Surgery Lecture 5: Intestinal Obstruction, Hernias, Appendicitis, & Portal Hypertension

INTESTINAL OBSTRUCTION
Causes of SB Obstruction: adhesions, hernias, cancer, gallstone ileus, intussusception, volvulus, external
compression, abscesses, Crohns disease, diverticulitis, strictures
Perinatal period children w/ projectile vomiting is indicative of pyloric stenosis (typically an olive shaped lesion in the
mid-epigastrium)
Slightly older children w/ the presentation of nausea, vomiting, and a sausage shaped lesion of the lower quadrant
indicates intussusception (which is typically due to Meckels diverticulum).
o Meckels diverticulum: due to improper closure of the vitelline duct (SB congenital abnormality). Typically
follows the rules of 2s (2 types of epithelial tissues are usually involved, 2 cm in size, 2 feet from ileocecal
valve, occurs in ~2% of population, & occurs in children about the age of 2). Accounts for 50% of all lower GI
bleeds in pts <2 years old. Can result in a Littres hernia.
Older patients may get intestinal obstruction due to cancer. MC cause of obstruction is colon cancer (MC type is
adenocarcinoma). May also be due to diverticular disease (repeated bouts of inflammation will cause structuring of
the lumen of the colon and therefore cause difficulty with propulsion of wastes out / obstruction)
Post abdominal surgery: MC cause of intestinal obstructions in adults will be adhesions (sequelae of inflammation
due to surgery). Pt ends up w/ fibrous adhesions (or bands) that can cause obstruction of the bowel and stop
propulsion of wastes)

Symptoms: abdominal discomfort, cramping, nausea, abdominal distention, emesis, high-pitched bowel sounds
As patient becomes more distended, it may negatively impact the perfusion to the bowel risk of dead bowel
Large bowel obstruction (can be due to cancer or diverticulitis) will back up to the ileocecal valve.
If pattern of large bowel obstruction is seen w/ a large distended area on the R-side indicates closed loop
obstruction. Is a surgical emergency (theres no way for the colon to otherwise decompress if theres a competent
ileocecal valve, so colon may rupture & cause fecal peritonitis)
o Competent ileocecal valves only allows for unidirectional flow so fecal content will get backed up here.
Greatest risk of perforation is at the R-side of colon (where the diameter is greatest; Law of LaPlace: the
larger the radius, the larger the wall tension required to withstand a given internal fluid pressure).
o Incompetent ileocecal valve can have dramatic presentation of vomiting fecal matter (because everything that
is going in to the colon is being backed up the small bowel to the stomach and to the esophagus). Risk of
aspiration of fecal matter will need airway protection.
Diagnosis: flat plates (radiographs) may be useful in seeing gas patterns that indicate
an intestinal obstruction, (particularly small bowel obstructions). If pt is too sick to
stand upright, you can take a decubitus film
Air within the SB: markings that go all the way across (due to SB obstruction).
Classic radiograph finding of SB Obstruction: multiple air-fluid levels in a stepwise
pattern of intestines. Decubitus film will also depict multiple air fluid levels.
Air within the colon: markings that do not go all the way across (due to presence
of haustra; indicates colon obstruction)
Reason for Air in the Bowel: as bowel becomes more distended, it presses up
against the diaphragm, causing lung volumes to decrease. This causes more air
hunger & increased breathing causes increased air to go into the GI tract. Major
gas in air is nitrogen which isnt absorbed well across the GI mucosa so it is
trapped within the lumen. Bowel contents (fluid in the bowel) also start to build up due to obstruction.
CT scan: will locate the area of obstruction by finding the transition point (where the bowel collapses & distention
begins; this is typically where an adhesion is location in a pt with prior surgery).
o Pneumatosis intestinalis: air pockets within the wall; indicates a dying gut; very dangerous & is a surgical
emergency
o If the pt has blockage, should be done w/o contrast; otherwise dye would become inspissated (will sit there
& harden; dangerous situation) and because pt will have great fluid loss (in severe obstruction cases, the
bowel can become soaked / saturated and drip out fluid as ascites)
o Would use water soluble dye (never barium contrast; especially if perforation is suspected)
Treatment & Management

