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NUTRITION
Principles of Nutrition
Avoiding of malnutrition is the basic goal in nutrition
therapy as malnutrition increases the morbidity and
mortality of the disease process and prevents or delays
the recovery. Malnutrition increases the chance of sepsis,
delays wound healing, increases the respiratory complications, and decreases the efficacy and tolerance to radiotherapy or chemotherapy.
Whenever possible enteral route of nutrition should be
SRB's Manual of Surgery
used ideally. If that is not possible then parenteral nutrition
is used.
Overfeeding should be avoided as it leads into hyperglycaemia,
hepatic steatosis, raised BUN, and excess CO2 production.
Timing and type of nutrition is also important.
Nutrition therapy reduces protein wasting.
Immunomodulators like glutamine, arginine and omega 3 fatty
acids are also very useful. Glutamine is a nonessential amino
acid synthesised in skeletal muscle. It is essential for cell
proliferation during tissue repair. Glutamine helps GI mucosal
cell proliferation, maintains mucosal integrity, improves
immune function and prevents translocation of bacteria. It is
useful in inflammatory bowel disease, short gut syndrome,
burns, major trauma, and sepsis. Glutamine is used commonly
by enteral route even though IV preparations are now available
(but it is very unstable in solutions).
Note:
• Caloric requirement: Neonatal 100 kcal/kg/day; Adult 40 kcal/kg/day;
Adult with catabolism 60 kcal/kg/day.
• It is given as: Carbohydrates 50%; Fat 30–40%; Protein 10–15%.
• Caloric values: Carbohydrate 4 kcal/g; Protein 4 kcal/g; Fat 9 kcal/g.
Indications for Nutritional Support
Methods of Enteral Feeding
Gastrointestinal tract is the best route to provide nutrition.
Enteral feeding can be delivered by bolus, by gravity or using
mechanical pump.
¾
By mouth: Requires—common sense, cleanliness,
compassion.
¾
By nasogastric tube: Confirmation of the tube in the
stomach is made by injecting 5 mL of air down the tube
and listening through a stetho scope for its bubbling entry
into the stomach. Feeding rate is 30–50 mL/hours. A time
gap of 5 hours in the night is given to allow gastric pH
to return to normal.
Note:
Problems with tube feeding are: Blockage; nausea and vomiting, aspiration; hyperosmolarity; diarrhoea; tube discomfort; Cholestasis
¾
By enterostomy: Gastrostomy; jejunostomy.
Different preparations and formulas are available for enteral
feeding. Soluble fibre containing diets along with nutrients are
better to prevent diarrhoea.
Fig. 1.190: Nasogastric tube passed should be confirmed in place
using stethoscope. Tube is used for feeding purpose.
Preoperative nutritional depletion.
Postoperative complications: Sepsis, ileus, fistula.
Intestinal fistula: High type wherein output is more than 500
mL/day. It may be duodenal, biliary, pancreatic, intestinal.
Pancreatitis, malabsorption, ulcerative colitis, pyloric stenosis.
Anorexia nervosa and intractable vomiting.
Trauma—multiple fractures, fasciomaxillary injuries, head and
neck injuries. Burns, malignant disease; renal and liver failure.
Massive bowel resection causing short bowel syndrome.
ASSESSMENT
B
Body weight Mid-arm circumference
Triceps skin fold thickness Serum albumin
Lymphocyte count
Nutritional requirements: Carbohydrates, fat, proteins,
vitamins (includes fat-soluble vitamins also), minerals, trace
elements.
COMPLICATIONS OF ENTERAL FEEDING
B
Aspiration, wound infection and leak
Diarrhoea due to rapid feeding or hyperosmolarity
Hyperglycaemia, hypokalaemia
Refeeding syndrome due to severe hypokalaemia and hypophos-
phataemia
Advantages of enteral nutrition:
¾
Enteral nutrition preserves mucosal protein, digestive
enzymes, IgA secretion; prevents mucosal atrophy and
bacterial translocation.
¾
It is more physiological as nutrients pass through liver,
the first filter to process and store. Gallstone formation
is prevented (unlike long-term TPN) by stimulating gallbladder motility.
¾
It has got less serious complications. It is cost-effective.
¾
It supplies glutamine and short chained fatty acids to gut.
Contraindications of enteral nutrition
¾
Intestinal obstruction, GI bleed, paralytic ileus, severe
diarrhoea, high output fistula.
¾
Low cardiac output, haemodynamically unstable patient.
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If safe access to enteral feeding is not present.
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Anticipated complications if thought to be present should
be avoided.
GASTROSTOMY
It is the procedure wherein a tube is passed into the stomach
per abdominally for the purpose of enteral feeding.
Indications: Severe malnutrition; major surgeries; severe
sepsis; trauma; major head and neck surgeries; any conditions
where tube feeding is required for more than 4 weeks (e.g.
burns, severe sepsis). It keeps the small bowel function active.
Contraindications: Previous gastric surgeries; intestinal
obstruction; gastric outlet obstruction or gastric diseases.
