Nagzag Gi-2

Front 1

Esophagus starts at the level of __ and extends down to the _____.

Back 1

C6, stomach

Front 2

esophagus, 3 functional zones:

Back 2

UES, esophageal body, & LES

Front 3

-esophagus Blood supply:

Back 3

inferior thyroid, aorta, & the esophageal branch of the bronchial arteries.

Front 4

esophagus, Innervation: Intrinsic- Extrinsic-

Back 4

Intrinsic- the myenteric (Auerbach’s plexus), & submucosal (Meissner’s plexus). Extrinsic- sympathetic modulates motor activity, parasympathetic (CN IX,X,XI) causes muscular contraction & relaxation of the LES, & somatic.

Front 5

what increases LES tone

Back 5

Inspiration, esoph. distension, gagging, Valsalva maneuver, & acidity of contents, b-blockade, ingestion of a meal or increased intraabdominal pressure (via vagal pathways).

Front 6

what decreases LES tone?

Back 6

Distension, belching, vomiting, & swallowing.
-Swallowing initiates peristalsis. Peristalsis is mediated thru excitatory cholinergic activity.

Front 7

UES and upper esoph. body are ______ muscle.

Back 7

striated

Front 8

-LES and esoph. body are _____ muscle.

Back 8

smooth

Front 9

-**Tone of LES is maintained at ---mmHg (thru Vagal mediation mostly).

Back 9

20

Front 10

Esophageal Disorders
-Common symptom is ____

Back 10

dysphagia

Front 11

___________ is where muscles of the lower esophagus don’t relax so food can’t enter stomach) develops due to DM, stroke, ALS, amyloidosis, & scleroderma.

Back 11

-Achalasia

Front 12

________ is from chronic reflux, alcohol, tobacco, & hiatal hernia- likely to get carcinoma.

Back 12

-Barrett’s esophagus

Front 13

-Mallory-Weiss tear- at the
-S/Sx- pain and bloody vomit.
-Treatment:

Back 13

gastroesophageal junct. from persistant wretchning (likely from ETOH abuse).

Esophageal dilation is used to correct achalasia. Nifedipine SL can alleviate sx, surgical esophagomyotomy w/ fundoplasty is also used.

Front 14

-Hiatal hernia- a defect in the diaphragm that allows a portion of the stomach to migrate upward into the thoracic cavity.
4 types:

Back 14

Type I- sliding type- upper stomach moves in & out thru enlarged hiatus.
Type II- paraesophageal type- doesn’t slide in & out, but all or part of the stomach moves into the thorax and assumes a paraesophageal position.
Type III- both slides and has a paraesoph. position (combo type I & II).
Type IV- other organs are contained in the hernia sac forming a large paraesophageal hernia.

Front 15

-Hiatal hernia and ______ often exist together, but one doesn’t case the other. Most pts with hiatal hernia don’t have symptoms of reflux esophagitis so don’t require H2 blockers or antacids.

Back 15

peptic esophagitis

Front 16

hiatal hernia-

Major S/Sx:

Back 16

retrosternal burning pain after meals.

Front 17

-Common procedures for hiatal hernia repair:

Back 17

Nissen fundoplication, Belsey, Hill, & Collis (gastroplasty) procedures. Laparoscopic approach is common.
-If the thoracic approach is used= one-lung ventilation.
-Be prepared for Laparoscopic concerns, vent issues, etc.

Front 18

-Esophageal Diverticula-

Back 18

diverticular pouches off the esophagus.
*Pt at risk for aspiration!!!
-Surgery in 2 stages- 1st- mobilize the pouch, 2nd- excision with esoph. repair.
-Classified by location: epiphrenic- near the LES
traction- midesophagus
Zenker’s- upper esophagus. **pt at greatest risk for aspiration with Zenker’s diverticulum.

Front 19

-Esophageal Carcinoma- significant association with history of alcohol and tobacco abuse

Back 19

-Pts are: older, malnourished, and cachectic, often with other dz states
-usually preop chemo and radiation- so ask what chemo they are on- lost of side effects. Chemo increased incidence of intraop bleeding, cardiomyopathy (daunorubicin & doxorubicin [Adriamycin]), pulmonary lung fibrosis (from bleomycin=restrictive lung dz & prone to 02 toxicity), bone marrow suppression, fibrosis, friable tissues.
-Often have COPD from smoking & alcohol-related liver dz.
-Mets to liver and lungs are common from extensive lymphatics.

