Sabiston Small Bowel Flashcards
Anatomy , Lengths
duodenal length 20 cm
jejunal length at 100 to 110 cm
ileal length at 150 to 160 cm.
Anatomy , Jejunum Vs Ileum
jejunum :
larger circumference, thicker
can be identified during surgery by examining mesenteric vessels, only one or two arcades send out long, straight vasa recta to the mesenteric border
Ileum : blood supply to the ileum may have four or five separate arcades with shorter vasa recta
Mucosa of Small bowel
characterized by transverse folds (plicae circulares), which are prominent in the distal duodenum and jejunum
Blood Supply to Duodenum
Superior mesenteric artery > distal duodenum.
The celiac artery > proximal duodenum
Blood Supply to Small Bowel
-superior mesenteric artery (except for the proximal duodenum )
-SMA > courses anterior to the uncinate process of the pancreas and the third portion of the duodenum, it divides to supply the pancreas, distal duodenum, entire small intestine, and ascending and transverse colons.
-abundant collateral blood supply provided by vascular arcades coursing in the mesentery
Innervation
parasympathetic and sympathetic divisions of the autonomic nervous system
The parasympathetic fibers > the vagus nerve, traverse the celiac ganglion and influence secretion, motility, and probably all phases of bowel activity.
The sympathetic fibers > splanchnic nerves > located in a plexus around the base of the superior mesenteric artery
Location of myenteric (Auerbach) plexus and (Meissner plexus)
myenteric (Auerbach) plexus > muscularis propria (between the muscles)
(Meissner plexus) > networks of lymphatics, arterioles, and venules > in Submucosa
lamina propria Location and Role
between the epithelial cells and muscularis mucosae
Contains > plasma cells, lymphocytes, mast cells, eosinophils, macrophages, fibroblasts, smooth muscle cells, and noncellular connective tissue
protective role > rich supply of immune cells
Main functions of the crypt epithelium and Villous Epithelium
crypt epithelium > cell renewal, exocrine, endocrine, water, and ion secretion
villous epithelium > digestion and absorption.
What are the Four main cell types are contained in the mucosal layer
(i) absorptive enterocytes
(ii) goblet cells, which secrete mucus
(iii) Paneth cells, which secrete lysozyme, (TNF), and cryptdins, which are homologues of leukocyte defensin peptides related to the host mucosal defense system
(iv) enteroendocrine cells,produce the gastrointestinal hormone
What is the Main Cell in the Mucosa
Absorptive enterocytes
Function of The brush border of the small intestine
contains the enzymes
lactase, maltase, sucrase-isomaltase, and trehalase
split the disaccharides into their monosaccharides
Transport of the released hexoses (glucose, galactose, and fructose) is by
active transport.
The major routes:
sodium-glucose transporter 1 (SGLT-1), glucose transporter 5 (GLUT-5), and glucose transporter 2 (GLUT-2).
Protein Digestion
Pancreatic trypsinogen is secreted in the intestine by the pancreas in an inactive form > activated by the enzyme enterokinase, a brush border enzyme in the duodenum to an activated form of trypsin.
Bile Acid
-unconjugated bile acids absorbed into the jejunum by passive diffusion
-conjugated bile acids that form micelles are absorbed in the ileum by active transport
-then reabsorbed from the distal ileum and pass through the portal venous system to the liver for secretion as bile.
Vitamins Absorbtion
Calcium > duodenum and jejunum by active transport
facilitated by an acid environment and is enhanced by vitamin D and parathyroid hormone
Iron > as a heme or nonheme component > duodenum by an active process.
total absorption of iron is dependent on body stores of iron and the rate of erythropoiesis
Potassium, magnesium, phosphate, and other ions actively absorbed throughout the mucosa
Vitamin B1 > jejunum by an active process similar to the sodium-coupled transport system for vitamin C.