2. Kader-Senn temporary gastrostomy: It is serosal lined
temporary type similar to Stamm’s but instead of purse
string sutures, seromuscular interrupted sutures are
placed from stomach to peritoneum adjacent.
3. Percutaneous endoscopic gastrostomy (popular): Now
becoming common method (Figs. 1.198A and B).
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CHAPTER 1F General Surgery: Electrolyte and Nutrition
Fig. 1.191: Gastrostomy tube in place for enteral feeding.
A
C
Figs. 1.193A to C: Percutaneous endoscopic gastrostomy (PEG).
It is easier and acceptable method and less invasive.
B
4. Janeway’s mucus lined permanent gastrostomy by
creating mucosal entire thickness tunnel in the stomach
wall.
Problems in gastrostomy tube:
¾
Leak from gastrostomy site—gastric fistula.
¾
Trauma to other organs like colon, spleen.
¾
Infection, aspiration and pneumonia.
¾
Diarrhoea is common (30%); bloating, abdominal
cramps.
¾
Displacement, blockage of the tube.
A B
Figs. 1.192A and B: Types of gastrostomy: (A) Temporary
gastrostomy; (B) Permanent gastrostomy.
Types
¾
Based on duration of use: Temporary or permanent.
¾
Based on lining: Mucus lined (permanent) or serosal
lined (temporary).
¾
Based on technique:
1. Stamm temporary gastrostomy: After opening the
abdomen, anterior wall of the stomach is opened.
Feeding tube (Malecot’scatheter) is placed in position.
Two layers of purse string suturesare put around the
tube. Wound is closed. It is serosal lined temporary type.
In Witzel type serosal fold tunnelling is done around the
gastrostomy tube.
JEJUNOSTOMY
Jejunostomy for enteral nutrition is becoming more popular
because of—its comfort, easy to do, can be kept for long
time, lesser complication than gastrostomy.
Fig. 1.19 4 : Needle jejunostomy.
We will not know unless we begin.
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SRB's Manual of Surgery
A B
Figs. 1.195A and B: Percutaneous endoscopic gastrostomy (PEG). Guidewire passed through a trocar in the abdominal wall into the stomach is
pulled out across the oesophagus and mouth under visualisation using gastroscope. Gastrostomy catheter (tube) is passed along the guidewire
and pushed downwards across mouth and oesophagus to reach the stomach. It is further pushed along the abdominal wall through the trocar.
Gastrostomy tube is pulled out through abdominal wall and fixed. Trocar is removed. Placement of tip of gastrostomy tube can be confirmed
by doing gastroscope.
Indications are same as gastrostomy.
Types
¾
Witzel jejunostomy: Site of placing jejunostomy is 30 cm
from duodenojejunal junction.
¾
Needle jejunostomy using catheter of small gauge.
Contd...
Septicaemia; multiple trauma, short bowel syndrome
Severe pancreatitis, bowel ischaemia, peritonitis, ileus
Massive GI bleeding, unstable haemodynamically
High risk of aspiration
Hyperemesis gravidarum
Multiorgan failure, head injury, severe burns
TOTAL PARENTERAL NUTRITION (TPN)
All nutritional requirements are given only through intra-
venous route, not through gastrointestinal tract. It can be
through a central catheter through the subclavian/internal
jugular vein where the tip of venous catheter is at distal part
of superior vena cava.
It can also be a peripheral (Peripheral parenteral nutrition/
PPN) through a peripherally inserted central venous catheter
(PICC) or through a formal peripheral venous line.
INDICATIONS
B
Failure or contraindication for any enteral nutri tion for 7–10 days
High output abdominal fistulas, duodenal, biliary, pancreatic fistulas
Major abdominal surgeries of liver, pancreas, biliary, colonic
Contd...
About 5% of hospital admissions require TPN.
Technique
Using a needle and guide wire a Subclavian vein catheter is
passed just below the clavicle and fixed securely to the skin.
TPN is given through central vein and not through a periph-
eral vein.
Peripherally inserted central catheter (PICC) is also com monly
used (PPN).
Goals, Factors and Assessment in TPN
To decrease adverse effects of catabolism; to increase protein
synthesis, to reduce protein breakdown, to prevent weight
loss.
To support ongoing metabolism.
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To improve immune function, cardiac and respiratory func-
tion.
To maintain glycogen reserve in cardiac and respiratory
muscles.
To maintain acid, base and electrolyte metabolism.
Age, premorbid state, muscle mass, weight, serum albumin
should be assessed.
Underlying disease, its severity, therapies for the disease, GI
function should be assessed.
Fluid requirement is assessed by—1500 mL for 20 kg weight
+ 20 m
L/kg for additional weight.
Energy needed is calculated by calculating resting energy
expenditure (REE).
¾
By simple calculation: REE in kcal/day = 25 × weight in kg.
¾
Harris Benedict equation: REE in men = 66 + (13.7 ×
weight in kg) + (5 × height in cm) – (6.7 × age in years).
