Nutrition/Obesity

Question 1

Discuss the normal absorption of fat

Answer 1

In adults, 94% of dietary fat is absorbed

1. Emulsification
   
   • lipids need to be solubilised in aqueous environment ie suspended in water (emulsion) to expose large surface area to lipolytic enzymes
   • emulsification begins in UGI tract w mastication & gastric mixing –> fat droplets released are coated w ingested phospholipids to form a stable emulsion
   • additional phospholipids from bile added once emulsion reaches duo
2. Fat hydrolysis
   
   • begins in stomach by actions of lingual lipase (50% hydrolysis in adults), then pancreatic lipase (w colipase) in duo
     
     • FFAs released by lipolysis in stomach contributes to stimulation of secretion of panc lipase & colipase
     • also entry of gastric hydrogen ions into duo stimulates release of secretin which enhances panc bicarb secretion –> increases pH to ~6.5 which is optimal for fat digestion (hence ZES for example inhibits fat absorption)
     • bile salts further enhance fat solubilisation –> emulsion of microscopic micelles which also optimises action of panc enzymes
   • dietary & biliary phospholipids & cholesterol are further hydrolysed by phospholipase A2 & pancreatic cholesterol estase
3. now have complex soup of lipolytic products + other lipids + fat soluble vitamins whihc are mixed w bile salts –> small aggregates (micelles) or larger aggregates (liposomes)
   
   • allows 2-monoglycerides & FAs to be absorbed across apical membrane of enterocyte (not just passive, also protein-mediated transport processes)
   • most dietary lipids absorbed in prox 2/3 of jejunum
4. Bile salts remain in intestinal lumen –> TI where they are actively resorbed, enter portal circulation then are resecreted into bile (enterohepatic circulation)
5. Once within villus absorptive cells –> FAs transported to smooth ER –> triglycerides resynthesised
6. Triglycerides, cholesterol esters, phospholipid & apoprotein B48 form aggregate –> transferred to Golgi for further processing into fully mature chylomicron
7. Chylomicron binds to basolateral membrane & is transported to intestinal lymphatics to enter general circulation

Question 2

Describe the ideal composition of TPN

Answer 2

NB: Total energy requirement is ~25-35kcal/kg/day

In a surgically ill patient increased to ~2500kcal/day

• ~55% of calories given as CHO (14% dextrose soln)
  
  • Too little and gluconeogenesis kicks in
• ~35% of calories given as lipid emulsion
  
  • use a higher proportion in COPD paitents to reduce CO₂ production
• ~15% of calories given as protein (aa solution)
  
  • Daily requirement is ~0.8-1.0g/kg/day
  • Septic patients may require more (~double)
• Also need:
  
  • 15mmol linoleic and arachidonic acid per week
  • Vitamins; B₁₂, Vitamin-K, Folate, Zinc

Question 3

Describe the complications of TPN

Answer 3

1. Blood/serum related
   
   • Hyperglycaemia
     
     • IGT common
     • Responds well to Insulin
   • Electrolyte disturbance
     
     • Massive shifts in starvation esp Phosphate
2. Hepatic dysfunction
   
   • mild transaminitis and steatosis
   • most cases self-limiting
3. Respiratory dysfunction
   
   • CO₂ retention if too much CHO
   • Respiratory quotient increases
4. Line related
   
   • PTX during insertion
   • Line sepsis
   • Line breakage
   • Line thrombosis

Question 4

Outline your approach to assessment of nutrition.

Answer 4

1. Complete history and exam
2. Anthropometric measurements
   
   • BMI <18
   • Weight change of 5%-10% in last 6 months
   • Skin fold thickness (triceps most common but better if use multiple sites, but subject to intra- and inter-observer variability, limiting clinical use)
   • Bioelectrical impedence (less reliable in pts w oedema & electrolyte shifts)
3. Biochemical measurements
   
   • Albumin (t_1/2 of 21 days so may not fall for several weeks)
     
     • acts as a negative marker of the acute-phase response & so is lowered in malignancy, trauma & sepsis even in presence of adequate intake
     • so should not be used as assessment of nutritional STATE tho low concs point to increased nutritional RISK assoc w underlying disease
   • Other serum proteins: transferrin (t1/2 of 7 days), pre albumin (t_1/2 of 2 days)
     
     • but serum concs of these proteins also altered in stress, sepsis & cancer so also not useful
   • Anaemia
4. Functional assessment
   
   • Grip strength
5. Validated screening
   
   • Malnutrition Universal Screening Tool
     
     • 5 steps:
       
       • BMI - >20 = 0, 18.5-20 = 1, <18.5 = 2
       • note % Unplanned weight loss in previous 3-6mo (<5% = 0, 5-10% = 1, >10% = 2)
       • establish ‘acute disease effect’ (severity) & give this a numerical score (if pt acutely ill & there is, or will be, no nutritional intake for >5 days = 2)
       • add scores (total) from steps 1,2,3 together to get overall risk of malnutrition
       • make decision re what to do depending on score
         
         • 0 = low risk - repeat screening process at future time
         • 1 = medium risk - monitor oral intake for 3 days; if doesn’t improve dietitian rv
         • ≥2 = high risk - refer to dietician to try increase nutritional intake & should be policies in place for nutritional support given to these pts

Question 5

Name the three most important amino acids during times of starvation.

Answer 5

1. Alanine - for hepatic gluconeogenesis
2. Glutamate - fuel for enterocytes, hepatocytes, and white blood cells
3. Aspartate - for maintaining renal acid-base balance.

Question 6

What is immune-modulating nutrition?

Which patients have been shown to benefit from immune-modulating nutrition?

Answer 6

Nutrition enriched with arginine, nucleotides, and omega-3 fatty acids.

• Patients with mild sepsis (APACHE II <15)
• Patient with intra-abdominal cancer about to undergo surgery (5-7 days prior)
• Patients with ARDS.

Interestingly, contra-indicated in patients with severe sepsis.

Question 7

What are the causes of fat malabsorption?

Answer 7

• SB disease/resection
  
  • resection of >100cm of TI –> severe impairment of enterohepatic circulation of bile salts such that liver’s ability to upregulate de novo bile acid synthesis = inadequate to meet normal physiological needs for bile production –> fat malabsorption
  • NB loss of shorter segments of TI can still result in chronic diarrhoea even though may not result in fat malabsorption; bile acids that aren’t absorbed in SB may stimulate water & electrolyte secretion in colon (cholerrheic diarrhoea)
    
    • Bile salt binders (cholestyramine) can improve bile acid diarrhoea but may worsen diarrhoea from fat malabsorption (by increasing it)
• SIBO
  
  • deconjugation of bile acids by bacteria defunctionalises the bile acids
• Pancreatic exocrine insufficiency
  
  • chronic pancreatitis, pancreatectomy, CF
• ZES
  
  • inactivation of pancreatic lipase by acidification of duodenal contents
• Disorders of bile acid metabolism
  
  • inadequate synthesis (cirrhosis)
  • inadequate secretion of bile salts (cholestasis)

Question 8

How are carbohydrates normally absorbed?

Answer 8

• starch, sucrose & lactose = most abundant digestible carbs in human diet; must be broken down into monosaccharides prior to absorption
• some plant polysaccharides eg cellulose can’t be digested in SB lumen, though are fermented to a degree in the colon

1. Digestion of starch (amylose & amylopectin)
   
   • both salivary & pancreatic amylase contribute to their digestion –> oligo- and disaccharides
2. Oligo- and disaccharides (eg sucrose, lactose) are degraded by brush border enzymes (primarily disaccharidases –> monosaccharides)
3. These are absorbed by either active or passive transport
4. Carbs that aren’t digested & absorbed in SB –> bacterial degradation in colon
   
   • terminal phase of bacterial carb degradation = fermentation –> formation of SCFAs + CO2 + hydrogen + methane
   • excessive bacterial fermentation = reason for acidic stools, abdominal distension & flatulence in pts w various forms of carb malabsorption
   • SCFAs = available as an energy source as are efficiently absorbed from colon - allows body to recover a portion of the potential energy contained within indigestible food fibre & other undigested carbs

Question 9

What are some causes of carbohydrate malabsorption?