Start IVs, do fluid resuscitation (if taken to surgery w/o fluids given prior, anesthesia will cause pts to crash
hypotensively). Keep pt NPO
If history of surgery w/ no prior obstruction history will go to surgery (obstruction likely due to adhesions)
o Pt will need NG tube, decompression of GI tract, IV fluids
o Foley catheter to monitor urine output and response to resuscitation (low U/O poor volume status). Pts
may have high output renal failure however, but this is rare. Urine should go from dark concentrated urine to
diluted urine. Pt should get 4 hours of fluid resuscitation minimum.
Small Bowel Obstruction: must treat emergently; delaying tx can cause ischemia, leading to a dead bowel.
Colon Obstruction: may treat obstruction with colon resection, however, CANNOT anastomose or salvage obstructed
colon (dilated colon has great risk for leak). Must initially be managed w/ a colostomy.

Ostomies
Ostomy: operation that connects the GI tract to the abdominal wall or the lumen of another hollow organ
Stoma: opening of the ostomy (greek for mouth)
Colostomy: Connection of proximal portion of colon to abdominal wall (for stool drainage). Distal portion of colon will either
be brought up to become a mucus fistula or can be sewn + stapled and left inside the abdomen (Hartmanns procedure).
Are usually reversed when bowel has healed. End colostomy (proximal colon with an end stoma) is completely protective.
Hartmanns procedure: infected bowel is resected and distal colon is sewn & stapled into a blind pouch and then kept
inside the abdomen; proximal part of the colon is hooked up to colostomy bag.
This is eventually reversed when colon has time to heal 3 months later (when edema has gone down and the colon
has healed).
Mucus fistula: distal end portion colon connected to abdominal wall; no stool produced, just mucus. Alternative to
Hartmanns pouch; done so the end pouch is easily found for future reversal of colostomy procedure.
Ileostomy: terminal ileum is used instead to complete the loop (when the entire colon must be resected)
Primary Anastomosis w/ Loop Colostomy: whole loop of bowel brought to skin with
ostomy bag attached, to protect a distal anastomosis that is performed immediately.
Loop colostomy is done to divert the colon content to the colostomy bag to avoid
distal anastomosis (to allow it to heal). Is NOT 100% protective as some stool can
pass the ostomy & continue through to the anastomosis site; risky procedure.
When an anastomosis is done (e.g. for the small bowel) but the bowel doesnt
look healthy (is dusky looking), the adhesion as well as the bowel that is affected must be resected
Small Bowel Obstruction Treatment
Ostomies arent done for small bowels obstructions (are too difficult to control; too much fluid & bicarb lost, pancreatic
enzymes will macerate skin, etc.), so instead End-to-End Primary Anastomosis is done with an end to end anastomotic
(EEA) stapler.
Anastomosis has a large risk of leaking. The number one determinant of SB resection anastomosis leakage is
intraoperative hypotension. Decreased blood flow impedes the healing process and jeopardizes the anastomosis.
These pts will commonly get an abscess (pt will look better initially and then suddenly look worse).
If leak is suspected, CT scan w/ water soluble contrast should be done
Enterocutaneous fistula: a fistula from the bowel to the skin (typically from the small bowel). Due to damage to the
intestines; could be due traumatic injury or perforation of the bowel; usually iatrogenically caused (possible complication if
suture line breaks down)
Best way to manage is to surgical resect the fistula.
If not amenable to surgery, must do Total Parenteral Nutrition (TPN) and keep pt NPO for 4-6 weeks to allow the
fistula to self-heal (so long as certain factors arent present that would keep a fistula open)
Factors that keep the fistula tract open (F.I.E.N.D.)
o Foreign body (chronic irritation wont allow fistula tract to close)
o Inflammation (inflammatory response will keep fistula chronically active) or Infection
o Epithelialization (fistula will no longer be able to meet on itself and close)
o Neoplasm / Cancer (fistula cannot heal due to continuous cellular turnover)
o Distal obstruction distal to the fistula (content that is backed up into the fistula wont allow the
enterocutaneous fistula to close due to high pressures within the fistula)

HERNIAS
Hernias can occur in any age category. MC hernia is inguinal hernia in men &
women both. Femoral hernias are more common in women (but this doesnt mean
its the MC hernia in women overall!)
In the very young, hernias can present as an intestinal obstruction (obstruction
may be intermittent if the hernia is intermittent). Bulge may only be recognized
when baby cries & the mother is changing diaper. If the bulge becomes persistent
when it previously was not (was previously intermittent), this indicates an
incarcerated hernia (an irreducible hernia)