Front 20

#8- Anesthetic Considerations for Esophageal Disease

Back 20

-Pts are often on antacids, H2 blockers. & PPI’s- may need to give before surgery also.
-Often have reflux so use RSI with cricoid pressure to prevent aspiration!
-GETA is safest to minimize risk of aspiration- safe, secured, & sealed airway.
-Awake extubation- make sure pt has control of airway reflexes.
-In emergent situations- use bicitra.
-Gastrokinetic agents (reglan) with H2 blocker will stimulate GI motility speed up gastric emptying time.
-Use anticholinergics carefully!- they can Ø LES tone- chance of silent regurg.
-Sux ≠ LES tone, but barrier pressure (LES-gastric pressure) is unchanged as fasciculations ≠ gastric pressure.
-If pt has had radiation therapy, this can mess up the airway as it changes their anatomy. Have all airway adjuncts ready and have fiberoptic in the room. Nasal might be easier.

Front 21

-Two sections of the stomach:

Back 21

Fundus in the upper abdomen is thin-walled- for storage
distal stomach is thick-walled- mixes food & slow release

Front 22

-Blood supply of stomach

Back 22

R&L gastric arteries, R&L gastroepiploic arteries

Front 23

innervation of stomach

Back 23

Autonomic from 2 branches of Vagus- R celiac branch, L hepatic branch.

Front 24

-Endocrine function of stomach-

Back 24

pepsinogen from the chief cells & other secretions.

Front 25

endocrine function of stomach

Back 25

-In antrum- Epithelial & mucous cells produce mucous. G cells produce Gastrin.
-2 sphincters- LES at the gastroesophageal junction & the pyloric sphincter at the gastroduodenal junction.
-Stores food for up to 4 hours.
-Sight & smell of food stimulates acid & pepsinogen production.

Front 26

-Gastrin (from the G cells) is released with gastric distension & stimulates ____

Back 26

parietal cells to produce HCl.

-Pepsinogen & Gastrin secretion are vagally mediated.

Front 27

-Acid in the duodenum stimulates ___

Back 27

Secretin (which inhibits Gastrin=ØHCl) and stim. the pancreas to release bicarb.

-HCl is released by a H/K pump (need ATP). HCl secretion is stimulated by vagus, gastrin, & histamine (H2 receptor activation).
-H2 blockers, & PPI’s inhibit HCl production. Vagotomy Ø parietal cell response to Gastrin & histamine (anticholinergics have minor effects on parietal cell secretion).
-Acidity of the stomach also provides a protective barrier from pathogens.
-Parietal cells also secrete intrinsic factor, which is needed for vit B12 absorption.

Front 28

Peptic Ulcer Disease
-Chronic over abundance of HCl and ______ results in erosion of the protective mucous layer of the stomach and duodenum with ulceration and lesion formation.

Back 28

pepsin

- If LES is incompetent= esophageal involvement. Can also be in the duodenum.
-Men 45-65 & women >55 have highest incidence of duodenal ulcer. (pts have 2x # of parietal cells.)
-H. pylori infection is the most common cause.
-Chronic use of NSAIDS in the 2nd most common cause. Alcohol & steroids are minor causes.
-Critically ill pts are at great risk for gastritis (Curling’s ulcer) (≠’s M&M from hemorrhage)
-Other causes: hepatic cirrhosis, hyperparathyroidism, COPD, & RA. Emotional stress and alcohol have week correlational causes. Also chronic pancreatitis can cause it from Ø bicarb release into the duodenum.

Front 29

Gastric Ulcer Disease

Back 29

-develops as a result of degeneration of the stomachs mucosal barrier to gastric acid.
-There is normal acid secretion with hypochlorhydria.
-S/Sx: Pain & anorexia= metabolic abnormalities & weight loss..
-Surgical Treatment - antrectomy and plyoroplasty and vagotomy may be necessary if pt doesn’t respond to medical therapy.

Front 30

Gastrinoma -

Back 30

neoplasm arising from the pancreas or duodenum, releases overabundant quantities of gastrin = massive amts of HCl from the parietal cells (Zollinger-Ellison syndrome). If other neoplasias are also present (thyroid, parathyroid, pituitary, insulinoma)= multiple endocrine neoplasia type I.
-S/Sx: severe, intractable ulcer pain.
-Treatment: Surgical excision.
-Anesthesia: RSI, expect electrolyte and intravascular volume abnormalities (from diarrhea or vomiting)- ØK w/ metabolic acidosis common with vomiting & dehydration. Blood glucose monitoring if indicated, watch & treat any unstable hemodynamics. Want normothermic & normocarbic. Maintain renal function.