Answer 9

• deficiency in pancreatic amylase
• decreased disaccharidase activity in SB epithelium (eg lactase or sucrose-isomaltase deficiency)
• decreased absorptive intestinal surface area (eg celiac disease)
• unabsorbable carbs (eg sorbitol)

Question 10

How is protein usually absorbed?

Answer 10

1. Digestion begins in stomach by action of gastric pepsins, which are released as proenzymes (pepsinogen 1 and 2) and undergo autoactivation at low pH
   
   • amino acids released from gastric digestion play a role in releasing CCK from duo & jejunal endocrine epithelial cells; CCK critical for stimulating release of panc enzymes responsible for digestion of all 3 macronutrients
2. In duo, several pancreatic proteases act together to digest proteins –> amino acids or dipeptides + tripeptides
   
   • pancreatic enzymes also secreted as inactive proenzymes
     
     • bile salts trigger enterokinase to be released from duo; this converts trypsinogen –> trypsin
     • trypsin then catalyses conversion of all other panc proteases to active forms as well as auto-catalysing activation of additional trypsinogen
3. Amino acids, dipeptides or tripeptides can be absorbed through highly efficient sodium-dependent amino acid co-transporters at brush border membrane
   
   • passive but called secondary active transport since energy is indirectly provided by Na-K ATPase pump

Question 11

What are the causes of protein malabsorption?

Answer 11

• impaired pancreatic bicarb and protease secretion and/or activity (eg chronic panc or cystic fibrosis)
• generalised reduction of intestinal absorptive surface

Question 12

Discuss the absorption of vitamins and minerals

Answer 12

Proximal half of SB = predominant site for absorption of most vitamins & minerals, with notable exceptions:

• Vit B12 = absorbed by a specific ILEAL receptor that recognises the B12-IF complex; >100cm distal ileal resection will –> clinically signif vit B12 deficiency
• Bile acids also absorbed in TI
• Magnesium = primarily absorbed in distal SB & colon
  
  • malabsorption of Mg amplified by excess FAs in intestine of pts w untreated fat malabsorption; these bind to divalent cations eg Ca & Mg creating soaps
• Calcium = upper SB
• Iron = throughout SB esp duo
• Iodine = prox SB
• Folate = prox SB
• Zinc = prox SB (lesser extent ileum & LB)
• Copper = stomach & upper SB
• Fluoride = stomach & SB
• Chromium, selenium, manganese = SB

Question 13

How are minerals classified?

Answer 13

Macrominerals = need >100mg/day eg Na, K, Cl, Ca, Mg, PO4

Trace elements = need 1-100mg/day eg copper, fluoride, iodine, manganese, zinc

Ultratrace elements = need <1mg/day eg chromium, selenium

Question 14

What is the pathogenesis of obesity?

Answer 14

Multifactorial metabolic disorder involving gene and environmental factors along with dysfunction of the gut-brain-endocrine axis and the adipocyte-brain-endocrine axis

• familial predisposition - specific genes include FTO gene
• monogenetic causes rare - MC4R gene, POMT gene, leptin, ghrelin, neuropeptide Y
• gene-environment interactions - epigenetic changes
• gut microbiome - plays essential role in metabolism & the immune system; altered microbiome predisposes host to obesity & glucose intolerance
• dysregulation of hormonal control of satiety & appetite; ghrelin is secreted by gastric fundal cells and stimulates teh release of various neuropeptides form the hypotohalamus which creates an orexigenic state
• GBE axis fundamental for energy homeostasis
  
  • enteroendocrine cells sense luminal factors & screte gut hormones eg GLP1 which feed back via endocrine, paracrine, vagal & spinal efferent mechanisms to the hypothalamus
  • activation of metabolic control centres in hindbrain & hypothalamus to control energy homeostasis
• adipose tissue consists of both brown (non-shivering thermogenesis) & white fat
  
  • increase in fat mass assoc w obesity –> adipocyte dysfunction - adiposopathy/’sick fat’
  • white fat stores cholesterol & triglycerides and acts as an endocrine & immune organ
  • white adipocytes produce immune factors eg leptin, adiponectin (has antiinflammatory & antidiabetic properties), growth factors, adipocytokines (eg IL6, TNF), enzymes eg aromatase & 17beta-hydroxysteroid dehydrogenase
  • these contribute to inflammation & have significant effect on obesity-related comorbidities

Question 15

What is the rationale for bariatric surgery?

Answer 15

Medical therapy for severe obesity has limited short-term success and almost non-existent long-term success.

Multiple long-term folow-up trials comparing those who underwent bariatric surgery with those who didn’t have shown decreased mortality long-term after bariatric surgery

• Swedish Obese Subjects study was first prospective controlled trial to provide long-term data; weight loss at 20yrs of 18% vs -1%, reduced morbidity, overall mortality, cancer deaths, MI, first-time CV events
• other studies have also shown improvements in diabetes, OSA, dysplipidaemia & HTN
• multiple RCTs have confirmed superiority of bariatric surgery over medical management

Very cost effective (costs fully recovered within 2yrs)

Low M&M

Question 16

What are the mechanisms of action of bariatric surgery?

Answer 16

Main mechanisms are 1) reduced food intake, 2) malaabsorption and 3) alterations in the enteroencephalic and enteroinsular axis (altered food preferences & food reward and increased energy expenditure)

• Calorie restriction and malabsorption alone don’t fully explain metabolic effects; mechanisms seem to extend beyond magnitude of weight loss alone to include effects on CNS regulation of appetite & metabolism and improvements in insulin secretion & sensitivity

Enterocephalic endocrine axis: anatomic changes after bariatric surgery reduce pre-meal hunger and increase satiety; various components of GBE axis can explain this

• decreased postprandial secretion of ghrelin & thereby reduced hunger signals
• increased satiety via higher levels of peptide YY and GLP-1
  
  • peptide YY secreted by L-cells throughout small & large bowel in response to presence of nutrients in lumen of distal gut & has anorexigenic effect
• both of these hormones possibly have some effect on food preferences seen after LSG & RYGB; less fixation on energy-dense foods
• ghrelin reduced more by LSG than RYGB; peptide YY is increased by RYGB and unchanged by LSG
• metabolic surgery can increase number of gut peptide expressing EECs and therefore postprandial gut peptide secretion (eg PPY, GLP1)
• also, higher nutrient concs in distal segments & fast delivery to distal ileum post RYGB stimulates EECs to release these satiety hormones; and post sleeve, faster gastric emptying –> increased satiety hormones

Enteroinsular endocrine axis:

• improved insulin-action, beta-cell function & modulative effect of gut hormones in this axis play a role in T2DM remission
• GLP-1 = major player - released by L-cells in distal GI tract & levels increase in response to nutrients in distal midgut/hindgut
• in obese people, there is a delay in postprandial release of GLP-1 & overall reduced levels
• GLP-1 has anorexigenic effect secondary to delayed gastric emptying but more predominant action on enteroinsular axis; stimulates insulin secretion, increases insulin sensitivity of pancreatic cells & inhibits glucagon secretion
• elevated in response to both RYGB & LSG, more so in RYGB

Question 17

What are the criteria for bariatric surgery

Answer 17

• BMI >40
• or BMI >35 with associated comorbidities
• consider if BMI 30-35 with diabetes which can’t be adequately controlled with medical management particularly if other cardiovascular risk factors
• failed non-surgical attempts at weight loss for >2yrs
• understanding of and motivated for surgery
• accepts longterm follow-up
• nonsmoker for >6mo
• psychiatrically stable, no brain injury/Prader Willi
• no alcohol/drug use

Contraindications:

• weight >200kg or BMI >55
• steroid-dependent disease
• Crohn’s disease
• abdominal radiotherapy
• history of malignancy (other than low risk eg cutaneous SCC)
• major medical problems eg portal hypertension
• age = controversial; in adolescents recommended after major growth spurt; roughly <65-70

Question 18

What is the role of weight loss and optifast prior to bariatric surgery?