Hernia Complications
Incarcerated hernia: irreducible hernia. An incarcerated hernia can cause
obstruction; as the loop of bowel is caught in the hernia, food cannot normally
continue through the small bowel.
o Pts may get internally incarcerated hernias (located inside the pt which may not be externally visible) that
occur post-surgery. These are due to holes in the mesentery that arent properly closed; bowel loops can then
become trapped in these holes.
Strangulated hernia: incarcerated hernia that also has impinged blood supply; this may cause dead bowel due to
compromised vasculature to bowel. Presents w/ fever, severe pain, shock, hematemesis, abdominal free air
Incisional Hernia: MC cause is a technically difficultly from surgery (wound infection MC). Can cause significant
bulging and obstruction (depending on size). What gives a wound of strength and prevents the formation of a hernia is
the closure of the fascia. So whenever a pt ends up with a fascial defect incisional hernia will occur.
o Post-op wound infection wont allow fascial area to heal properly so pt will get a subsequent hernia
o With infection, pt will have secondary wound healing and granulation; thus wont look as cosmetically
appealing as a primary incision would look
Types of Hernias
Inguinal hernias: occur at various ages. In elderly, ask why pt is getting a hernia now. MC hernia in men + women
both. May be direct or indirect, based on hernias location in relation to the inferior epigastric arteries.
o Direct Inguinal Hernia: within Hesselbachs triangle, due to weakness of abdominal wall itself (transversalis
fascia). Older pts will more commonly get these
o Indirect Inguinal Hernia: hernia through internal ring of the inguinal canal; may enter the scrotum. Due to a patent
vaginalis fascia (congenital, from birth). MC hernia in both men and women. For elderly pts, should ask why it is
presenting now. Can be due to increased abdominal pressure from:
Diverticular ds and/or luminal obstruction from cancer (will lead to bearing down)
COPD with use of accessory muscles to assist in breathing (will exhale more forcibly)
Obstruction in urination due to enlarged prostate (will lead to bearing down)
o Indirect inguinal hernias + femoral hernias greater likelihood of becoming incarcerated (even more likely in
hernias w/ small holes because when bowel gets through, theres less chance for it to be reduced back)
Obturator Hernia: internal hernia that goes through the obturator foramen, which also contains the obturator nerve so
will cause anesthesia or pain (Howship-Romberg sign: decreased pinprick sensation or pain along the medial
aspect of the affected thigh). Occurs more in females than males.
Umbilical hernia: hernia through the umbilical ring (associated w/ ascites, pregnancy, or obesity). Usually a very small
defect so can become incarcerated or strangulated. Very common; will typically close by itself. Is more common in
young children (will typically allow 4 years to allow hernia to close by itself;
otherwise youd intervene surgically). Can occur with older pts as well
Richters Hernia: hernia partially bulges through the ring (not the full loop of
bowel, only the anti-mesenteric border / one sidewall of the bowel).
Physicians may see a mass in groin and assume its an abscess and I&D it,
but it could actually be an incarcerated strangulated femoral hernia thats only
partially through the defect. Better to use needle first rather than attempt I&D
with a scalpel if youre unsure.
Pantaloon hernia: combination of direct and indirect hernia straddling the
inferior epigastric vessels. Protrudes through the floor of the canal as well as the internal ring
Femoral hernia: travels beneath the inguinal ligament, down the femoral canal, medial to the femoral vessels
PANCREATITIS

A non-bacterial infection and non-infectious inflammation of the pancreas. Primarily caused by alcohol or gallstones
(both can cause a blockage of ampulla of Vater backing up of normally inactive enzymes into pancreas and become
active). This will cause an auto-ingestion of cells in pancreas.
BAD HITS (Causes): Biliary (gallstones), Alcoholism, Drugs, Hypertriglyceridemia / Hypercalcemia, Idiopathic,
Trauma, or Scorpion sting
o Drugs can cause pancreatitis: corticosteroids, HIV drugs,
o thiazide diuretics, furosemide, birth control, Valproic acid
o Trauma from improper seatbelt wearing (due to pancreas overlying vertebral bodies; rapid deceleration
causes pancreas to slam against vertebral bodies and be injured)
Anatomy: Superior Mesenteric Vein runs posteriorly
Duct of Wirsung: main pancreatic duct:
Duct of Santorini: accessory pancreatic duct
Symptoms: epigastric pain radiating to the back, typically alleviated by leaning forward; nausea and vomiting, significant
SIRS response, hemorrhage of pancreas retroperitoneally (Grey Turners Sign) or hemorrhage that goes to umbilical
region (Cullens sign)