In women = 655 + (9.6 × weight) + (1.8 × height) – (4.7
× age). Activity/disease/thermal factors are also added.
¾
Indirect calorimetry: It is more accurate method done
using special instrument. REE: = (3.9 × VO
VCO
) – 61.
2
) + (1.1 ×
2
Components Used in TPN/PPN
Carbohydrates: Dextrose is less costly (1 gram dextrose
3.4 kcal); can be used in 50–70% concentration during PN.
It supplies calories, stimulates insulin release and glucose
oxidation, prevents muscle protein breakdown, has got
nitrogen sparing ability. Problems of carbohydrate/dextrose
are—low calorie value compared to fat, requires large fluid
volume to infuse, hyperglycaemia, causes more CO
tion, because of high osmolality it causes thrombophlebitis
in 10% or above concentration. Rate of administration of
dextrose is 5 mg/kg/min.
Fat: Fat gives high calorie (1 gram—9 kcal), essential fatty
acids. It is given as emulsion containing long chain triglycerides. It contains soyabean/sunflower oil with egg yolk phospholipids (emulsifying factor), glycerin (isotonic). Fat has got
low osmolality (260 mosm/L); it is available as 10%, 20%,
30% emulsions. Advantages of fat in PN are—high calorie,
prevents hyperglycaemia, glucose and nitrogen sparing, less
CO
production, less insulin production; it prevents essential
2
fatty acid deficiency (for this purpose 3 days a week dose is
given), reduces thrombophlebitis. Problems of lipids in PN
are—hypertriglyceridaemia, sepsis, fat embolism, fat overload,
hepatic dysfunction, pancreatitis, delayed gastric emptying.
Lipid emulsions are avoided in hyperlipidaemia, anaemia,
acidosis, obesity. Lipid emulsion is a good culture media for
bacteria and fungi; so care should be taken to prevent sepsis.
Triglyceride level should be monitored weekly; if it is more
than 400 mg%, infusion is discontinued. Mixture of long and
medium chain fatty acids is better tolerated and efficient.
Amino acids: They are source of proteins. Calorie value of
amino acid is 4 kcal/gram. 6.25 gram protein has 1 gram
produc-
2
nitrogen. In PN 20% of energy comes from amino acids; rest
from dextrose and fat. Daily protein need is 0.8–1.5 gram/kg.
Protein supplement should be less in patients with CRF and
hepatic encephalopathy. Its need is more in burns, trauma,
enteropathy, sepsis. Protein supplement should not exceed
1.7 gram/kg/day; if so will cause raised urea production.
Uses of amino acids in PN—in protein anabolism; prevents
catabolism. Proper monitoring by doing BUN or ammonia
level is essential during amino acid therapy.
Vitamins, electrolytes, trace elements and minerals:
Electrolytes like sodium, potassium, magnesium, phosphate,
calcium; fat-soluble vitamins like A, D, E, K; water-soluble
vitamins; trace elements like chromium, copper, iodine, iron,
manganese, selenium, zinc are all used in PN.
MONITORING THE PATIENT
B
By body weight, fluid balance, blood glucose, electrolytes, blood
urea, LFT, serum calcium, magnesium, phosphate should be done
at regular intervals.
A weight gain more than one kg/day signifies fluid overload.
Complications
Technical: Air embolism; Pneumothorax; Bleeding; Catheter
displacement, sepsis, blockage; Infection, thrombosis.
Biochemical
¾
Electrolyte imbalance: Hyponatraemia, hypokalaemia,
hypophosphataemia.
¾
Hyp erosmolarity; Hyperglycaemia—common.
¾
Dehydration; Azotaemia
¾
Altered immunological and reticuloendothelial function.
Others: Dermatitis; Anaemia and increased capillary perme-
ability; Cholestatic jaundice (It is common); Severe hepatic
steatosis; Metabolic acidosis; Candida infection (candidiasis),
staphylococcal infection (10–15%).
Contraindications: Cardiac failure; Blood dyscrasias; Altered
fat metabolism.
Note:
Anabolic steroid durabolin 25 mg IM weekly is given to improve nitrogen
balance.
HOME PARENTERAL NUTRITION
B
It is becoming popular
It is commonly used in western countries
It is indicated in short bowel syndrome or any other conditions
wherein enteral feeding is not possible but patient can be sent
home with provision for home parenteral nutrition
Patient himself uses the total parenteral nutrition (TPN) fluids as
advised at home. He will be with TPN catheter
Patient should attend TPN clinic weekly for follow-up or immedi-
ately whenever complications arise
Patient will be comfortable psychologically and often can attend
his job also
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CHAPTER 1F General Surgery: Electrolyte and Nutrition
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REFEEDING SYNDROME
are common problems. All these conditions are called as
comorbidities.
Refeeding syndrome is occurrence of severe fluid and elec-
trolyte imbalance in severely malnourished individual while
starting the proper feeding enteral or parenteral nutrition. It
is more common in TPN.