Vitamin B2 > the upper intestine by facilitated transport.
vitamin B12 > terminal ileum.
derived from cobalamin, freed in the duodenum by pancreatic proteases, binds to intrinsic factor
Vitamin B6 > simple diffusion into the proximal intestine
Motility
Sympathetic activity inhibits motor function
parasympathetic activity stimulates it.
motilin, its peak plasma level during phase III (intense bursts of myoelectrical activities resulting in regular, high-amplitude contractions) of migrating myoelectric complexes
The gut-associated lymphoid tissue is localized in four areas
-Peyer patches > activate and prime B and T cells
-lamina propria lymphoid cells
-Paneth cells
-intraepithelial lymphocytes > unique subtype of T cells.
major protective immune mechanisms for the intestinal tract is
the synthesis and secretion of IgA.
produced by plasma cells in the lamina propria
Which Primary colonic cancers Present Like SBO
Tumors arising from the cecum and ascending colon
MC Cause of SBO
Adhesions 60%
Malignant 20%
Hernia 10%
Crohns 5%
Early in the course of an obstruction
intestinal motility and contractile activity increase > diarrhea
Later in the course of obstruction
intestine becomes fatigued and dilates > water and electrolytes accumulate intraluminally and in the bowel wall itself > massive third-space fluid loss > dehydration and hypovolemia
proximal obstruction vs Distal obstruction
Proximal > dehydration, hypochloremia, hypokalemia, and metabolic alkalosis
Distal > large quantities of intestinal fluid into the bowel; however, abnormalities in serum electrolyte levels are usually less dramatic.
Sepsis in SBO
-the jejunum and proximal ileum Normally have only 103 to 105 (CFU/mL) of bacteria.
-With obstruction (most commonly Escherichia coli, Streptococcus faecalis, and Klebsiella spp.) > reaching concentrations of 109 to 1010 CFU/mL.
increase in the number of indigenous bacteria translocating to mesenteric lymph nodes and even systemic organs
> amplifies the local inflammatory response leading to intestinal leakage and subsequent increase in systemic inflammation.
higher obstruction vs Distal
Higher > Nausea and vomiting , hyperactive bowel sounds
distally > less emesis;
initial and most prominent symptom is cramping abdominal pain, minimal or no bowel sounds are noted
As the obstruction becomes more complete with bacterial overgrowth, the vomitus becomes more feculent, indicating a late and established intestinal obstruction.
Plain abdominal film signs of SBO
Supine :
-Dilated gas or fluid filled small bowel >3 cm
-Dilated stomach
-Small bowel dilated out of proportion to colon
-Stretch sign
-Absence of rectal gas
-Gasless abdomen
-Pseudotumor sign
Plain abdominal film signs of SBO
Upright or Left Lateral Decubitus :
-Multiple air fluid levels
-Air fluid levels longer than 2.5 cm
-Air fluid levels in same loop of small bowel of unequal lengths
-String of beads sign
why put NGT in SBO
-empties the stomach
-reducing the hazard of pulmonary aspiration of vomitus
-minimizing further intestinal distention from swallowed air
Radiation enteropathy causing SBO Tx
can be treated nonoperatively with tube decompression and the potential addition of corticosteroids, particularly during the acute setting.
In the chronic setting, laparotomy will be required with possible resection of the irradiated bowel or bypass of the affected area.
If intestinal viability is questionable
the bowel segment should be completely released and placed in a warm, saline-moistened sponge for 15 to 20 minutes and then reexamined.
If normal color has returned and peristalsis is evident, it is safe to retain the bowel
Another options : Doppler probe, administration of fluorescein and Intraoperative near-infrared angiography or second-look laparotomy 18 to 24 hours after the initial procedure.
consideration of laparoscopic management in SBO
-mild abdominal distention
-proximal or partial obstruction;
-anticipated single-band obstruction
-and those with low risk of strangulation or perforation
laparoscopic found to be of greatest benefit in
-patients with fewer than three previous operations
-were seen early after the onset of symptoms
-and were thought to have adhesive bands as the cause.
the most effective means of limiting the number of adhesions
is a good surgical technique :
-gentle handling of the bowel to reduce serosal trauma
-avoidance of unnecessary dissection
-exclusion of foreign material from the peritoneal cavity
-the use of absorbable suture material when possible,
-avoidance of excessive gauze sponge use,
-the removal of starch from gloves
-adequate irrigation and removal of infectious and ischemic debris
-preservation and use of the omentum around the site of surgery or in the denuded pelvis
Causes of ileus.