Front 31

-Histamine-2 (H2) receptors antagonist: antagonism of gastric H2 receptors inhibits HCl production and raises gastric pH (≠ pH, Ø volume)

Back 31

Cimetidine (tagament), ranitidine (zantac) and famotidine (pepcid) - Cimetidine INHIBITS cytochrome P450 enzymes found of hepatic microsomes - thereby interfering with its normal function of metabolizing drugs. PROLONGS the action of drugs metabolized in the liver - warfarin, phenytoin, phenobarbital, diazepam, propanolol. Rantidine has less effect and famotidine the least.

Front 32

-Antacids-

Back 32

increase pH but increase volume

Front 33

-Gastrokinetics- Metoclopramide (reglan) -

Back 33

increases tone of LES, increases gastric motility, decreases tone of pyloric sphincter and relaxes duodenum – (NO EFFECT on pH, but decreases volume).

Front 34

-Proton Pump Inhibitors- ( PPI’s)

Back 34

inhibit the hydrogen/potassium pump thereby, preventing secretion of HCI into the lumen of the stomach - omeprazole, esmeprazole, lansoprazole, pantoprazole, rabeprazole (increase pH, variable effect on volume).

Front 35

(Mendelson’s syndrome)

Back 35

*** The incidence & severity of aspiration is reduced when the pH is >2.5 & volume <25ml!!!

Front 36

#11- Anesthetic Considerations in Gastric Disease & Gastrotomy Procedures

Back 36

-Pts can be acutely ill (bleeding)= emergent surgery or stable.
-Laparoscopic is common (≠ PIP’s, ≠ ETCO2, ≠ SVR, etc.)
-Give bicitra, reglan, & H2 blockers as indicated.
-GETA with aspiration precautions- RSI with cricoid pressure!!!
-Correct Hypovolemia, Anemia (Watch blood loss!), & Coags (crystalloids, collioid, PRBC’s, Platelets, FFP, Cryo, etc), & electrolytes.
-Invasive monitoring if pt has other preexisting acute conditions.
-Labs: CBC, Coags, T&S, chemistries, etc.
-Postop Complications: Pain, hemorrhage, hypovolemia, hypothermia, & ileus. May need ICU care postop.
-Epidural for post op pain.

Front 37

-Common Procedures (other than a total or partial gastrectomy) for Gastric Dz:

Back 37

-Billroth I- resect distal stomach & end-to-end gastroduodenostomy.
-Billroth II- resect distal stomach & end-to-end gastrojejunostomy.
-Laparotomy with oversewing of the ulcer & apply a omenal patch.
-Vagotomy is usually performed for gastric ulcer surgery to Ø HCl secretion.

Front 38

Gastrostomy

Back 38

-Surgical placement of a tube thru the abdominal wall for gastric decompression & feeding.
-Can be permanent or temporary & are often for pts that are neuro incapacitated & have compromised airway reflexes (at high risk for aspiration).
-Performed perutaneously with endoscopic guidance or thru a small laparotomy incision.
-Usually just sedation with local anesthetic is used unless pt requires laparotomy with endoscopic placement- then use GETA!

Front 39

#12- Postgastrectomy Syndromes
-Recurrent ulcer disease-

Back 39

-After surgery for PUD or gastric ulcers, it’s common to have loss of pyloric sphincter function, loss of stomach’s reservoir function, & parasympathetic denervation.
-Recurrent ulcer disease- Can be caused by an unrecognized gastrinoma and unsuccessful vagotomy.
Sx: typical ulcer pain
Tx: H2 blockers, repeat vagotomy

Front 40

#12- Postgastrectomy Syndromes
-Early postprandial dumping-

Back 40

Results from rapid gastric emptying of hyperosmolar chyme from stomach into sm. intestine. Fluid moves from the extracellular tissues into the intestine.
S/Sx: Nausea, cramping abd. Pain, weakness, explosive diarrhea, dizziness, diaphoresis, flushing, & palpitations that occur within the 1st 1/2 hr after a meal.
Tx: medically or revise the gastroenterostomy to a Roux-en-Y reconstruction (provides a peristaltic conduit for drainage of pancreatic & biliary secretions into the jejunum) which significantly reduces the incidence reflux.