It causes hypomagnesaemia, hypocalcaemia and hypophos-
phataemia leading into myocardial dysfunction, respiratory
changes, altered liver functions, altered level of consciousness, convulsions and often death.
Gradual feeding and correction of magnesium, phosphate
and calcium and other electrolytes is important.
Condition is common in chronic starvation, severe anorexia
SRB's Manual of Surgery
and alcoholic patients.
Infertility is common in married morbid obese women due
to improper ovulation, polycystic ovary disease. Urinary
incontinence is common in morbid obese women (stress
incontinence and detrusor instability). Pregnancy in morbid
obese patient is considered as high-risk pregnancy. Gestational diabetes, hypertension, are common. It is better these
women to undergo bariatric surgery prior to pregnancy which
definitely reduces the complications during pregnancy. Such
individual after bariatric surgery needs more iron and vitamin
supplements.
Evaluation of the patient—cardiac and respiratory assess-
ment; lipid profile; blood glucose; renal and liver status
OBESITY AND MORBID OBESITY
assessment; anaesthesia risk assessment.
Obesity is a condition where weight is more than 20% above
the normal. Body mass index (BMI) is weight in kilogram
divided by height in metres squared [wt in kg/(Ht in meters)2].
Morbid obesity is a condition wherein BMI is more than 40
kg/m2. It is often also defined as weight 100 lbs or more; or
100% over ideal body weight.
Weight more than double the expected weight to that age and
height of the individual is also often called as morbid obesity.
Body weight exceeding BMI 50 kg/m2 is called as superobesity.
Causes of Obesity
Familial, hyperinsulinism, hyperadrenocorticism, hyogonadism.
Abnormal eating behaviour: Hormones which control eating
are—ghrelin from stomach; insulin from pancreas; leptin
from fat; PYY 3–36 from colon. Hypothalamus is the center
in CNS which controls eating.
Nutritional status BMI (kg/m2)
• Underweight • <18.5
• Normal • 18.5–24.9
• Overweight (Preobesity) • 25.0–29.9
• Obesity • >30
– Class I – 30.0–34.9
– Class II (Moderate) – 35.0–39.9
– Class III (Severe/Morbid) – 40.0
• Superobesity • >50
• Super superobesity • >60
Obesity is more common in young women. Child of a normal
weight parents has 10% chance to become obese. If both parents
are obese then child has got 80% chances to develop obesity.
Problems with Morbid Obesity
Obstructive sleep apnoea, degenerative joint disease, back
pain, hypertension, GERD, gallstones, type II diabetes,
hyperlipidaemia, arrhythmias, venous diseases, DVT, skin
diseases, urine incontinence, infertility, ventral hernias,
obesity hypoventilation syndrome, polycystic ovarian disease,
hirsutism, gynaecomastia, steatohepatosis, malignancies—
Medical Management
General: Diet, life style changes, exercise.
Drugs: (1) Orlistat is a selective inhibitor of gastric and
pancreatic lipases that reduces the absorption of lipids from
intestine. (2) Sibutramine is a noradrenaline and 5 HT reuptake inhibitor which act as appetite suppressor.
Surgical Treatment (Bariatric Surgery)
Bariatric surgery causes long-term durable weight loss. Patient’s
eating behaviour is reduced to slow ingestion of small boluses
of food and or also reducing the absorptive surfaces.
Types of Bariatric Surgery
Restrictive wherein caloric intake is reduced. Purely gastric
restrictive procedures are vertical banded gastroplasty (VBG)
and laparoscopic adjustable gastric banding (LAGB).
Malabsorptive wherein absorption of calories and nutrients
from food is reduced. Biliopancreatic diversion (BPD) and
biliopancreatic diversion with duodenal switch (BPD-DS) are
malabsorptive procedures.
Combined wherein both methods are used. Roux-en-Y gastric
bypass (RYGB) is both restrictive and malabsorptive types.
Gastric bypass reduces GI polypeptide ghrelin level secreted
from fundus of stomach and duodenum. Ghrelin acts on
specific receptor in CNS—hypothalamus to initiate appetite.
This stimulation is reduced to decrease appetite. In restrictive
only procedure ghrelin level raises and so appetite stimulation
is not controlled.
Indications for Bariatric Surgery
Body mass index (BMI) more than 40 kg/m2 or BMI more than
35 kg/m
American Association of Bariatric Surgery (ASBS) published
indications and approved surgeries.
2
with comorbidity is indication for bariatric surgery.
Contraindications
Patients who are unfit for general anaesthesia (cardiac/renal/
respiratory/hepatic causes) or who are unable to adjust post-
operative life styles or psychiatric patients are contraindications
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for bariatric surgery.
Cholecystolithiasis After Bariatric Surgery
Gallstone formation is common after bariatric surgery (50%).
It is due to rapid weight loss. If gallstones are present at the
time of bariatric surgery it is essential to do laparoscopic
cholecystectomy during bariatric procedure. It is controversial about doing prophylactic cholecystectomy during
bariatric surgery even though it is practiced in many places.