Answer 18

• used to give weight loss targets; now know this may predict the pt’s biological ability to lose weight but may not predict outcome after surgery - preop psych factors don’t predict long-term weight loss outcomes
• weight loss of ≥5% can reduce operative time & potentially operative risk by making surgery technically easier though this doesn’t necessarily equate to reduced complications
• BMI >55 is one of leading causes for complications & death after RYGB so desirable for this group to lose weight
• most will prescribe 1-4wks of pre-op low-calorie liquid diet to hel preduce stiffness & size of liver - easier to retract, better exposure of GOJ

Question 19

Preparation for bariatric surgery

Answer 19

• MDT input
• optimise comorbidities
• optifast to make liver more compliant +/- weight loss target (less used now)
• nutrition screen - iron studies, B12/folate, vits A,B,C,D
• advise against pregnancy for 12mo afterward bc inc risk fetal nutrition
• stop oestrogen therapy preop due to DVT risk

Question 20

Deciding which bariatric operation

Answer 20

• all operations improve diabetes control; trend towards RYGB being superior to sleeve & band at 1yr & by 2yrs, superior durability in diabetes control
• RYGB superior to sleeves by 1yr for HTN resolution
• RYGB superior by 2yrs for dyslipidaemia
• RYGB superior to sleeve for resolution of OSA in short term
• RYGB may be preferred for people w Barrett’s, severe/complicated GORD or bile reflux
  
  • hiatus hernia alone doesn’t preclude bariatric surgery - repair hiatus & proceed w whichever operation
• RYGB may be preferred for BMI >50
• sleeve may be preferred for pts w iron deficiency anaemia, SB Crohn’s, ?severe arthritis requiring NSAIDs

Advantages of sleeve include technically simpler, lower complications?, pylorus preserved (avoidance of dumping), less hernias & malabsorption, can convert later, still get diabetes remisison in >25%

Question 21

Steps for lap RYGB

Answer 21

Gastric pouch <30mL, roux limb 100cm (150cm if super-obese), BP limb 80-100cm (150cmm if super obese)

34Fr orogastric tube. Stack at pt’s left shoulder. Modified Lloyd Davies, slight head up.

Pouch first approach.

• Optical entry with 12mm port LUQ (0 degree scope). Further ports.
• Liver retraction, assess oesophageal hiatus, mobilise hiatal fat pad & take down angel of His
• at 5cm distal to GOJ, dissect lesser curve fat from gastric wall to create tunnel to lesser sac
• use blue 45mm GIA to staple stomach perpendicular to lesser curve; then staple vertically to angle of His with 1-2 blue 60mm - gastric pouch <30mL
• lift transverse colon superiorly +/- split greater omentum if bulky, find DJ flexure & measure SB 50-100cm
• lift SB loop over transverse colon to gastric pouch & make a small access hole in antimesenteric border of the loop; insert cartridge of a 20mm blue stapler in here & into a corresponding access hole in the most dependent part of the gastric pouch staple line (usu at junction of 1st & 2nd staple lines)
• close access hole with 1 or 2 layers of absorbable suture round a 34Fr orogastric tube
• once GJ formed, divide SB loop w a linear stapler proximal (ie BP limb side) to GJ
• anastomose BP limb to Roux limb 100-150cm distal to GJ with a 45mm linear stapler
• close stapler access hole w absorbable suture
• close mesenteric windows with non-absorbable suture

Question 22

Expected outcomes for bariatric procedures

Answer 22

• EWL
  
  • RYGB 60-85%
  • SG 55-80%
  • SAGB70-85%
  • BPD 79%
  • Band 50-60%
• RYGB: diabetes >50%, HTN 40%, GORD >90%
• Sleeve: diabetes remission 25%

Question 23

Complications of RYGB

Answer 23

• mortality 0.1-0.3%
• leak 1% (usu GJ)
• VTE 0.23% if prophylaxis (most common cause of death)
• SBO 4% lifetime incidence (adhesions 50%, internal hernia 30%, anastomotic stricture/kinking at JJ (13%)
  
  • closing mesenteric defects leads to quarter the incidence of internal hernia associated BO, adds 4mins to op time
  • also can get gastric remnant syndrome
• stomal/anastomotic stenosis 6% (usu GJ, balloon dilate or refashion; JJ refashion)
• marginal ulcer 2-10% (near GJ)
• gastrogastric fistula 1-2% (–> marginal ulcer or weight gain)
• early dumping syndrome up to 50% when high levels simple carbs
• late dumping syndrome 1-2%
• iron & B12 deficiency; also calcium, thiamine, folate
  
  • iron def 15-40%, IDA 20% - bypass duo & prox jej
  • vit B12 def 15-20% but rarely causes anaemia - delayed mixing w IF
• (significant) late regain up to 20%

Question 24

What are the two types of dumping syndrome after RYGB?

Answer 24

• Early dumping syndrome
  
  • occurs in up to 50% when high levels of simple carbs ingested
  • rapid onset usu within 15mins
  • result of rapid emptying of food into SB & bc of hyperosmolality of food, rapid fluid shifts from plasma into bowel –> hypotension & SNS response
  • colicky abdo pain, diarrhoea, nausea, tachycardia
  • avoid foods high in simple sugar content & replace w diet consisting of high fibre, complex carb & protein-rich foods + small frequent meals + separate solids from liquids by 30mins
  • usu self limiting & resolves within 2-3mo
• Late dumping syndrome/reactive hypoglycaemia
  
  • 1-2%
  • usu 1-3hrs after ingestion of carb-rich meal, typically months to yrs after surgery
  • neuroglycopenic sx (dizziness, fatigue, diaphoresis, weakness) assoc w low serum glucose levels
  • exact aetiology uncertain but prob includes combo of late dumping, beta cell hyperfunction & an exaggerated incretin response
  • dx can be confirmed by oral glucose tolerance test
  • same mx as above, low carb, agents like diazoxide, acarbose, octreotide usu successful

Question 25

What are the 3 defects that should be closed during RYGB to prevent internal hernia?

Answer 25

1. Mesocolic - only if Roux limb brought retrocolic
2. Peterson’s - space between Roux limb mesentery & mesocolon
3. Mesenteric - at site of jejunojejunostomy

Question 26

What is a one anastomosis gastric bypass?

Answer 26

• modification of loop gastric bypass
• create gastric pouch as for RYGB & anastomose a loop of jejunum as an antecolic & antegastric loop gastrojejunostomy - use a point 150-180cm distal to ligament of Treitz
• closure of mesetneric window not routine
• excess weight loss comparable to RYGB & comparable/superior to LSG
• ?similar to RYGB in induction of remission of T2DM
• higher rates of alkaline bile reflux

Question 27

Steps for lap sleeve gastrectomy

Answer 27

Stack at pt’s left shoulder. Modified Lloyd Davies. Head up.