Front 41

#12- Postgastrectomy Syndromes
-Late postprandial dumping-

Back 41

less common than early dumping. Due to rapid gastric emptying & absorption of a high carb load in the intestine= hyperglycemia. Insulin is released to counter the hyperglycemia= hypoglycemia. Sx similar to insulin shock.
S/Sx: Diaphoresis, tremulousness, & dizziness occur 1-3 hours after eating a high carb meal.
Tx: Medial management.

Front 42

#12- Postgastrectomy Syndromes
-Obstruction at the anastomosis=

Back 42

dilation of the loop & increase in hepatobiliary & hepatic secretions. Also called afferent loop syndrome.
S/Sx: occurs after eating a meal and is relieved by projectile, bilious vomiting. Vomit lacks food because the food passes into the intestine & is absorbed.
Tx: Roux-en-Y reconstruction.

Front 43

#12- Postgastrectomy Syndromes
-Excessive Reflux-

Back 43

seen especially after gastrojejunostomy.
S/Sx: epigastric pain, bilious vomiting, anemia, & weight loss.
Tx: Roux-en-Y reconstruction.

Front 44

#12- Postgastrectomy Syndromes
-Anesthesia Concerns:

Back 44

-Consider the pts nutrition & metabolic status
-Pt may be anemic (decrease intrinsic factor=decrease vit B12 absorption).
-Prevent aspiration- RSI with cricoid pressure.
-Aggressive preop & intraop fluid & electrolyte replacement as necessary.

Front 45

-peritoneal Innervation-

Back 45

sympathetic & parasympathetic.
-Pain that is nonspecific, dull & cramping is mediated by C fibers.
-Parietal visceral innervation from somatic spinal fibers at levels T7-L2.
-Pain that is sharp is mediated thru A delta fibers.
-Parietal pain can be localized.
-Visceral pain can be referred because of common shared nerve plexus.

-Most intraabd. organs are insensitive to cutting & electrical stimulation, but are sensitive to distension, stretching, torsion, & compression.
-Peritoneal circulation cleans contaminants from the peritoneal cavity but may also facilitate transmission of pathological substances.
-The peritoneum is secretory- serves in the development of ascites, & it’s ability to perform peritoneal dialysis

Front 46

-Peritonitis

Back 46

is inflammation of the peritoneal cavity. Can be primary or secondary.
-Primary peritonitis- results from direct bacterial contamination of the peritoneum. It’s rare & is associated with immunocompromised pts & those with cirrhotic liver disease.
-Secondary peritonitis is result of perforation of the gut with translocation of bacterial flora and toxins - may be caused by inflammation, neoplasia, ischemia, and trauma.

Front 47

Small Intestine

Back 47

-3 divisions- Duodenum (20cm), Jejunum (100-110cm and is larger & thicker than the ileum & has less blood supply), & Ileum (150-160cm).
-Mesentary- rich in lymphatics & blood vessels, tethers the sm. intestine.
-Blood Supply: Superior mesenteric artery- to jejunum, ileum, & prox, transverse colon.
Venous drainage: thru superior mesenteric vein which joins the splenic vein and then is joined into the portal vein.
-Serosa- outer layer of visceral peritoneum.
-Muscular layer- 2 layers of smooth muscle; longitudinal & circular. Auerbach’s plexus (myenteric) lies between the 2 layers.
-Submucosa- strongest layer of connective tissue. Within it lies Meissner’s plexus, which controls local blood flow & secretions.
-Mucosa- inner layer with folds of millions of villi ,which greatly increase the absorptive surface area of the small intestine. 3 layers: muscularis mucosa (deepest), lamina propria (connective tissue), & epithelial layer (covers the villi).

Front 48

small intestine innervation -

Back 48

Parasympathetic thru vagus nerve & celiac ganglia which controls motility & secretion. Sympathetic stim is thru the splanchnic nerves from the celiac plexus which controls secretion, vascular integrity, & bowel motility. Also carries pain afferents.

Front 49

small intestine

Back 49

-Mucosa provides a barrier from pathogens entering. Has a rich reservoir of IgA & plasma cells. IgA-Antigen binding cause mucous secretion=prevents bacterial & viral uptake. IgA also binds with, incapacitates, & facilitates enzymatic destruction of bacteria. Lymphocytes provide specific antibodies for antigens & are in Peyer’s patches. The mucosa also provides many hormones that regulate GI function.
-An electrical rhythm is generated in the muscle layers, which cause motility after eating. This peristalsis activity mixes chyme with digestive enzymes & exposes it to absorptive surfaces.
-Sympathetic influence generally inhibits motility.
-Parasympathetic influence increases motility.