- After laparotomy
- Metabolic and electrolyte derangements (e.g., hypokalemia, hyponatremia, hypomagnesemia, uremia, diabetic coma)
- Drugs (e.g., opiates, psychotropic agents, anticholinergic agents)
- Intraabdominal inflammation
- Retroperitoneal hemorrhage or inflammation
- Intestinal ischemia
- Systemic sepsis
Ileus vs SBO
-Plain abdominal radiographs may reveal distended small bowel as well as large bowel loops.
-In cases that are difficult to differentiate from obstruction, barium studies may be beneficial
Etiology of Crohns
-infectious : Mycobacterium paratuberculosis and enteroadherent E. coli.
-immunologic : Humoral and cell-mediated immune reactions , cytokines, such as interleukin (IL)-1, IL-2, IL-8, and TNF-α
genetic : NOD2, MHC, and MST1 3p21
Environmental factors : smoking
the single strongest risk factor for development of Crohns disease
-is having a first-degree relative with Crohn disease
-The most important gene in Crohn disease development is NOD2
The NOD2 gene is associated with a decreased expression of
antimicrobial peptides by Paneth cells.
Which Gene is a predictor of ileal disease, ileal stenosis, fistula, and Crohn-related surgery.
NOD2
Which gene can distinguish Crohn disease from ulcerative colitis
CARD15 > strongly associated with Crohn disease
CARD15, leads to impaired activation of
the transcription factor nuclear factor kappa B (NF-κB)
tumor suppressor gene play a role in the pathogenesis of Crohn disease and development of Crohn disease–related cancers
The FHIT gene located on 3p14.2
Environmental factors that increase the risk of Crohn disease
medications (oral contraceptives, aspirin, [NSAIDs]), decreased dietary fiber, and increase fat intake.
dysbiosis in which organisms increase the risk
decrease in intraluminal Bacteroides and Firmicutes
increase in Gammaproteobacteria and Actinobacteria
Ileal involvement has been shown with mutations of
IL10, CRP, NOD2, ZNF365, and STAT3
ileocolonic involvement has been shown with mutations
ATG16L1, TCF4, and TCF7L2
colonic involvement has been associated with mutations
HLA, TLR4, TLR1, TLR2, and TLR6.
What characteristic can distinguish it from ulcerative colitis
rectal sparing
Gross pathologic features at exploration
1- thickened gray-pink or dull purple-red loops of bowel
2- areas of thick gray-white exudate or fibrosis of the serosa.
3- skip areas
4- extensive fat wrapping caused by the circumferential growth of the mesenteric fat around the bowel wall, (creeping fat)
5- bowel wall thickened, firm, rubbery, and almost incompressible
6- uninvolved proximal bowel may be dilated secondary to obstruction
7- Involved segments adherent to adjacent intestinal loops or other viscera, with internal fistulas
8- The mesentery of the involved segment is thickened, with enlarged lymph nodes
9- On opening of the bowel, the earliest gross pathologic lesion is a superficial aphthous ulcer noted in the mucosa.
on opening the bowel, the earliest gross pathologic lesion is
superficial aphthous ulcer noted in the mucosa.
With disease progression, the ulceration becomes results in transmural inflammation
characteristics of The ulcers
linear
may join to produce transverse sinuses with islands of normal mucosa in between
thus giving the characteristic ‘‘cobblestone appearance’’
Characteristic histologic lesions of Crohn disease are
noncaseating granulomas with Langerhans giant cells.
Granulomas appear later in the course and are found in the wall of the bowel or in regional lymph nodes
massive gastrointestinal bleeding in CD can occasionally occur, particularly in
duodenal Crohn disease > chronic ulcer formation
long-standing Crohn disease can develop
Dysplasia
Adenocarcinoma
MC in the Ileum
Extraintestinal cancer with CD
squamous cell carcinoma of the vulva and anal canal
Hodgkin and non-Hodgkin lymphomas
especially those treated with immunomodulators
Serologic markers useful in the diagnosis of Crohn disease.