Interstitial Pancreatitis: pancreas will appear swollen. Continued insults to pancreas can result in multiple calcifications
(chain of lakes appearance in LUQ region on plain radiograph)
Hemorrhagic Pancreatitis: can become boggy and necrotic. The
more inflmxn the pancreas has, the greater chance of mortality

Diagnosis: Ransons criteria (criteria changes after 48 hrs), Balthazar

criteria (via CT scan, will help you understand whats going on with the
pancreas), BISAP criteria (bedside investigation of acute pancreatitis,
very easy to use), Glasgow criteria
o Bathalzar Score looks specifically at CT appearance of pancreas; lets you know percentage of edema and
necrosis. Must be done with IV contrast. Pts w/ straightforward pancreatitis dont need an emergent CT scan
however, only would if its necrotic pancreatitis). Criteria looks at enlargement, inflmxn of pancreas & fat,
necrosis & amount of fluid collections.
Ransons Criteria

On Admission
GA LAW

Glucose >200
Age >55

LDH >350
AST >250

WBC >16k

After 48 Hours
C & Hobbs

Ca+ <8
Hematocrit drop >10%

PaO2 <60 mmHg

Base deficit >4

BUN increase >5

Sequestration of fluid >6L

Amylase and lipase may be elevated (lipase is more sensitive & specific for acute pancreatitis). HOWEVER, in
chronic pancreatitis, pts ability to produce these enzymes will be impaired so they wont be elevated at all. May have
NORMAL amylase and lipase so many criteria dont include these enzymes as a part of their scoring.
Do scan to rule in / rule out things. Scan in pancreatitis doesnt have to be done until 24hrs later, to look for particular
findings such as pancreatic abscess if pt has high lymphocytosis, fever, SIRS response, etc. (suggestive of abscess;
this pts will need antibx)

Treatment & Management

Fluid resuscitation (fluid sequestration will occur in the retroperitoneal space)
Long Tiger feeding tube (bypasses the duodenum and goes to posterior pyloric position; position is assessed
radiographically). Pancreatitis is extremely catabolic (so nutrition is very important)
Pancreatitis equivalent to a 20-30% 3rd degree burn will need solutions with protein. Pts may end up with
retroperitoneal fluid loss. May require up to 200-300cc per hour to keep up with their fluid loss.
Hypoxemia can occur due to elevated lipase causing injury to surfactant (necessary for functioning alveoli).
Possible hypocalcemia w/ tetany symptoms, so must monitor calcium (Ca can precipitate out into retroperitoneum)
Antibiotics of choice for severe pancreatitis w/ abscess formation: Meropenem or Ertapenem
Chronic pancreatitis pts (intractable pain due to dilated & distended ducts) will need insulin and replacement of
pancreatic enzymes (proteolytic enzymes of amylase & lipase). Would give Viokase

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o

Repeated bouts of pancreatitis will burn out the endocrine and the exocrine function of the pancreas; thus pt
will become a very brittle diabetic
These pts will have steatorrhea (foul smelly bulky stools that float due to high fat content)

Surgery is very rare in pancreatitis

o If pt has acute necrosis, they may require surgery. May require pancreas to be marsupialized (necrotic tissue
is scooped out)
o Another indication of surgery: pseudocyst (dont have epithelial layer). Pt will have pancreatitis with
hyperamylasemia that was treated and that went down and later suddenly comes back up.
Cannot drain cyst until it forms (until it forms a thick wall). Must wait 4-6 weeks.
Can cause early satiety due to pressing on stomach. May see displacement of gastric bubble
medially due to pseudocyst.
Can be drained intraoperatively or through gastroenterology (and drain the cyst into the stomach, and
put a stent into the stomach).

Intractable pain will be major problem (pain due to dilated ducts); would treat via Puestows Procedure.
o Purpose is to find a way for the pancreatic duct to drain. Pancreas is transected (cut it half), loop of jejunum is
brought up, and then pancreatic duct is sewn into little holes on each side of the jejunum so the pancreatic
duct will drain into the jejunum. This will relieve the pain and pressure on pancreatic ductal system.