Front 50

Large Intestine

Back 50

-Approx. 3-5 feet in length. Has 3 strips of longitudinal muscle, & numerous outpouchings (haustrations).

Front 51

Large Intestine
-Blood Supply-

Back 51

Superior mesenteric artery: perfuses right colon to midtransverse.
Inferior mesenteric artery: perfuses midtransverse colon to superior rectum.
Venous: middle & superior veins to the portal vein.

Front 52

Large Intestine
-Innervation-

Back 52

Sympathetic: T10-T12 (right colon), L1-L3 (left colon), & the presacral
nerves off the aortic plexus (rectum).
Parasympathetic: Vagus nerve (R&transverse colon), & nerves from S2-S4 (descending colon, sigmoid, & rectum).

Front 53

Large Intestine
-Function-

Back 53

to store & expel wastes. R colon also absorbs water, Na, K, & Cl, and also converts primary bile acids to secondary bile acids. (Na conservation is very efficient).

Front 54

Malabsorption Syndromes

Back 54

-Caused by diseases that disrupt the mucosal integrity of the intestines & actual loss of absorptive surface area (from surgical resection). These disorders affect the absorption of nutrients, carbs, amino acids, & fats. Where & how much sm. bowel is resected affects which vits, minerals, & electrolytes will be deficient.

Front 55

Malabsorption Syndromes s/s

Back 55

-S/Sx: Unexplained weight loss, steatorrhea (fatty stools), & diarrhea.

Front 56

Malabsorption Syndromes

Complications:

Back 56

-Gluten-sensitive enteropathy- also known as celiac sprue & tropical sprue.
S/Sx: eventual megaloblastic anemia, fatigue, weight loss.
Tx: diet & steroids.
sm. bowel ulceration & predisposes pts to CA (tx with folic acid & ABX)

Front 57

Malabsorption Syndromes

-Fat malabsorption-

Back 57

deficiency in absorption of fat sol vits (ADEK). Low vit K causes coagulation disorders & bleeding dyscrasia.

Front 58

Malabsorption Syndromes

vit/protien....

Back 58

-Vit B12 deficiency causes anemia (also low Fe absorption causes anemia), neuropathy, & glossitis.
-Protein malabsorption- may result in peripheral edema & ascites.
-Vit D malabsorption- causes low Ca absorption. S/Sx:Tetany, osteomalacia & fractures.

Front 59

Maldigestion Syndromes

Back 59

-Usually caused by abnormal or deficient pancreatic secretion.
-*Hallmark sign is Steatorrhea (fatty stools)
-*Chronic pancreatitis is the major & most common cause of pancreatic insufficiency. Cystic Fibrosis, fistulas, gallstones, & neoplastic dz are also causal factors for pancreatic dysfunction.

Front 60

Inflammatory Bowel Disease

Back 60

-Incidence- in US btwn 2-300,000 have it & 30,000 new cases dx each yr.
-Two types – Crohn’s disease and ulcerative colitis

Front 61

Inflammatory Bowel Disease

-Crohn’s –

Back 61

involves the distal ileum & Lg colon. Deeper mucosal layers are involved= Øabsorption.
-S/Sx: Diarrhea, mod to severe abd pain & cramps, & frequent anal complaints. Rectal bleeding is less common.
-Deficient in: magnesium, phosphorus, zinc and potassium; also vit B12, folic acid (from sulfasalazine treatment), & Fe=anemia (anemia can also be from occult blood loss).
-Protein-losing enteropathy is common.
-Impaired bile circulation causes nutrient deficiencies- proteins, zinc, mag, phos, fat-sol vits (ADEK), & vit B12.
-Can develop fistulas & abcesses.
-Increased Ca oxlate absorption= kidney stones & gallstones.
-Medical therapy - sulfasalazine (blocks prostaglandin synthesis producing anti-Inflammatory and antibacterial effects), steroids, antimicrobial (flagyl), and immunosuppresive agents (cyclosporine, methotrexate, & tacrolimus). Also monoclonal antibodies are being used. TPN for severe weight loss, cachexia (weakness & wasting of body from severe chronic illness), & malnutrition.
-Surgical therapy - resection of diseased colon, fix obstruction, drain abcesses. Surgery is limited & reserved to current problem. It is not curative & will most likey come back. There is a higher prevalence of carcinoma with Crohn’s.