• 12mm optical port entery with 0 degree scope + further ports
• Retract liver, assess oesophageal hiatus. 34-40Fr bougie.
• Devascularaise & mobilise greater curve from 4cm proximal to pylorus to GOJ
• Mobilise hiatal fat pad & take down angle of His, exposing left crus of diaphragm
• Fire consecutive staplers from 5cm prox to pylorus up to GOJ along the bougie. Avoid catching distal oesophageus in staples. Important to preserve left gastric vessels & lesser curve blood supply and to prevent twisting/spiraling of gastric tube.
• Once resected, remove stomach via one of 12mm port sites
• Haemoclip lateral aspect of staple line to cut edge of greater omentum

Mechanisms:

• restrictive
• removal of fundus –> decreased ghrelin –> decreased hunger, increased satiety
• accelerated gastric/duo emptying –> exposure of distal SB to food

Question 28

Complications of lap sleeve gastrectomy

Answer 28

• mortality 0.1%
• bleeding 0.6% (intra-luminal, intra-abdominal or at trocar/incision sites)
• leak 1-3% (present 1-4wks post-op)
  
  • acute (within 7 days), early (within 1-2wks), late (after 6wks), chornic (after 12wks
• stricture up to 4%
• GORD & Barrett’s 10-20% at 5yrs
  
  • if pre-existing GORD, 50% will have worse reflux post, 10-20% improved mianly due to weight loss
• nutritional deficiencies: Fe, Ca, B12, thiamine
• weight regain
• revision rate 20% (primarily for weight regain or GORD)
• gallstones

Question 29

What is a biliopancreatic diversion +/- with duodenal switch?

Answer 29

original BPD:

• divide duo from pylorus, removign pylorus (or distal half of stomach) & dividing ileum 150-250cm from ICV
• distal ileum anastomosed to stomach and prox ileum anastomosed to TI 50-100cm from ICV

BPD with DS:

• sleeve gastrectomy with preservation of pylorus & creation of Roux limb with short common channel
• divide duo distal to pylorus, proximal to bile duct
• ileum divided 150-250cm from ICV and distal end anastomosed to duodenum
• proximal end anastomosed to TI 50-100cm from caecum
• ie 50-100cm common channel with long BP limb & alimentary limb ~150cm

Excess weight loss 70-80% at 2yrs & highly effective at treating comorbid conditions

Cons:

• technically complex
• 2-4BM a day with flatulence & bloating & foul-smelling stools
• malnutrition - fat-soluble vitamin & zinc deficiency common 60-90%, protein malnutirtion in 12%, Wernicke’s

Question 30

What is a lap adjustable gastric band?

Answer 30

A purely restrictive procedure that compartmentalises the upper stomach by placing a tight, adjustable prosthetic band around the entrance to the stomach. The band consists of a soft, locking silicone ring connected to an infusion port placed in teh subcut tissue. The port may be accessed by a syringe and needle in order to inject or rmeove saline.

Advantages include that it is adjustable, with a low incidence of nutritional deficiencies. Weight loss is relatively poor however and removal rates are high.

Question 31

Complications of lap gastric band

Answer 31

• obstructed band
• slipped band/gastric prolapse
• band erosion
• port infection
• enlarged gastric pouch
• GORD
• Failure to lose weight

Question 32

Management of slipped gastric band/gastric prolapse

Answer 32

• on plain xray band should lie at ~45 degrees to vertical (normal phi angle supposedly 4-58degrees)
  
  • anterior prolapse: angle >45 degrees to vertical (ie band tipped horizontally)
  • posterior: angle <45 degrees to vertical (ie band tipped vertically, sometimes “o sign”
  • may also see air-fluid level above band
• causes obstruction, pain +/- gastric necrosis
• management:
  
  • remove fluid from band; if resolution of obstruction/pain –> semi-elective operation otherwise acute
  • operative options:
    
    • removal (remove port then lap port through same hole)
    • repositioning
    • just releasing and leaving in situ
    • if capsule is restrictive will need to release this too

NB can also get obstructed non-slipped band from overfilling or poor eating habits (eating too fast or too much at a time) +/- enlarged gastric pouch with time

• management - empty band, then investigate underlying cause ?behavioural, often can ccautiously refill later w education on eating habits or in more severe/recurrent cases, need to remove band

Question 33

Discuss gastric band erosion and its management

Answer 33

• Incidence 1-2%
• Aetiology theories:
  
  • intraop events (undetected damage, excessive tension)
  • overfilling of band causing relative ischaemia
  • perigastric placement
• Presenting features:
  
  • often asymptomatic or v subtle
  • weight loss failure/lack of satiety
  • band or port issues:
    
    • late port site infection - should always trigger check gastroscopy
    • requiring increased fluid volumes
    • turbid fluid in band
  • rarely acute event: pain, peritonitis, abscess, dehydration
• Ix:
  
  • may be missed on barium swallow but if seen is indicated by contrast on both sides of band
  • CT if pt unwell, to identify associated collections
  • diagnose by endoscopy: white prosthesis within lumen, needs retroflexed view
• Mx:
  
  • removal of band
  • if buckle in lumen, endosocpic removal possible (divide tubing & remove port either before or during procedure, then endoscopicaclly divide band & remove via mouth)
    
    • post-procedure contrast swallow
  • buckle not in lumen: remove surgically
    
    • lap +/- open removal (may be difficult)
    • technique varies; may involve anterior gastrotomy
    • closure of defect - suture closure, omental patch
    • if buckle not seen in lumen and pt well, can wait for significant erosion then remove endoscopically

Question 34

Management of gastric sleeve leak

Answer 34

• incidence 1-3%, present 2-4wks post-op
• often at prox staple line
• symptoms vary: pain, nausea, decreased oral intake or fever; majority not overtly septic or unwell
• pathophysiology
  
  • ischaemia
  • dynamic mechanical forces around crura and prox staple line
  • possible elevated intragastric pressures
  • varied presentation depending on severity/chronicity:
• diagnosis
  
  • CT scan & oral contrast - fluid +/- gas-filled collection adjacent to stomach +/- contrast leak
  • gastroscopy: usu pinhole defect in prox stomach
• classification (radiological)
  
  • Class 1a: phlegmon assoc w staple line
  • Class 1b: phlegmon w small localised locules of gas associated w the staple line
  • Class 2a: fluid collection w localised locules of gas
  • Class 2b: extensive fluid and gas collection
  • Class 3a: contained contrast leak
  • Class 3b: free intraperitoneal contrast leak
  • Class 4: chronic fistula
• management - varies
  
  • if sick/poor source control/free gas - consider emergency operation
  • management of sepsis
    
    • source contorl (endoscopic, perc, operative drain)
    • antibiotics/antifungals, resuscitation
    • nutritional support
  • management of defect - many options
    
    • endoscopic: stent, pigtails, plugs, glue, clips, endovac, pyloric botox, dilatation
    • surgical: omental patch, serosal patch, T-tube, loop drainage, gastric bypass, total gastrectomy
  • other considerations: PPI, psychological, social/financial support

Question 35

Follow-up for bariatric patients

Answer 35

• 24mo follow-up with bariatric service including monitoring nutritional intake (macros, vitamins, minerals), monitoring for comorbidities, medication review, dietary & nutritional assessment, physical activity advice & support, psychological support
• after d/c from bariatric service, annual monitoring of nutritional status

Nutritional monitoring & supplementation

• lifelong multivitamin (2 for first year) including vitamin B (including folate & thiamine), iron, calcium, vitamin D, selenium, zinc and vitamins A, C and E
• vitamin B12 as required
• initially blood test at 1, 3-6 and 12mo post op then annually - FBC, U&E, LFTs, ferritin, thiamine, folic acid, vitamin D, Ca, vit B12, lipids
  
  • and for RYGB and BPD/DS also monitor copper, zinc, selenium, vitamin A +/- Vit E & K

Question 37

Discuss malnutrition following bariatric surgery

Answer 37

• can occur with any bariatric procedure, irrespective of weight loss, but more common in malabsorptive procedures
• may present with any of
  