-Perinuclear antineutrophil cytoplasmic antibody
(target proteins bactericidal/permeability increasing protein [BPI], lactoferrin, cathepsin G and elastase)
-Anti–Saccharomyces cerevisiae antibody (ASCA)
useful in differentiating Crohn disease from ulcerative colitis
-outer membrane porin of flagellin (anti-CBir1),
-outer membrane porin of E. coli (OmpC-IgG)
> predict development of IBD even in Low risk patients
inflammatory markers specific to the intestine
- Stool lactoferrin, an iron-binding protein in the secretory granules of neutrophils
- fecal calprotectin, a protein with antimicrobial properties released by squamous cells in response to inflammation,
- both calprotectin and lactoferrin levels correlate with CT enterography (CTE)
-Helpful screening tools for detecting early small bowel Crohn disease
Montreal classification of Crohn disease
see
MRE may be superior to CTE in detecting
intestinal strictures and ileal wall enhancement
the gold standard for the diagnosis of Crohn disease.
Ileocolonoscopy with biopsies of the terminal ileum
Endoscopic advances that allow better evaluation of the small intestine include
-single-balloon enteroscopy
-double-balloon enteroscopy
-spiral enteroscopy
the most well-established technique is double-balloon enteroscopy, which allows increased enteral intubation (240–360 cm)
push enteroscopy (90–150 cm)
ileocolonoscopy (50–80 cm)
Best Modality for identification of intestinal ulceration.
capsule endoscopy has been found to be superior to any other modality in the identification of intestinal ulceration.
criterion for an abnormal finding is the presence of three or more ulcers in the absence of NSAID use.
Aminosalicylates
-Sulfasalazine (azulfidine) is an aminosalicylate with 5-aminosalicylic acid
-use in maintenance therapy has fallen out of favor
-Mesalamine, a slow release of 5-aminosalicylic acid
-If remission is achieved with induction,continued for maintenance
-SE: interstitial nephritis (1%)
Corticosteroids
-Budesonide, high first-pass hepatic metabolism, allows targeted delivery to the intestine mitigating the systemic effects of steroid therapy.
-The preferred primary treatment for patients with mild to moderately active Crohn disease with localized ileal disease
-9 mg/day
-prednisone, in moderate to severe CD.
-not ideal for maintenance therapy (50% become “steroid dependent,”)
-Parenteral corticosteroids indicated for severe disease once the presence of an abscess has been excluded
-40–60 mg daily
How to taper Steroids ?
tapered by 5 to 10 mg/ week until 20 mg
and then by 2.5 to 5 mg weekly until cessation
What Should you do when starting steroids ?
-Dual-energy x-ray absorptiometry scan
-calcium and vitamin D supplementation
-consideration of bisphosphonate therapy
Antibiotics
-metronidazole
-ciprofloxacin
-rifaximin
-clofazimine
-ethambutol
-isoniazid,
-rifabutin
-used in septic complications and beneficial in perianal disease.
Immunosuppressive agents
-AZT and 6-MP are effective for maintaining steroid-induced remission
-weekly IV MTX is effective for both induction and maintenance therapy.
SE: pancreatitis, hepatitis, fever, and rash.
chronic liver disease, bone marrow suppression, and the potential for malignant transformation.
What regulates Immunosupressive Therapy ?
thiopurine methyltransferase (TPMT), which is the primary enzyme that metabolizes AZT and 6-MP
decreased TPMT activity > increased risk of fatal bone marrow suppression
Any test can be done before starting immunosupressive therapy ?
TPMT genotype testing > determine genetic predisposition to adverse outcomes
MTX side effects
hepatotoxicity
myelosuppression
not used in pregnant women.
Other agents help in fistula?
FK-506 inhibits the production of IL-2 by helper T cells
effective for fistula improvement, but not fistula remission