Front 62

Inflammatory Bowel Disease

-Ulcerative Colitis –

Back 62

inflammatory dz of the mucosa of the distal colon & rectum. Fraught with remissions & exacerbations. Affects females>males. 1st peak incidence btwn 15-20 yrs, 2nd peak btwn 55-60yrs. Causes: genetics & phycological factors. Pts with ulcerative colitis are also at increased risk for developing carcinoma.
-S/Sx: Chronic-bloody diarrhea, abdominal pain, malaise, & fever. Acute- severe abd. pain, profuse rectal hemorrhage, high fever, N/V, anorexia, profound weakness, pallor, & weight loss.

-Toxic megacolon - severe colonic distention that can cause shock=bacterial overgrowth. Errosive inflammation & perforation allows for systemic release of endotoxins. S/Sx: fever, tachycardia, abd. distension, pain ileus, dehydration, electrolyte abnormalities, anemia, low albumin.
-Pts with ulcerative colitis may also have arthritis, liver dz, iritis, erythema nodosum, & ankylosing spondylitis.
-Medical Tx- sulfasalazines, antidiarrheal agents, and steroids.
-Surgical Tx- reserved for intractable complications. Proctocolectomy with ileostomy is curative for colitis but not Crohn’s.

Front 63

Inflammatory Bowel Disease


-Anesthesia Considerations for Inflammatory Bowel Dz-

Back 63

- Thorough H&P, with special attention to Fluid & Electrolyte status as pt may have sepsis, liver dz, anemia, arthritis, low albumin, among other abnormalities.
-Prophylactic steroid coverage is likely indicated (Hydrocortisone 100mg IV)
-TPN concerns- hyper & hypoglycemia (check blood sugar), metabolic acidosis, renal or hepatic dysfunction.
-Possible invasive monitoring with extensive organ disease.
-Correct fluid, electrolyte, & hematologic abnormalities if necessary before surgery.
-GETA with RSI & Epidural for postop pain control.
-Anticholinesterases are okay to use.

Front 64

Diverticulitis/Diverticulosis

Back 64

Diverticulitis/Diverticulosis
-Diverticulosis - numerous mucosal outpouchings in the lg colon (mostly in the sigmoid-65%). Caused by weakened wall & increased intracolonic pressures.
-Diverticulitis - inflammation of the diverticula .
- S/Sx: abd pain, ileus, n/v/d, rigid abd, distention, dehydration, & fever- progression of symptoms may lead to hypovolemia, hypokalemia and shock. The presence of free intraperitoneal air suggests perforation & surgery is urgent. (also urgent for abcesses [indicated by air in retroperitoneum], bleeding, & sepsis)
-Medical treatment: is aggressive & is the first line of treatment (surgery is reserved for emergencies and for symptoms refractory to medical therapy).
-corticosteroids, ABX, fluid replacement.
-Surgical intervention- fecal diversion, abscess drainage and resect diseased bowel.
-Complications of diverticulitis- bowel obstruction, fistulas, & abcesses (which all may need surgery). Abcesses may be extensive. Bleeding is uncommon, but can be occult or massive from erosion of vessels. Can mimic appendicitis if present in R colon or cecum. Sx of diverticulitis may also mimic Crohn’s Dz.

Front 65

Abdominal Compartment Syndrome

Back 65

Abdominal Compartment Syndrome
-Normal abd. pressure is <10mmHg.
-At 10mmHg- hepatic arterial blood flow is decreased.
-At 15mmHG- CV status is impaired.
-At 15-20mmHg- oliguria occurs. Anuria occurs at 40mmHg.
-Causes of acute ACS include obstruction, arterial thrombosis, ruptured AAA, postop & posttraumatic complications. Chronic ACS- PG, acites, tumors.

-S/Sx: Ø CO from Ø preload, ≠ SVR, ≠ intrathoracic pressure (Ø compliance & lung volumes), ≠ HR, ≠ pulm shunt fraction & atelectasis, Ø renal function.
-Tx: decompressive laparotomy and pts may not tolerate closure of abdomen after surgery from edema. Opening the abdomen releases the pressure 7 may have profound consequences of systemic perfusion. Reperfusion washout of by-products of anaerobic metabolism releases an array of cardiac depressant & vasodilatory mediators into circulation. Prepare for severe hypotension, acidosis, & hypoxia.
-Anesthesia- Have fluids and pressors ready, invasive monitoring, Benzo’s or just Scopolamine may be all the anesthesia used in extremely labile patients.
-Mortality rate is 42%, as most pts develop systemic inflammatory response syndrome, sepsis, and multiorgan system failure.