  • significant weight loss (>1-2kg/wk)
  • macronutrient deficiencies (hypoalbuminaemia, sarcopenia)
  • micronutrient deficiencies (anaemia, vitamin deficiencies)
• management
  
  • diagnose anatomical problem eg stricture/ulcer
  • support nutrition
    
    • supplements, feeding tube
    • be aware of severe vitamin/mineral deficiencies and supplement these
    • monitor for refeeding syndromee
  • MDT approach
  • monitor with regular blood tests (see separate slide)

Commonly encountered problems

• protein-calorie malnutrition
• neurological complications
  
  • vit B12, thiamine & copper deficiency can lead to devastating neurological complications, more likely after procedures that re-route SB
  • early dx important; delays may be assoc w signif morbidity & mortality
• anaemia
  
  • up to 15% of pts can develop IDA in absence of any overt blood loss
  • BPD/DS highest risk, followed by RYGB, SG, GaB
  • most anaemia due to iron def but B12, folic acid & copper deficiencies can also cause anaemia & should be investigated depending on supplementation regimen & response to treatment w iron
• hair loss & derm complications
  
  • hair loss common presumably related to catabolic state but severe alopecia rare
  • hair loss and/or derm manifestations usu suggest zinc deficiency
  • deficiencies of niacin (B3) or vit A may give skin rash
• bone health
  
  • obese people have higher prevalence of vit D deficiency; bariatric surgery may worsen due to poor intake/absorption of vit D and/or calcium

Question 38

Through what mechanisms does malnutrition affect post-operative recovery?

Answer 38

Disturbances in function at organ & cellular level can manifest as following:

• impairment of normal homeostatic mechanisms
• muscle wasting & impairment of skeletal muscle function
• impaired resp and cardiac muscle function
• atrophy of smooth muscle in GI tract
• impaired immune function
• impaired healing of wounds & anastomoses

Question 39

What is refeeding syndrome?

Answer 39

• inability of a pt’s metabolism to handle macronutrients
• after ~10days w/o nutritional intake, metabolism adapts to state of starvation
• refeeding w full ‘normal’ required amounts of macronutrients will induce a sudden reversal of this adaptation, w an anabolic drive that may result in catastrophic depletion of available K, PO4 & Mg
• before refeeding, serum biochem may be normal so possibility of re-feeding must be anticipated on hx alone
• also thiamine is another nutrient liable to become depleted in this situation
  
  • is a cofactor of pyruvate kinase, which is required for glucose to undergo oxidative phosphorylation; w/o it glucose is metabolised to lactic acid
  • must replenish before feeding is commenced in starved pt to prevent development of Wernicke-Korsakoff syndrome
  • risk of this much higher in pts w hx of chronic excess ETOH
  • always consider thiamine in pts who have had no nutritional intake for >1wk in presence of an unexplained metabolic acidosis

Question 40

Why is enteral feeding preferred? What are relative contraindications?

Answer 40

• in absence of nutrients into intestinal lumen, intestinal mucosal changes: loss of height of villi, decrease in cellular proliferation, mucosa becomes atrophic
• decreased activity of enzymes found in assoc w the mucosa & permeability of mucosa to macromolecules increased
• stimulation of intestinal tract by nutrients = important for release of many gut-related hormones, incl those responsible for gut motility & stimulation of secretions necessary for normal maintenance of the mucosa
• gut acts as a barrier to bacteria, both physically & by release of chemical & immunological substances
  
  • atrophy of intestinal mucosa = assoc w increased translocation of bacteira & endotoxin from gut lumen into portal venous & lymphatic systems…extent to which it contributes to sepsis unclear

(Relative) contraindications:

• intestinal obstruction
• ileus
• high-output intestinal fistulas
• D&V?
• major intra-abdominal sepsis?

Question 41

What are the advantages of jejunostomy over gastrostomy?

Answer 41

• less stomal leakage
• gastric & pancreatic secretions reduced bc stomach bypassed
• less nausea, vomiting or bloating
• reduced risk of pulmonary aspiration

Question 42

What are the categories of nutrient solutions available for enteral nutrition?

Answer 42

1. Polymeric diets
   
   • ‘nutritionally complete’
   • for pts w inadequate oral intake but good intestinal function
   • contain
     
     • nitrogen source: whole protein
     • energy source: complex carbs & fat
     • vitamins, trace elements & electrolytes in standard amounts
2. Elemental diets
   
   • required if pt unable to produce an adequate amount of digestive enzymes or has reduced area for absorption (eg severe panc insufficiency or short-bowel syndrome)
   • contain
     
     • nitrogen source: oligopeptides (free amino acids aren’t as easily absorbed as dipeptide & tripeptide mixtures)
     • energy source: glucose polymers & medium-chain triglycerides
   • bc each oligopeptide molecule contributes as much to osmolarity of solution as one molecule of intact protein, can be difficult to provide complete requirements w/o producing side-effects assoc w an osmotic load eg dumping & diarrhoea
3. Special formulations
   
   • developed for pts w particular diseases
     
     • high hepatic encephalopathy risk: increased concs of branched-chain aas & low in aromatic aas
     • pts on artifical ventilation: higher fat conc but lower glucose energy content
     • diets containing key nutrients that modulate immune response
4. Modular diets
   
   • not common but allow provision of a diet rich in a particular nutrient for specific pts
   • eg diet may be enriched in protein if pt is protein-deficient or sodium if Na-deficient

Question 43

Delivery of enteral nutrition & complications

Answer 43

• used to start at lower rate or strength for first few days to reduce GI complications; not required unless risk of re-feeding syndrome
• can be cyclical (eg 16hrs on, 8hrs off) or continuous
• administer via volumetric pump to avoid risk of large bolus
• if reduced LOC or bedbound, head elevated to 25degrees to reduce risk of pulmonary aspiration
• aspirate stomach q4h & if >100mL, w/h feed & recheck aspirate after 2hrs; restart when vols <100mL; if >400mL aspirate in 24hrs, stop feed
  
  • can give erythromycin or metaclopramide to improve gastric emptying
• complications
  
  • GI: diarrhoea, nausea, vomiting, abdo discomfort & bloating, regurgitation
  • Resp: aspiration of feed/stomach contents
  • Mechanical: dislodgement of feeding tube, blockage of tube, leakage of stomach/SB contents onto skin w jejunostomies or gastrostomies
  • Metabolic: excess or deficiency of glucose, electrolytes, minerals or trace elements
    
    • less common than with PN

Question 44

Indications for parenteral nutrition

Answer 44

• nonfunctioning or inaccessible GI tract
• high output enteric fistulas (enteral nutrition may stimulate GI secretion)
• not possible to provide sufficient intake of nutrition enterally (eg bc short segment of residual bowel or malabsorption, severe burns, major trauma)

Question 45

Complications of CVL placement

Answer 45

• catheter-related sepsis: up to 40%
• thrombosis of central vein: up to 20%
• pleural space damage; pneumothorax (5-10%), haemothorax (2%)
• major arterial damage: subclavian artery 1-2%
• catheter problems: thrombosis 1-2%, embolism <1%, air embolism <1%
• miscellaneous problems: brahical plexus damage <1%, thoracic duct damage <1%

Question 46

What are the potential nitrogen and energy sources in parenteral nutrition?