APPENDICITIS
MC surgical procedure in the Western Hemisphere. Difficult diagnosis in very old, very young, and in diabetic pts (due to
impaired pain reception, so may present as advance appendicitis due to going unnoticed). Nausea or vomiting may be
more pronounced in very young. Omentums ability to seal off and wall off appendicitis is also impaired in the elderly
Types of Abdominal Pain:
Visceral Pain: dull, crampy, deep, aching (due to stretching, contraction; traction, compression, torsion; or certain
chemicals)
Parietal Pain: sharp, severe, persistent
Epigastric: foregut
Periumbilical: midgut
Lower Abdominal: hindgut

Differing locations of the appendix: rabbit appendix (can be very long and extend in the pelvis, and possibly cross the
midline and cause LLQ pain (very rare, but still a possibility), retrocecal, and retroileal
Other causes of RLQ pain: ask about pulmonary, GI, GU, GYN, and even hematologic causes of abdominal pain
o If pt had recent upper respiratory infection, can result in mesenteric adenitis (RLQ pain due to greatest
concentration of lymph nodes; so as body clears recent infection, pain occurs due to stretch of enlarged
lymph nodes in that area). Consider this if right-shift (lymphocytosis on WBC differential, indicates upper
respiratory infxn commonly caused by viruses)
o Can also be due to Crohns disease or OB/GYN disease (e.g. ovarian cyst, endometritis, tubo-ovarian
abscess secondary to PID, tubal pregnancy)
o Diaphragm is innervated by the Vagus nerve and the thoracic dermatome. T10 is also shared with the R and L
lower quadrants as well as the diaphragm. So lower lobe pneumonia causing diaphragmatic irritation can
present as right lower quadrant pain. So must look at a CXR prior to operating on a pt with suspected acute
appendicitis before they are taken the operating room (to rule out lower lobe pneumonia)

Symptoms: RLQ pain, some vomiting, anorexia, left shift (bandemia / elevated stab count) in WBC differential
Classic Presentation of Appendicitis: starts periumbilically because its poorly localized, then it shifts to RLQ due to
local inflammation from bacterial transudate.
The appendix can still secrete at high intraluminal pressures (which are high due to obstruction) gets distended.
This distention causes the pain periumbilically. As it gets more distended + inflamed, it starts to irritate the parietal
peritoneum and the pain moves to the RLQ.
Signs: McBurneys sign (deep tenderness at McBurneys point), rebound tenderness, Rovsings sign (LLQ rebound
tenderness), Obturator sign (pain upon internal rotation of leg), Markle sign (pain when heel is hit, due to localized
peritonitis), mass effect
Mass effect (typically in RLQ and is usually implies pt has an appendiceal abscess or appendiceal phlegmon)

o
o
o

o
o

Phlegmon means the appendix is inflamed and the body is trying to contain the inflammation; so the omentum
and bowel are matted to the appendix (and this can be felt on physical examination).
Have to do a CT scan to diagnose an abscess formation
Abscess typically occurs due to perforated appendix which is walled off as an abscess; emergent
appendectomy NOT indicated. As long as pt is doing well and is stable, can put them on antibiotics
(moxifloxacin or metranidazole are preferred, because you can easily continue these as PO-based
outpatient prescriptions)
Then bring pt back 6 weeks later and perform interval appendectomy (must treat local abscess first and allow
local inflammation to quiet down before you can remove the appendix)
Wouldnt want to perform surgery due to no clear dissection plains would do more harm than good

Diagnosis: via history & physical examination, 4 views of chest and abdomen, CBC w/ differential, Ultrasound (can
identify the appendix and show if theres any luminal obstruction), Amylase / Lipase, Beta HCG, leukocytosis (w/ left shift),
mass effect, anorexia, abnormal urinalysis
Other Tests for Dx: flat plate of the abdomen, barium enema, CT scan
Diagnosis is based on physical examination primarily. Even if all labs are normal (normal WBC count, CT scan, or
ultrasound), if pt has physical findings they have appendicitis; take to operating room
o Exquisite RLQ pain, rebound, obturator sign, anorexia are going to the operating room. (You dont need
your appendix to survive. Appendectomy a common and safe surgical procedure).
o You dont want the appendix to rupture, especially in females. Can causes tubal adhesions causing
infertilitly and tubal pregnancies
If pathology report indicates periappendicitis indicates another intaabdominal process occuring that is causing
external inflammation of appendix (but not of the appendix itself). So some other pathology may have been missed.
So when during laparotomy, must check other structures to make sure no other process is being missed.
Treatment: take pts to operating room before appendix ruptures!
Appendectomy; Interval Appendectomy (if abscess formation); Laparoscopy vs Laparotomy (open or closed)
Rocky-Davis (transverse) or McBurney (traditional oblique) incision at McBurneys Point
Hydration & Antibiotics
Fowler Position (head up position; attempt to control where an abscess would form if one happens to form. In reality,
this is pointless. Abscess can develop anywhere in the peritoneal cavity due to fluid circulation in cavity)