Advantages are—it prevents future gallstone formation at the
time of bariatric surgery (loss of access); it prevents difficulties in approaching CBD in case needed endoscopically due
to surgery. Disadvantage is cholecystectomy adds additional
1 hour time for bariatric surgery increasing the risk of immediate complications. Patients who are not having gallstones at
the time of bariatric surgery, should receive ursodeoxycholic
acid 300 mg twice daily for 6–12 months of post-bariatric
surgery period. Often stomach is anchored to abdominal wall
as access part to biliary system for future need.
Preoperative Preparations and Evaluation
Complete cardiac, respiratory/renal/hepatic evaluation.
Lipid profile and blood glucose assessment.
Obstructive sleep apnoea in obese patient should be assessed
using polysomnography and be treated.
Risk assessment for DVT should be done.
If GERD symptoms are present gastroscopy should be done.
USG abdomen to identify gallstones should be done; if gall-
stones present it is of usual practice to do cholecystectomy
along with bariatric procedure.
Nutritional evaluation and dietician advice for preoperative
and postoperative diet management.
Psychological screening is needed to all patients to counsel
their postoperative care and diet.
Separate theatre table is needed for morbid obese patient.
Equipments should be long and flexible. In laparoscopic
surgery, special ports and instruments are needed.
DIFFERENT SURGERIES (Refer Table Below)
Note: Differnet Procedures are Disscussed Below
Vertical Banded Gastroplasty (VBG); Mason (1982)
• It is a purely restrictive type with creation of a calibrated stoma in
the lesser curvature which is reinforced by an encircled mesh with
a proximal gastric pouch. After laparotomy Ewald’s stomach tube
is passed per orally to place against lesser curve. A 2.5 cm circular
window is created in the body of stomach near lesser curvature 8 cm
below the angle of His. After this, four lines of linear vertical stapling
are done from circular opening towards angle of His. This staple line
ideally should be divided using another cutting linear stapler to reduce
chances of dehiscence. This creates a 50 m
A 1.5 × 7 cm polypropylene mesh is placed around the lesser curve
through circular opening and sutured to create a 5 cm collar stoma. It
is not used at present; it is only of historical importance.
• VBG causes only medium term weight loss; its efficacy is less compared
to other procedures. Complications of VBG are—stricture at stoma
(20%), vomiting (30%), reflux (20%), staple line dehiscence (40%),
conversion into other procedures. Mortality is 0.3%.
• VBG is technically easier to do; it has got very less chances of long-term
metabolic and nutritional deficiencies.
Laparoscopic Adjustable Gastric Banding (LAGB)
• It is also a restrictive type (1992, Guy Bernard) to create a narrow
stoma just below the OG junction. It is used in adolescents and elderly.
It is contraindicated in hiatal and paraoesophageal hernias. It is done
using laparoscopy.
• Under general anaesthesia, with patient in reverse Trendelenburg position
six laparoscopic ports are placed. Using pars flaccida method, retrogastric
tunnel is created; a silicone band is passed through the tunnel to encircle
the cardia just below the OG junction; tail of the band is buckled and
locked. Stoma diameter is determined by inserting a calibration tube.
Stomach over the band is imbricated using interrupted sutures except
the buckle area. Silicone tube end is brought out through the abdominal
wall to connect access port. It is used for band volume adjustment by
injecting or withdrawing the saline.
L proximal gastric pouch.
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CHAPTER 1F General Surgery: Electrolyte and Nutrition
Complications of obesity Obesity and surgery Treatment for obesity
• General: Difficulty in work, fatigue, depression,
back pain, arthritis and gout
• Cardiovascular: Hypertension, stroke,
thrombophlebitis, pulmonary embolism
• Pulmonary: Hypoventilation, poor respiratory effort
• GIT: Hiatus hernia with reflux, changes in liver,
pancreatitis, gallstones
• Endocrine: Diabetes mellitus
Note:
Many of these patients after bariatric surgery require
plastic surgery for abdominal contour (panniculectomy, abdominoplasty) after weight reduction.
• Hernia and gallstones are more
common in obese individual
• Burst abdomen, incisional hernia are
more common in obesity
• Delay in recovering from anaesthesia
• Infertility is more common
• General: Dieting, exercise
• Drugs: Orlistat, Sibutramine
• Surgeries:
– Restrictive
Vertical banded gastroplasty
Laparoscopic adjustable
gastric banding (LAGB)
Jaw wiring
– Malabsorptive
Biliopancreatic diversion (BPD)
Biliopancreatic diversion with
duodenal switch (BPD-DS)
Jejunoileal bypass
– Combined
– Roux-en-Y gastric bypass (RYGB)
open or laparoscopic
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Fig. 1.196: Vertical banded gastroplasty (VBG).
SRB's Manual of Surgery
Fig. 1.197: Laparoscopic adjustable gastric banding (LAGB).
• Gastrograffin study is done on 1st postoperative day to assess band
position and lumen patency. Patient is advised to have liquid diet for
one month. Band adjustment is done under fluoroscopic guidance in
2 months. Adjustment is done to achieve weight loss at a rate of 2 kg/
week. Efficacy of LAGB is 55%.