Answer 46

• Nitrogen sources
  
  • solutions of crystalline L-amino acids containing all essential & a balanced mixture of non-essential amino acids required
  • Aas that are rel insoluble (eg L-glutamine, L-arginine, L-taurine, L-tyrosine, L-methionine) may be absent or present in inadequate amounts
    
    • L-glutamine has key roles in metabolism but despite being one of most abundant aas, use is limited by instability; not contained in routine PN - can be added in different form but no evidence for improved morbidity or mortality
• Energy sources
  
  • energy supplied as balanced combo of dextrose & fat
  • glucose = primary carb source & main form of energy supply to majority of tissues
  • during critical illness, body’s preferred calorie source = fat (fasted or fed states)
    
    • glucose utilisation may be impaired & metabolised through other pathways; results in increased production & oxidation of fatty acids, resulting in increased CO2 (excreted through the lungs)
    • in addition, if glucose only energy source, may develop essential fatty acid (linolenic, linoleic) deficiency
  • fat (eg soyabean oil emulsions) provides a more concentrated energy source
    
    • provision of exogenous lipids also been assoc w problems:
      
      • IV fat emulsions can impair lung function, inhibit reticuloendothelial system & modulate neutrophil function
      • fish oils as source of fat rich in omega-3 polyunsaturated fatty acids appears to be assoc w reduced incidence of hepatic dysfunction

(also need trace elements, vitamins, enough fluid volume & electrolytes)

Question 47

Complications of parenteral nutrition

Answer 47

• glucose disturbances
  
  • hyperglycaemia: excessive admin of glucose w inadequate insulin response eg sepsis
  • hypoglycaemia: rebound hypoglycaemia occurs if glucose stopped abruptly but insulin concs remain high
• lipid disturbances
  
  • hyperlipidaemia: directly through excess administration of lipid or indirectly through excess calories that will be converted to fat or decreased metabolism (eg renal failure, liver failure)
  • fatty acid delivery: essential fatty acid delivery –> hair loss, dry skin, impaired wound healing
• nitrogen disturbances
  
  • hyperammonaemia: occurs if deficiency of L-arginine, L-ornithine, L-aspartate or L-glutamate in infusion; also occurs in liver diseases
  • metabolic acidosis: caused by excessive amounts of chloride & monochloride amino acids
• electrolyte disturbances
  
  • hyper/hypokalaemia: excessive/inadequate K admin or reduced/excessive losses
  • hypocalcaemia: inadequate Ca replacement, loss in pancreatitis, hypoalbuminaemia
  • hypophosphataemia: inadequate phosphorous supplementation, also tissue compartment fluxes
• liver disturbances
  
  • elevations in AST, ALT, ALP & GGT may occur bc of enzyme induction secondary to amino acid imbalances or fatty liver from excess calories
• ventilator probs - if excessive amounts of glucose given, the increased production of CO2 may precipitate ventilatory failure in non-ventilated pts

Question 48

Monitoring pts on parenteral nutrition

Answer 48

• accurate fluid balance & daily weighs
• daily calorie & nitrogen intake
• daily renal & liver function; twice-weekly phosphate, calcium, magnesium, albumin & protein concs, Hb, WCC, Hct till pt stabilised
  
  • then weekly or fornightly measurements
• monitor BSLs; may need IV insulin on sliding scale
• check catheter site & length regularly
• when feeding prolonged, other assessments eg muscle function, nitrogen balance, measurement of trace elements & vitamins regularly to ascertain progress

Question 49

What is intestinal failure?

Answer 49

Encompasses a spectrum of conditions that manifest as an inability to maintain adequate nutritional, fluid and electrolyte homeostasis without supportive therapy

Can be transient or prolonged

• vast majority transient w/o significant gut pathology, frequently occur secondary to postop ileus
• prolonged involves loss of funcitonal gut lasting months-yrs, some pts requiring permanent PN - eg due to massive gut loss after surgery or loss of functioning intestine available for absorption

Question 50

What is the aetiology of intestinal failure?

Answer 50

4 broad groups

• Loss of intestinal length
  
  • from multiple resections (eg Crohn’s) or one massive (eg ischaemic event, volvulus, trauma, necrotising enterocolitis or gastroschisis)
  • relationship between amount of resected bowel & degree of IF influenced by age of pt, site of resection & presence/absence of colon (and also function of residual bowel eg Crohn’s)
  • normal SB ~600cm; important not how much removed but how much remains
  • ~<100cm in presence of ileostomy or <50cm w colon present = likely to result in dependence on PN at 3mo
    
    • when ≤2m, most clinically impaired eg diarrhoea; when ≤1m, most require home PN
    • children can adapt better & may function w shorter bowel
• Loss of functional intestinal length
  
  • enterocutaneous fistula = commonest cause of this mechanism of IF - bypasses normal functional SB
    
    • can also have hidden internal fistulas
• Loss of intestinal absorptive capacity
  
  • inflammatory conditions of SB can result in non-functioning enterocytes that reduce absorptive capacity
  • eg IBD, scleroderma, ayloid, coeliac disease, radiation enteritis
• Loss of intestinal function
  
  • eg ileus, pseudo-obstruction, gastroparesis, autonomic neuropathy

Question 51

What are the three stages of intestinal failure?

Answer 51

• Stage I: hypersecretory phase - 1-2 months
  
  • usually of the 7 litres secreted daily by duo, stomach, SB, pancreas & liver, about 6 litres are reabsorbed prox to ICV & further 800mL absorbed in colon –> 200mL left in faeces
  • lack of absorption –> high vol losses = copious diarrhoea and/or high stoma/fistula outputs
  • main focus = fluid & electrolyte replacement & PN may be required to maintain nutrition
• Stage II: adaptation phase - 3-12months
  
  • series of histological changes in intestinal mucosa that permit enhanced mucosal absorption within residual intestine
  • triggers for adaptation = maintenance of fluid & electrolyte balance & gradual introduction of enteral feeding - see below
  • degree of adaptation varies w age, underlying disease extent & site of resection (ileum has better capacity for adaptation than jejunum)
• Stage III: stabilisation phase - max intestinal adaptation will take up to 1-2yrs
  
  • ​extent & route of nutritional support will vary
  • overall goal = pt to achieve as normal a lifestyle as poss (at home)

NB re adaptation:

• will only occur if there is enteral feeding; pts who are wholly dependent on PN have mucosal atrophy which is reversed on re-feeding enterally
• stimulation to adapt 3fold:
  
  • direct absorption of enteral nutrients –> local mucosal hyperplasia
    
    • increased crypt cell proliferation –> lengthening of villi & deepening of crypts –> increased surface area
    • bc ileum has shorter villi is able to adapt further, but more frequently resected
  • enteral nutrition –> release of trophic hormones & a paracrine effect
  • increased fluid & protein secretion w subsequent reabsorption –> increased enterocyte workload & adaptation

Question 52

Discuss fluid and electrolyte issues in the context of intestinal failure

Answer 52

• sodium absorption in SB = actively linked to absorption of glucose & certain amino acids
• water absorption = passive & follows sodium
• jejunum = freely permeable to water, so contents remain isotonic
  
  • if luminal Na conc is low, sodium moves into lumen; absorption of Na and hence water only occurs when conc is >100mmol/L
• Na absorption normally occurs in ileum & colon
  
  • in absence of ileum & colon, net sodium losses = high - ie in presence of high fistula or jejunostomy
    
    • daily net loss of Na 300-400mmol & water 3-4L
    • so sodium replacement v important
    • oral fluid concentrated in sodium will help reduce enteric fluid losses
    • need minimum oral sodium of 100mmol
• colon absorbs up to 6-7L, 700mmol Na and 40mmol K per day - connection of colon in continuity w residual SB will significantly reduce water & sodium losses
• K absorption usu ok unless <60cm SB, in which case 60-100mmol IV K needed
• Mg usu absorbed in distal jejunum & ileum; loss of these will result in significant Mg loss & deficiency
  
  • this in turn may precipitate Ca deficiency bc hypomagnesaemia impairs release of PTH