If no perforation or infection close the wound with primary intention healing

In the non-perforated, non-purulent, non-leaking appendix, can close everything up until the fascia (postappendectomy). You must keep the subq tissue + skin open (is a contaminated wound).
A few days later, send sample of wound to test for infection. If results are negative, you can close the wound.
Allows for better cosmetic result, (this is delayed primary closure / tertiary intention healing). Will heal with
same tensile strength as primary intension healing.

PORTAL HYPERTENSION TREATMENT

Portal HTN causes a reversal of bloodflow, resulting in bleeding esophageal varices, retroperitoneal dilated veins, and
hypersplenism. Must control bleeding and control portal pressures. Best definitive treatment option: liver transplant
Non-operative
Direct: tamponade (Sengstaken-Blakemore Tube), sclerosing, banding
Indirect: vasopressin, propranolol, somatostatin (octreotide), paracentesis, Transjugular intrahepatic portosystemic
shunt (TIPS)
All GI bleeding has to be scoped (especially if massive GI bleeding). Scoping can be diagnostic or therapeutic. Ideally,
want to band the varices or can sclerose them (by injecting sclerosing agents around the varix).
Be careful however, because if sclerosing agent gets INTO the varix, then it can get into the portal system, sclerose
and block off the portan vein.
If no chance of scope: use Sengstaken-Blakemore Tube to temporize the bleeding (this is if you have no choice and
have no one to scope the pt). Otherwise best to endoscope the pt first (to rule out Mallory Weiss for example).
Propanolol: effected way of decreasing portal pressure
Ascites under pressure can cause extrinsic compression on the portal system and increases the bleeding in portal
system even more, so if you control the ascites then you can control the bleeding.

TIPS (transjugular intrahepatic portosystemic shunt): done by Interventional Radiology

Allows you decompress the portal system directly into the systemic venous
system. This is dangerous because when you bypass the liver, you bypass the
deamination of the blood. You will get a tremendous amount of amines in the
blood as a result (ammonia).
When you bypass the liver, you bypass the deamination of blood; therefore
causing high levels of hepatic encephalopathy, due to high levels of amines in the
systemic circulation now
Operative
Designed to allow for decrease of pressure by anastomosing the portal system with the venous systemic system. Best
option: Warrens shunt.
Direct: transesophageal ligation / transection, devascularization, GE resection
Indirect: portal-systemic shunts
Variceal Control
Packed cells & FFP (coagulation factors will affected from liver damage; cryoprecipitate for low fibrinogen)
Reduction of ammonia load (by getting rid of blood in GI system or it will cause a continuous source of ammonia load)

Vasopressin + Nitroglycerin
o Vasopressin used with Nitro to counteract the intense vasoconstriction
o Pitressin (Vasopressin) dose 0.2 0.6 units / minute; 50% response rate.
o Numerous side effects: cardiac arrhythmias, mesenteric ischemia
Propanolol: decrease the pressures
Somatostatin (Octreotide)
Sengstaken-Blakemore (Minnesota) balloon tamponadeGastric balloon under traction with esophageal balloon
inflated to 35-40 mm Hg. Successfully stops bleeding in 80% but rebleeding common (because it doesnt fix
underlying issue). High risk of complications: aspiration, esophageal perforation, esophageal erosions
Endoscopic Sclerotherapy
o Sclerotherapy and binding are used for emergent situation, but the endoscopist wont be able to see anything
from bleeding so cant treat unless above methods are used first to decrease the bleeding so that scoping can
be done with definitive banding therapy
o Successfully stops acute bleeding in 90%. Considered one of the best emergent treatment (also binding).
o Does not alter mortality. Will usually require multiple attempts.
o Complications: perforation, ulceration, pulmonary aspiration, repeated therapy may obliterate varices
Endoscopic Band Ligation
o Success rates similar to sclerotherapy. Lower complication rate. Long term efficacy requires further study
o Best emergent treatment option (other best is sclerotherapy)
Transjugular Intrahepatic Portal-systemic Shunt (TIPS): effective in emergent portal decompression (buys more
time to stabilize + resuscitate the pt). Shunts may close over time. Long term efficacy requires further study.
Surgical bypass
o Last resort; multiple decompression procedures possible.
o Nonselective Bypass: by anastomosing the portal system to the
systemic circulation, youre just dumping ammonia to the IVC,
causing encephalopathy.
End to Side Portacaval Shunt: anastomosing portal vein
directing into IVC. Horrible procedure; maximal loads of
ammonia is dumped into systemic circulation
Side to Side Portacaval Shunt: hole in the side of the portal vein with some portal blood going to the
liver, but majority will go into IVC still will have significant encephalopathy
Interposition grafts (Portacaval, Mesocaval, Mesorenal)