• Complications of LAGB are—spleen/stomach injury; bleeding; band
slippage (10%); band erosion (7.5%); tube related complications;
vomiting; pouch dilatation; reflux. Conversion rate is 3%; mortality is
less than 0.5%.
Jejunoileal Bypass
• Proximal jejunum is divided and proximal cut end is anastomosed to
distal ileum just proximal to ileocaecal valve to reduce the absorptive
surface area of small bowel.
• Complication rates were higher and so procedure is not practiced. Colon
in these patients absorbs high level of oxalate causing nephrocalcinosis.
Bypassed bowel promotes bacterial growth causing endotoxic-induced
liver injury, cirrhosis, liver failure. Complications like protein, vtamin K,
vtamin B
arthritis, osteoporosis are common.
deficiencies; gallstone formation; enteritis and diarrhoea;
12
Roux-en-Y Gastric Bypass
• It is commonly done combined procedure. It can be done by open
or laparoscopic method. Proximal stomach is dissected between 1st
and 2nd branches of left gastric branches. Vagii nerves and nerves of
Latarjet are retained carefully. Stomach is transected at this proximal
site to create a proximal gastric pouch (15 m
BMI is 40–50). It is usually carried out through linear stapler. Jejunum
is transected 45 cm from ligament of Treitz. A side to side jejunojejunal
anastomosis is done using stapler 75 cm distal to the distal cut end.
Proximal Roux part of the distal jejunal cut part (75–150 cm, based on
patient’s preoperative weight) is brought out through the transverse
mesocolon towards the created proximal gastric pouch and gastrojejunostomy is done to this proximal gastric pouch. Mesenteric defect
is closed. Stomal integrity is checked on table by air distension and
methylene blue infusion. Gastrograffin study is done in 24 hours to
assess pouch size, stomal patency and distal obstruction. Oral food is
started in 24 hours and patient is discharged in 4 days.
L if BMI is >50; 30 mL if
• It was the first malabsorptive procedure done for obesity. Now this
technique is not done due to high incidences of complications.
Fig. 1.198: Jejunoileal bypass procedure (JIB).
Fig. 1.199: Roux-en-Y gastric bypass procedure (RYBG).
• RYGB is more useful in weight loss compared to purely restrictive
types. 5 years weight loss is 60–75%. It also prevents progression of
noninsulin dependent diabetes mellitus, controls hypertension, sleep
apnoea, hyperlipidaemia, asthma, arthritis, GERD.
• Complications are—Roux obstruction, anastomotic leak, acute distal
gastric dilatation, stomal stenosis, marginal ulcer, dumping syndrome,
internal hernias, vitamin B
deficiency, iron deficiency anaemia. Distal
12
gastric dilatation needs emergency intervention which is usually due to
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jejunojejunal obstruction.
Laparoscopic RYGB (1994, Wittgrove, Clark, Trembly)
• Technique is similar to open RYGB. Anastomoses are done using
endoscopic stapler. GJ between gastric pouch and Roux jejunum is
done either using linear stapler through laparoscopic port after making
a gastrotomy in the pouch which is later sutured after staple firing;
or using circular stapler anastomosis is done wherein anvil is initially
passed transorally often under endoscopic guidance across the pouch
into the Roux jejunum; or using hand sewing with absorbable sutures.
Omentum is released from the colon and is covered over the GJ.
Mesenteric defect and Patterson Brown defect are closed. A Bronlin
antiobstructive stitch is placed between Roux and biliopancreatic
limbs. Integrity of anastomosis is checked using insufflation of air,
methylene blue. Complications are similar to open RYBG. Conversion
rate is 9%. Advantages of LRYBG to open RYBG are—faster recovery,
less postoperative pain, less wound related complications, less morbid
one. Disadvantage of LRYBG is availability of facility, technical expertise,
and steep learning curve.
• Now technique is modified to antegastric, antecolic one which has
become popular (Gagner).
Biliopancreatic Diversion (BPD) (Nicola Scopinaro, Italy)
• It is done in patients who had failed restrictive procedure or who are
superobese.
Fig. 1.201: Biliopancreatic diversion with duodenal switch
procedure (BPD-DS).
to create gastric reservoir (200 mL) along lesser curve. Duodenum just
distal to first part is divided using stapler; proximal cut end is sutured
to proximal upward pulled end of the distal ileal segment of earlier
transected ileum, 250 cm from ileocaecal valve. Biliopancreaticoduodenal with proximal jejunoileal segment is later stapled to distal ileum
50 cm proximal to ileocaecal valve. Duodenal switch reduces the rate
of marginal ulcer and dumping syndrome.
• Results of BPD/BPD-DS are—excellent for weight reduction compared
to restrictive procedures. But they need lifelong supplement of vitamins,
fat-soluble vitamins, calcium, and iron. Technically BPD is easier to do
when compared to BPD-DS.