Question 53

Discuss the absorption of nutrients in the context of intestinal failure

Answer 53

• Carbs, proteins & water-soluble viatmins
  
  • upper 200cm of jejunum absorbs most carbs, protein & water-soluble vitamins
  • nitrogen = macronutrient least affected by a decrease in absorptive surface & utilisation of peptide-based diets rather than protein-based ones has demonstrated no benefit
  • water-soluble vit deficiencies = rare in pts w short gut though thiamine deficiency been reported
• Fat, bile salts & fat-soluble vitamins
  
  • fat & fat-soluble vitamins absorbed over lenght of SB, so loss of ileum will impair absorption
  • bile salts also reabsorbed in ileum; bile salt deficiency will contribute to reduced fat absorption
  • vit D supplements often given empirically along w Ca supplements
  • vit A & E deficiencies been reported but usually just need to be aware that visual or neuro sx may indicate deficiency & monitor infrequency
  • if wholly dependent on PN then replacement & vit K injections required
  • most pts have lost TI so need vit B12 replacement
  • trace elements not a prob - normal levels in PN pts on long term PN
  • loss of bowel –> decreased absorption but also rapid transit so reduced time for absorption which will exaverbate nutritional deficiencies

Question 54

What is the role of the colon in short-bowel syndrome?

Answer 54

• has significant absorptive capacity, not only for fluid & electrolytes but also for SCFAs
  
  • SCFAs = energy substrate & ~500kcal may be derived this way
  • estimated that having a colon = equivalent to ~50cm SB for energy purposes
• colon will also slow intestinal transit, particularly if ICV present –> improved absorption
• frequent problem for pts w large bowel in continuity = diarrhoea
  
  • excessive carb entry into colon may –> osmotic diarrhoea
  • or choleric diarrhoea from failure to absorb bile saltes completely
    
    • colonic bacteria deconjugate & dehydroxylate these into bile acids, which stimulate water & electrolyte secretion
  • in more extreme cases, bile salt depletion may occur to point of steatorrhoea from incompletely digested long-chain fatty acids
• renal stones:
  
  • bile salts increase colonic permeability to oxalate
  • undigested fatty acids bind calcium in preference to oxalate so resultant increase in enteric oxalate uptake & hence increased renal stone formation
• gallstones:
  
  • increased frequency of mixed stones, poss bc of interruption of enterohepatic circulation
• D-lactate acidosis?

Question 55

Discuss what happens following ileal resection

Answer 55

• more significant than jejunal resection due to absorption of B12 & bile salts
  
  • reduced ileal surface area –> reduced B12 absorption & reduced bile acid pool –> reduced fat absorption, steatorrhoea
  • resection of 50-100cm of ileum may cause diarrhoea (or less if ICV gone too)
  • vit B12 replacement likely required if >100cm TI resected
• reduced fat absorption –> reduced calorie intake &
  
  • increased osmotic pull inside lumen –> diarrhoea
  • reduced absorption of fat-soluble vitamins
• increased Ca oxalate absorption –> increased urinary oxalate stones
  
  • unabsorbed FAs combine w calcium –> prevent formation of insoluble Ca oxalate & allow oxalate to remain available for absorption
  • FAs & bile salts in colon –> increased colonic permeability to oxalate
• lack of enough bile salts to solubilise cholesterol in bile –> gallstones
• increased colonic bile acid conc stimulate Na & H2O secretion
• after resection, intestine undergoes a process of adaptation (over up to 2yrs)
  
  • mucosa becomes hyperplastic, villi lengthen, wall thickens, crypts deepen, intestine elongates

Question 56

What are the criteria for referral to a nationally designated intestinal failure unit?

Answer 56

• persistence of intestinal failure beyond 6wks w/o any evidence of resolution and/or complicated by venous access probs
• multiple intestinal fistulation in totally dehisced abdominal wound
• intestinal fistula outside the expertise of the the referring unit (eg recurrent in a non-specialist unit) or 2nd or 3rd recurrences in a colorectal centre
• <30cm residual SB
• recurrent venous access problems where all upper limb & cervical cenous access routes obliterated
• persistent intra-abodminal sepsis complicated by severe metabolic derangement not responding to rad/surg drainage of sepsis & provision of nutirtional support
• metabolic complications relating to high-output fistulas & stomas adn to prolonged IV feeding, not responsive to medication & adjustment of the feeding regimen
• disorders of hepatic & renal function assoc w IVN that are resistant to metaboic & nutritional supplementation
• chronic intestinal failure. in a hospital w/o adequate experience/expertise to manage the medical/surgical & nutritional requirements of such pts

Question 57

What are the steps of management after a surgical catastrophe resulting in proximal stoma or fistula

Answer 57

1. Resuscitation
2. Restitution - SNAPP
   
   • Sepsis
   • Nutrition
     
     • fluids & electrolytes (first stage of IF = hypersecretory, w high outputs & gastric hypersecretion)
       
       • daily IV requirements:
         
         • water: losses + 1L
         • Na: losses (100mmol/L effluent) + 80mmol
         • K: 80mmol
         • Mg: 10mmol
     • nutritional support
       
       • early return to enteral nutrition
       • requirements depend on size, weight, activity levels, metabolic status
       • generally males 25-30kkcal/kg/day, females 20-25kcal/kg/day of NON-protein energy, PLUS 1-1.5g/kg/day of protein
       • plus vitamins and minerals
     • reduction of output
       
       • allow solids but restrict to 500mL water orally per day; electrolyte solution rather than plain water to reduce intestinal fluid & electrolyte losses
       • High dose PPI to reduce gastric hypersecretion
       • Loperamide & codeine
     • cholestyramine may be used for hyperoxaluria, but no role for those w jejunostomy & in those w colon in continuity may reduce jejunal bile salt conc to steatorrhoea
     • r/v long-term meds - enteric-coated tablets unlikely to be useful
     • dietary modification
       
       • oral feeding introduced gradually, remaining fluid-restricted
       • in early part of 2nd clinical stage may need total PN as gastric hypersecretion in response to even small enteral feed can destabilise fluid balance
       • little & often +/- overnight enteral feeds to make use of absorption time
       • oral mag oxide 12-16mmol/day started & IV gradually withdrawn
       • roughly, stoma/fistula losses
         
         • <1500mL - oral replacement alone
         • 1500-2000mL - Na & H20 replacement, usu as subcut/IV, no PN
         • >2000mL/day - PN (can adapt with time however for up to 2yrs)
     • aims:
       
       • no thirst/signs of dehydration, acceptable strength, energy & appearance
       • gut loss <2L/day
       • urine >1L/day
       • urine Na >20mmol/L (if less, likely deficient)
       • serum Mg >0.7mmol/L
       • body weight within 10% normal
     • as move into 3rd stage of max adaptation, assess for common vitamin/mineral deficiencies & complications
     • consider fistuloclysis or distal enteral feeding
       
       • ensure no obstruction in distal bowel & efferent limb of fistula can be cannulated easily
       • using fistula output can reduce need for PN
   • Anatomy (mapping)
     
     • in terms of planned mx & prediction of long term outcome - residual SB length, define anatomy of ECFs
     • contrast scans (eg SB follow-through or enema, fistulograms); also CT or MR enteroclysis
   • Protection of skin
     
     • stoma bacgs
     • consider refashioning of stoma or creating stoma proximal to more distal fistula (eg enterovaginal)
   • Planned surgery
     
     • delaying surgery for 6-12mo reduces mortality & fistula recurrence rates
       
       • avoid early surgery (1-6wks) - bad adhesions
       • rare to wait >12mo
       • requirements for definitive surgery: no infection, nourished, softening scars or abdo wall
3. Management - reconstruction
   
   1. close stoma/close fistulas
   2. surgery to increase nutrient & fluid absorption by either slowing intestinal transit or increasing intestinal surface area = not commonly done in adults
      
      1. reversed SB segments, colonic interposition, SB lengthening with tapering (Bianchi technique) or serial transverse enteroplasty (STEP) procedures

Question 58

What are the factors influencing spontaneous enterocutaneous fistula closure and what are the key points re surgical closure of these?