Front 66

Colonic Polyps

Back 66

Colonic Polyps
-Four categories: neoplastic, inflammatory, hamartomatous, & unclassified.
-Neoplastic are adenomas and the potential for malignancy increases if size is >1cm. They can be removed by colonoscopy or if lesion is sessile- need colon resection as may be malignant.
-Inflammatory polyps are small and low potential for malignancy.
-Hamartomatous polyps are small juvenile polyps with minor to nill neoplastic potential.
-Unclassified polyps include familial adenomatous polyposis coli- genetic autosomal dominant with multiple adenomatous polyps. Requires a total colectomy with ileostomy if neoplastic (likely). Also unclassified is Turcot syndtome (polyps with CNS tumors) & Gardener’s syndrome (polyposis with cutaneous tumors & osteosarcoma.
-S/Sx: painless frank or occult rectal bleeding. Bleeding can cause anemia. Cramping abdominal pain- especially in kids.

Front 67

Carcinoma of the Colon

Back 67

-Is highly treatable and often curable when localized to the bowel - 2nd most frequently diagnosed malignancy in the US as well as the 2nd most common cause of cancer death. Surgery is primary treatment & results in cure 50% of the time. Causes 60,000 deaths and >140,000 new cases are dx annually.
-Causes: diet high red meat intake & low in fiber, genetic predisposition, & inflammatory bowel disease.
-Occult stool testing for blood is standard screening method along with rectal exam & colonoscopic exam with biopsy. Pt may be anemic and fatigued & have sx of obstuction.

Front 68

Volvulus of the Colon

Back 68

(Obstruction)
-Obstruction of blood supply leads to necrosis of the bowel. The bowel twists & rotates around the mesentery. Mostly occurs in the sigmoid colon.
-S/Sx: acute, severe, colicky abdominal pain & distension, hypovolemia, & fever.
-Tx: Endoscopic reduction with rectal tube placement- has high success rate and permits later surgical resection. Surgery may be necessary & if gangrene is seen on laparotomy, resection is performed with a colostomy & mucus fistula.

-Many pts are elderly or debilitated & have associated dz: Alzheimers, Parkinson’s, MS, paralysis, pseudobulbar palsy, schizophrenia, & dementia (neuropsychotropic drugs Ø bowel motility).

Front 69

Pseudomembranous Colitis

Back 69

-Associated with inflammatory bowel dz, uremia, intestinal ischemia, Hirschsprung’s disease, shigellosis, and antibiotic therapy (mostly with Clindamycin & Lincomycin)
-ABX associated colitis is caused by Clostridium difficile enterotoxin.
-S/Sx: fever, diarrhea, abd. pain, distention, & shock caused by dehydration & bacterial infection.
-Tx: stop the offending ABX, supportive therapy- fluids, etc, & start vancomycin &/or metronidazole (flagyl)- directed against C.diff.

Front 70

Ischemic Bowel Disease

Back 70

-Caused by bowel not getting enough perfusion/oxygen and symptoms are similar to other disease processes.
-Causes: advanced atherosclerosis, shock, vasculitis, hypercoagulopathy, cross-clamping during AAA surgery.
-Can be localized or systemic.
-Definitive diagnosis is endoscopic exam with biopsy. Xray that shows free air= perforation.
-S/Sx - fever, vomiting, rectal bleeding, abd cramping present for weeks to months. The
development of sudden rectal bleeding and left-sided abd pain and pertioneal signs strongly suggest ischemic bowel disease. Pt may have concomitant ischemic heart disease & Peripheral vascular dz.
-Tx: If no necrosis - ABX, fluid resuscitation
If necrosis or perforation- then emergent laparotomy with poss. bowel resection & colostomy. Stable pts may also have vascular reconstruction.

Front 71

Diseases of Rectum or Anus

Back 71

-May be neoplastic and require surgery, chemo & radiation.
-Rectal prolapse is repaired with rectosigmoidectomy or proctopexy- in elderly.
-Perirectal abscesses & fistulas may require I&D.
-Hemorrhoids- dilation of submucosal veins. Internal are painless- ligation or excision. External are painful and tend to thrombose- excision.
-Anesthesia: regional (spinal or epidural), local infiltration with sedation. May need GETA for some cases depending on pt. position (prone & lithotomy).