• Complications of BPD/BPD-DS are—anemia (30%); protein deficiency
(20%); dumping syndrome; marginal ulcer (in BPD 10%; in BPD-DS it
is 1%); osteoporosis; night blindness; biliopancreatic limb obstruction;
staple line leak; staple line bleed; DVT; subphrenic abscess. Vitamin B
deficiency is specific.
Ileal Interposition with Sleeve Gastrectomy
103
CHAPTER 1F General Surgery: Electrolyte and Nutrition
12
Fig. 1.200: Biliopancreatic diversion procedure (BPD).
• Distal subtotal gastrectomy is done with formation of proximal gastric
pouch (of 400 mL in BMI 40–50; 200 mL in BMI >50). Ileum is
transected 250 cm proximal to ileocaecal valve; distal ileal segment is
brought up to anastomose into the proximal gastric pouch. Proximal
biliopancreatic jejunoileal limb is anastomosed into distal ileal segment
50 cm proximal to ileocaecal valve as end to side stoma. Additionally
cholecystectomy should be done.
• Modification of BPD with duodenal switch (BPD-DS) has become more
popular. Here sleeve gastrectomy along the greater curvature is done
The lazy man is always occupied with his laziness.
It is done mainly in type II diabetes. Often they are associated with obesity,
dyslipidaemia, hypertension, nephropathy and neuropathy. Two types of
ileal interposition with sleeve gastrectomy are done.
Type 1: Sleeve gastrectomy is done. 170 cm of ileum with mesentery is
isolated 30 cm from ileocaecal junction. Jejunum is transected 50 cm from
duodenojejunal flexure. Isolated 170 cm ileal segment is interposed 50 cm
distal to DJ junction with end-to-end anastomosis on both ends.
Type 2: After doing sleeve gastrectomy, gastroduodenal junction is
transected; cut proximal end of duodenum is closed. 170 cm ileal segment
with mesentry is isolated and interposed between cut end of stomach and
side of jejunum 50 cm distal to DJ flexure.
G. Shock
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C hapter Outline
·
Shock
·
Stages of Shock
·
Effects of Shock
·
Clinical Features of
Shock (Hypovolaemic
Shock)
·
Assessment, Investigations and Monitoring
·
Central Venous Pressure
SHOCK
Shock is defined as a state of cellular and tissue hypoxia with
either reduced oxygen delivery or poor oxygen utilisation
or increased oxygen consumption with circulatory failure
(collapse) and poor perfusion.
Normal aerobic metabolism is not maintained due to hypoper-
fusion. Shock is meant by ‘inadequate perfusion’ to maintain
normal organ function. It may be initially reversible but becomes
irreversible eventually if not treated leading multiorgan failure and
death. Shock can be hypovolaemic (16%), cardiogenic (16%),
distributive(septic (62%), neurogenic/anaphylactic (4%),
acute adrenal insufficiency) or obstructive (2%) or endocrine
(hypothyroidism, thyrotoxic crisis, adrenal insufficiency).
At cellular level hypoxia causes change of normal aerobic to
anaerobic metabolism causing lactic acidosis. Intracellular
potassium is released into circulation. Lysosomes from
cells get released into blood causing cell lysis. Hypoxia and
acidosis through complements release free oxygen radicals
and cytokines which damage capillary endothelium. Eventually cardiovascular, respiratory, renal, endocrine and GIT will
be affected presenting as systemic features.
CAUSES OF SHOCK
B
1. Hypovolaemic shock—due to reduction in total blood volume.
It may be due to:
a. Haemorrhage
– External from wounds, open fractures
– Internal from injury to spleen, liver, mesentery or pelvis
b. Severe burns, which results in loss of plasma
c. Peritonitis, intestinal obstruction
d. Vomiting and diarrhoea of any cause
2. Cardiac causes
a. Acute myocardial infarction, acute carditis
b. Acute pulmonary embolism wherein embolus blocks the
pulmonary artery at bifurcation or one of the major branches
·
Pulmonary Capillary
Wedge Pressure
·
Systemic Inammatory
Response Syndrome
·
Multiple Organ
Dysfunction Syndrome
·
Oxygen Therapy
·
Cardiac Arrest
Contd...
Contd...
c. Drug induced
d. Toxaemia of any causes
e. Cardiac surgical conditions like valvular diseases, congenital
heart diseases
f. Cardiac compression causes
i. Cardiac tamponade due to collection of blood, pus, fluid in
the pericardial space which prevents the heart to expand
leading to shock.
ii. Trauma to heart
Septic shock—is due to bacterial infections which release toxins
3.
leading to shock
x 4. Neurogenic shock—due to sudden anxious or painful
stimuli causing severe splanchnic vessel vasodilatation. Here,
patient either goes for cardiac arrest and dies or recovers fully
taneously—spinal cord injury/anaesthesia can cause neuro-
spon
genic shock
5.