Answer 58

• 70% of postop fistulas heal, usu within first 6wks of starting PN
• factors preventing healing may be
  
  • specific to fistula itself
  • general, including ongoing sepsis, nutritional deficiency or infiltration of tract by underyling disease eg malignancy, Crohn’s, TB
• factors influencing spontaneous fistula closure:
  
  • unfavourable vs favourable
    
    • jejunum vs ileum
    • short & wide fistula (<2cm tract, >1cm defect) vs long & narrow
    • mucocutaneous continuity vs discontinuity
    • discontinuity of bowel vs continuity
    • active vs no active SB disease
    • distal obstruction vs no distal obstruction
  • FRIIENDS: foreign body, radiation, infection, inflammatory bowel, epithelialisation of tract, neoplasm, distal obstruction, steroids
  • malnourished
  • gastric, beyond lig of Treitz, ileal
• surgery depends on what’s found
  
  • goals: eliminate fistula, re-establish GI continuity, tension-free closure of abdomen
  • carefully choose entry point
  • mobilise SB carefully
  • resect fistula-bearing segments of bowel en bloc including any cutanous abdominal wall components of the fistulous tract
  • re-anastomose remaining ends of bowel; if anastomosis likely to be in area of residual sepsis, stoma usu advisable
  • measure residual length
  • tension-free abdominal wall closure - may necessitate component separation abdominoplasty in order to obtain fascial closure or ?biological mesh or tissue flaps
    
    • risk of refistulisaton high if abdo wall done w cross-linked porcine collagen mesh or synthetic mesh

Question 59

What are the indications for small bowel transplantation?

Answer 59

Because survival is poorer than that of pts on home PN, indication is SBS not maintainable on dietary supplements, and in whom PN no longer possible due to severe complications (including lack of access sites bc of central venous occlusion, or cholestatic liver disease progressing to fibrosis & cirrhosis)

• possibility of gut-lengthening operations must be considered first

Question 60

What is the recipe for St Mark’s Solution?

Answer 60

1L of water + 6 tablespoons glucose + 1 x 5mL teaspoon of salt + 1 heaped 2.5mL half teaspoon of sodium bicarb - provides 100mL of sodium per litre.

Can add cordial for palatability

WHO recommendations similar but also contain 20mmol of KCl.

Question 61

St Mark’s intestinal failure protocol

Answer 61

• Stage 1: Establish stability
  
  • restrict oral fluids to 500mL daily
  • achieve & maintain reliable venous access
  • give IV normal saline until conc of sodium in urine >20mmol/L
  • maintain equilibrium by infusion
    
    • fluid: calculated from previuos day’s losses & daily body weight records
    • sodium: 100mmol/L for every liter of previous day’s intestinal loss + 80mmol
    • potassium: 60-80mmoL daily
    • magnesium: 8-14mmol daily
    • calories, proteins, vitamins, trace elements: only if enteral absorption inadequate
• Stage 2: Transfer to oral intake
  
  • continue IV maintenance therapy
  • start low-fibre meals
  • start anti-diarrhoeal meds 30-60mins before meals
  • start gastric antisecretory drugs
  • start oral rehydration solution & discourage drinking around mealtimes
  • restrict intake of non-electrolyte drinks to 1L daily
  • encourage snacks & supplementary nourishing drinks, within above limits
  • consider need for enteral tube feeding
  • start oral mag oxide capsules, 12-16mmol daily
  • if intestinal losses remain high, start octreotide 50-100mg sc tds
  • gradually withdraw IV therapy
• Stage 3: Rehabilitation
  
  • patient and family education
  • detailed stoma care
  • refer to community continence service if intestinal continuity & incontinence from liquid stools
  • work towards home PN if continuing intestinal losses >2L/day
• Stage 4: Long-term care
  
  • regular monitoring & rv of therapy
  • vit B12 if >1m of TI resected
  • r/v other nutrients eg zinc, iron & folic acid and also fat-soluble vitamins

Question 62

What is a high vs low output enterocutaneous fistula?

Answer 62

< 500mL/24hrs vs >500mL/24hrs

Question 63

Causes of enterocutaneous fistula

Answer 63

• ECF = commonest cause of IF
• Commonest cause of fistula = Crohn’s; then
  
  • abdo surgery
    
    • most commonly anastomotic breakdown, also mesh, VAC on open abdomen next to bowel
  • colorectal cancer
  • diverticular disease
  • radiation

Question 64

What are the nutritional requirements per day?

Calories

Volume

Electrolytes Na, K, Cl, Mg, PO4

Ratio of CHO/lipid/protein

Answer 64

Calories 35-40kCal/kg/day

30mL/kg/day

Na 1.5mmol/kg

K 1mmol/kg

Cl 1.3mmol/kg

Mg 0.2mmol/kg

PO4 1mmol/kg

50/30/20

Question 65

What are the criteria for referral to intestinal failure unit?

Answer 65

1. Persistence of intestinal failure after 6 weeks with no evidence of resolution/complicated by venous access problems
2. Multiple fistula in a total dehisced abdominal wall
3. Fistula above the expertise of the hospital
4. Total or near total excision of SB resulting in <30cm
5. Recurrent venous access problems in patient needing parenteral support
6. Persistent abdominal sepsis not responding to perc/surgical drainage
7. Metabolic complications not repsonsive to medical
8. Chronic intestinal failure in a hospital not used to dealing with it

Question 66

What are the 4 causes of intestinal failure?

Answer 66

1. Loss of length
   - Crohn’s, vascular accident, volvulus, trauma

(50cm with colon, 100cm without, PN dependence at 3 months)

2. Loss of functional length
   - EC fistula
3. Loss of absorptive capacity
   - IBD, scleroderma, amyloid, celiac, rad colitis
4. Loss of intestinal function
   - ileus, pseudoobstruction, gastroparesis

Question 67

What are the three phases post IF?

Answer 67

1. Secretory

1-2 months

Focus on fluid and electrolyte correction

2. Adaption

Histological changes to allow increased absorption

3-12 months

3. Stabilisation

Question 68

What are the indications for bariatric surgery?

Answer 68

• BMI of 40 or greater
• BMI of >35 and obesity-related comorbidity:
  
  • Hypertension
  • Diabetes
  • OSA or OHS
  • Osteoarthritis
  • NASH, GORD, Hyperlipidaemia
  • Asthma, Venous stasis disease
• Clearance by dietician
• Clearance by mental health professional
• No medical contraindications to surgery

Question 69

What is the definition of malnutrition

Answer 69

BMI <18.5

unintentional weight loss of >10% in past 3-6months

BMI <20 and unintentional weight loss >5% in past 3-6months

Question 70

How does Loperamide work?

Answer 70

Loperamide is a synthetic opioid with µ-agonist activity and coincidental calcium channel blocking actions.

By slowing gut transit, increasing fluid reabsorption, and reducing secretion, Loperamide thickens stool and reduces stool frequency.

It also has direct sphincter actions, attenuating the ano-rectal inhibitory reflex and increasing resting anal pressure.

Question 71

Discuss the classification and pathology of small bowel malabsorption

Answer 71

• Failure of intraluminal digestion
  
  • Cholestasis, pancreatic insufficiency, bacterial overgrowth, surgical procedures, lactose intolerance
• Failure of mucosal absorption
  
  • Coeliac’s, Whipples, IBD, Inflammatory Bowel Disease, Radiation enteritis, Tropical sprue.