Front 72

Radiation Enteritis

Back 72

-Colon is susceptible to radiation injury because of rapid renewal of epithelial lining.
-Radation injury results from therapy to malignant bladder, uterus, ovaries, & cervix dz.
-Sx similar to ulcerative colitis from inflammation & atrophy. Strictures, obstruction, & ulceration may occur. May need surgery to correct these- a diverting colostomy or bowel resection. Pts prone to increased intraop bleeding and 3rd spacing as may have adhesions and increased friable tissues.

Front 73

Appendicitis

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-Occurs mostly in late teens and early 20’s, with males>females.
-Obstruction of appendiceal lumen is the cause= stasis of mucous & bacterial overgrowth occurs & secrete endotoxins that damage the epithelium which causes inflammation, ulceration, & eventual perforation. Abscesses are formed=causes possible sepsis.
-S/Sx: localized rebound tenderness/pain in RLQ, fever, N/V, high WBC (sometimes).
-Tx: Appendectomy- laparoscopic or open, ABX, fluid replacement. GETA with RSI!

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#15- Anesthetic Considerations in Elective Surgery of the Colon

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Patient may undergo aggressive preop preparation - bowel preps (to clean the bowel from feces & bacteria)- predisposes the patient to water and electrolyte imbalance that may have deleterious influence on CV function, hemodynamics and systemic organ perfusion. Pt could also be anemic from chronic bleeding. Malnutrition with hypoalbuminemia, may be present.
Presence of an adynamic colon or obstruction commonly necessitates evacuation of stagnant stomach and upper intestinal contents via nasogastric drainage. This preop intervention may be superimposed on a dehydrated pt or one who is electrolyte depleted. Fluid and electrolyte derangements therefore may be of sufficient magnitude to require postponement of the procedure until volume and electrolyte resuscitation has been accomplished.
-**These pts need LOTS of fluids- replace all losses & 3rd space losses, etc. Replace electrolytes before surgery- especially K!!!

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-Carcinoid Tumor-

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slow growing malignancies composed of enterochromaffin cells usually found in GI tract (also in the lungs are rarely ovarian). They release vasoactive substances such as serotonin, bradykinin, histamine, tachykinins, kallikrein, adrenocorticotrophic hormone, prostaglandins, vasoactive peptide, and others. 5 to 10% of pts with carcinod tumors develop carcinoid syndrome (liver usually able to clear these substances). These substances can produce profound CV instability.
-Two factors enhance the release of carcinoid hormones: direct physical stim, & b-adrenergic stimulation.

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-Carcinoid Syndrome-

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s/s: flushing (kinins, histamine), diarrhea ( serotonin, prostaglandinds), Heart disease- tricuspid/pulmonic regurg, pulmonic stenosis, supraventricular tachys, & atrial ectopy (serotonin), bronchoconstriction & bronchospasm (serotonin, bradykinin, substance P, histamine), hypotension/low CO (kinins, histamine), abd pain (sm bowel obstruction), hepatomegaly (metastases), hyperglycemia, hypoalbuminemia, & edema.

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#16- Anesthetic Considerations for Carcinoid Syndrome

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-Anesthesia-
-use drugs with minimal hepatic metabolism
-Correct hypovolemia & electrolytes
-Avoid histamine releasing drugs (morphine, pentothol, atracurium, & mivacron)
-Etomidate or propofol for induction.
-Vecuronium, Cis-atracurium, or Rocuromium are OK.
-Avoid regional anesthesia- severe & refractory hypotension
-Avoid Ketamine- sympathetic stim.
-Avoid Ephedrine- don’t want b stim.
-Use Neosynephrine to tx hypotension (a-adrenergic agonist)
-Octreotide- somatostatin analogue is used to blunt vasoactive and bronchoconstrictive effects- it mimics the inhibitory action of somatostatin on the release of GI hormones and those derived from carcinoid tumors. (also used to tx GI hemorrhage-vasoconstricts those vessels)
-Aprotinin (isn’t this off the market?) - inhibitor of kallikrein - reversal of bronchospasm and hypotension.
-Bronchospasms- resistant to ketamine & inhaled agents- use b-agonist (albuterol & terbutaline, theophylline, etc).