Anaphylactic shock—is due to Type 1 hyper sensitivity reaction
Respiratory causes
6.
a. Atelectasis (collapse) of lung
b. Thoracic injuries
c. Tension pneumothorax
d. Anaesthetic complications
Other causes
7.
a. Acute adrenal insufficiency (Addison‘s disease)
b. Myxoedema
Pathophysiology of Shock
Any cause of shock
↓
Low cardiac output
↓
Vasoconstriction occurs as a compensation to perfuse vital
organs like brain, heart, kidneys, liever
↓
Because of vasoconstriction and tachycardia
↓
Dynamic circulation increases
↓
Tachypnoea occurs to increase the oxygen saturation
↓
Peripheral veins (capacitance vessels) constrict diverting
blood from splanchnic system towards essential vital organs
↓
Decreased renal blood flow reduces the GFR and thereby the
urine output
↓
Renin angiotensin mechanism gets activated causing further
vasoconstriction and aldosterone release
↓
Causes salt and water retention
↓
ADH is released
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↓
Further concentration of urine occurs
When shock persists cardiac output falls further
↓
Hypotension and tachycardia occurs leading to poor perfusion
of coronaries
↓
Hypoxia—metabolic acidosis
↓
Release of cardiac depressants
↓
Cardiac (pump) failure
Hypoxia
↓
Anaerobic metabolism
↓
Lactic acidosis
↓
Cell wall damage
↓
Sodium and calcium enter
the cell
↓
Potassium leaks out of the cell
↓
Causes hyperkalaemia, hyponatraemia and hypocalcaemia
↓
Intracellular lysosomes break down releasing powerful
enzymes which destroy own cell
↓
SICK CELL SYNDROME
free radical production, altered complement activation, failure to have
a localisation of inflammation. It is severe type of reversible shock.
↓
Which will lead to established microvascular occlusion, cellular dysfunction, sick cell syndrome, DIC and PUMP failure.
↓
M
ODS (Multiorgan dysfunction syndrome) (Irrever sible shock)—of
lungs, kidneys, liver, clotting system and brain.
STAGES OF SHOCK
B
x Stage of hypoperfusion and hypoxia: Aerobic metabolism
changes to anaerobic leading to lactic acidosis (metabolic
acidosis).
x Stage of compensatory shock: It is neuroendocrine response to
maintain the perfusion of vital organs like brain, lungs and heart.
Noradrenaline, renin-angiotensin and antidiuretic hormone (ADH)
gets activated causing vasoconstriction of organs like gastrointestinal, kidney to divert the blood to heart, lungs and brain.
x Stage of decompensatory (progressive) shock: Here compensa-
tory mechanism fails; cell perfusion decreases causing raised
intracellular sodium but low intracellular potassium. Microcirculation fails beginning the failure of kidneys, liver and lungs.
x Stage of irreversible (refractory) shock: Here cellular ATP
metabolism is lost completely leading into MODS and MOF
(multiorgan failure).
Note:
• Distributive shock is one in which there is vasodilatation, decreased
vascular resistance, hypotension, altered microvascular perfusion
with arteriovenous shunting, altered cellular oxygen metabolism. It
is seen in septic shock, spinal trauma, adrenal crisis and anaphylaxis.
• Obstructive shock occurs due to mechanical impediment of circulation due to pulmonary embolism, tension pneumothorax or cardiac
tamponade, aortic stenosis.
105
CHAPTER 1G General Surgery: Shock
Platelets are activated forming small clots
in many places
↓
Disseminated intravascular coagulation (DIC) (Consumption
coagulopathy)
↓
Further bleeding.
STAGES OF SHOCK
Factors like infection, trauma, burns,
haemorrhage, hypovolaemia
↓
Hypoxia and its effects.
↓
SIRS (Systemic inflammatory response syndrome) is due to vaso-
dilatation, increased endothelial per meability, thrombosis, leucocyte
migration and activation.
↓
All these lead to altered cytokines level, abnormal NO (nitric oxide)
synthesis, abnormal arachidonic acid metabolism, neutrophil activation,
In time of test, family is best.
EFFECTS OF SHOCK
Heart: Low perfusion → low venous return → decreased cardiac
output → hypotension → tachycardia. Persistent shock causes
hypoxia and release of myocardial depressants leading to further
cardiac damage.
Lung: Interstitial oedema → decreased gaseous exchange →
pulmonary arteriovenous shunting → tachypnoea → Adult/Acute
respiratory distress syndrome (ARDS) and pulmonary oedema.
Metabolic: Shock leads to hypoxia, which activates anaerobic
metabolism leading to lactic acidosis. Antidiuretic hormone
(ADH) is released which increases the reabsorption of water
from renal tubules. Other hormones released are ACTH,
prostaglandins, histamine, bradykinin, and serotonin to compensate the effects of shock to increase the perfusion of vital organs
like heart, brain and lungs.
Cellular changes occur in persistent shock due to release of
lysosomal enzymes, which alters the cell membrane permeability
causing cell death—sick cell syndrome.
Sympathetic overactivity alters the microcirculation leading to
capillary dysfunction.
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