biliopancreatic diversion
with duodenal switch (BPDDS), along with gastric bypass (RYGBP), is among the
surgical techniques leading to weight loss and its maintenance over time [2].
BPDDS includes three specic components: (1) a longitudinal gastrectomy, providing caloric restriction and decreasing acid production while maintaining normal
gastric emptying; (2) a 250cm total alimentary limb whose role is to reduce caloric
absorption; and (3) a 100cm common channel where the bolus mixes with biliopancreatic juices, resulting in decreased absorption of protein and fat [3].
As with any surgical technique, BPDDS outcomes are more satisfactory when a
patient undergoes regular multidisciplinary follow-up after surgery. Indeed, 20% of
bariatric patients achieve <50% excess weight loss after surgery, largely due to psychological issues regarding general psychopathology (for instance, depression and
anxiety); dysfunctional eating behaviors (DEB) like binges, food addictions, and
emotional eating; as well as some personality traits where impulsivity is a central
phenomenon [4]. Such conditions need to be properly identied in the preoperative
evaluation and treated when they persist despite having been managed before surgery, in order to guarantee the best results in terms of weight loss.
H. Tonelli (*)
Caetano Marchesini Clinic, Curitiba, PR, Brazil
Neuroscience and Social Cognition at FAE Business School, Curitiba, PR, Brazil
A. Minski
Curitiba, PR, Brazil
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. Teixeira et al. (eds.), Duodenal Switch and Its Derivatives in Bariatric and
Metabolic Surgery, https://doi.org/10.1007/978-3-031-25828-2_47
431
Соседние файлы в папке Библиотека им академика М.И. Перельмана