Selective Bypass (best surgical bypass option)

Distal splenorenal: splenic vein is connected to the renal vein (Warrens shunt)
Selectively decompress the problematic area, which is the anastomosis between
the spleen and the veins given off to the lower portion of the esophagus (allows
decompression of area of spleen)
Done by taking the splenic vein and rerouting it the left renal vein. The portal
system is untouched except for the splenic vein (so will still get primary feeding
into the liver but it is still damaged).
Complications: Intraoperative bleeding, Hepatic coma, Renal failure / hepatorenal syndrome (fatal), early
postoperative bleeding, or Rapid ascites formation

Ascites
Hepatitis (whether viral or fatty liver infiltration due to alcoholism) liver damage ascites
Rapid development of ascites formation occurs w/ history of hepatitis
o Pt either has portal vein thrombosis or
o Tumor blocking the portal vein (in absence of recent surgery)
o But if they had surgical decompression done then its an issue of the surgical decompression

Treatment: Bedrest, dietary modification, sodium restriction, diuretics, peritoneovenous (Denver) shunting
o Denver shunt: shunt with one-way valves from the peritoneal cavity that drains subcutaneously into the
jugular vein so acidic fluid can be drained directly into the venous system
o Pts can get DIC from this however, and fluid can be infected. If pt presents with acute abdominal pain, be
careful of spontaneous peritonitis w/ infection of the peritoneal fluid.

Other Management
Splenectomy treatment for hypersplenism may indicated when WBC <4000 and platelets <100,000.
Encephalopathy follows hepatic failure.
Hyperammonemia both from endogenous and exogenous sources; levels > 125 ug/dl (ammonia will be first test in the
morning, put on ice)
Three stages: mental confusion, exaggerated reflexes hypertonicity flaccidity, coma
Hepatic frost (white froth around mouth), liver flaps, & asterixis possible
Treatment
o Reducing intestinal load, reducing production, & increasing metabolism
o Protein restriction, glucose in diet
o Diuresis necessitates potassium supplementation (w/ furosemide in particular, must give potassium
supplements but be careful of hyperkalemia)
o Lactulose (will get rid of ammonia)
o GI purging (via Magnesium citrate, will cause GI tract to purge itself)
o GI decontamination can be done by using antibiotics that are poorly absorbed from GI tract so bacteria no
o

longer is breaking down RBCs decrease in ammonia problem

Antibx such as neomycin and erythromycin, (specifically to decrease the bacteria in the GI tract)

Child-Pugh Criteria for Hepatic Reserve

Perioperative Mortality
Measure
A
B
C
Class A:
0 5%
Bilirubin
<2.0
2-3
>3.0
Class B:10 15%
Albumin
>3.5
2.8-3.5
<2.8
Class C:
>25%
PT increase
1-3
4-6
>6
Ascites
None
Slight
Moderate
Correct w/ FFP, vitamin K, & blood. Anticipate
Neuro
None
Minimal
Coma
bleeding and liver complications.
Encephalopathy possible from liver failure. Hepatic coma possible as well.
Monitor ammonia levels (most accurate level taken in the morning). Give kayexalate if high.
Ammonia levels high due to possible GI bleed (breakdown of blood causes protein buildup). Consider gastric
decontamination if ammonia levels high to get blood. May have to give PO antibx to target bacteria that are breaking
down blood (e.g. erythromycin, neomycin)