GI (9%) Flashcards
APPENDICITIS
-Inflammation of the vestigial vermiform appendix
Appendix = small one ended tube attached to the cecum (vermiform = “worm-shaped”)
Function of appendix = unknown
- suggested that it might be a safe-house for gut flora, or perhaps plays a part in the lymphatic / immune system
- or perhaps just a useless vestigial organ
- One of the most common causes of acute abdomen
- Approx. 10% of population develops appendicitis at some point
- One of the most frequent indications for emergent abdominal surgery worldwide
Appendicitis = most frequent in 20s-30s
More common in men
** MC CAUSE of appendicitis = OBSTRUCTION **
⦁ Fecalith (hard fecal masses - “poop rock”)
⦁ Calculi or foreign body (ex: undigested seeds)
⦁ Lymphoid hyperplasia
⦁ Infectious process or inflammation
⦁ Benign and malignant tumors**
⦁ Fibrosis
⦁ Parasites (endemic areas) - ex: pinworms
In adults, appendicitis is most often caused by fecalith obstruction of the appendix.
In children, appendicitis is caused by lymphoid hyperplasia obstructing the appendix.
LYMPHOID HYPERPLASIA = more common in children / adolescents = lymphoid follicle growth occurs when young, reaches max size during adolescence - can sometimes obstruct the tube. Can also get inflamed after certain viral infections or even immunizations)
PATHOPHYSIOLOGY
⦁ The intestinal lumen (including appendix) is always secreting mucus and fluids to keep pathogens from entering blood stream and to keep tissue moist
⦁ Even with obstruction, the appendix continues to secrete mucus and fluids within obstruction –> increased pressure + enlarges the appendix –> pushes on AFFERENT VISCERAL NERVE fibers nearby, causing abdominal pain
⦁ Gut flora is trapped in appendix and continues to multiply (Ie: E. coli and Bacteroides fragilis) –> signals immune system –> increase in WBC (leukocytosis) and pus accumulation in the appendix
⦁ Increased pressure from mucus / fluids / bacteria / WBCs - can push and compress on blood vessels that supply appendix with oxygen
- without oxygen supply –> ischemia –> necrosis
- no longer secrete mucus / fluids keeping pathogens out, so can invade the wall with bacteria
⦁ As the appendiceal cells die, the wall becomes weaker –> at risk for rupture / perforation –> allows all the bacteria to escape into peritoneum –> causes patients to often experience peritonitis and have rebound tenderness (pain when pressure is removed)
MC complication with Ruptured Appendix
⦁ Periappendiceal Abscess = forms from ruptured appendix and outflow of accumulated bacteria
Common organisms in gangrenous + perforated cases: ⦁ E. coli ⦁ Peptostreptococcus ⦁ Bacteroides fragilis ⦁ Pseudomonas sp.
SYMPTOMS OF APPENDICITIS ⦁ RLQ PAIN ⦁ may have periumbilical / epigastric pain first (50-60%), followed by RLQ pain ⦁ anorexia = lack / loss of appetite ⦁ nausea / vomiting follow pain ⦁ Fever
Initial “atypical” or nonspecific symptoms of indigestion, flatulence, bowel irregularity, diarrhea, generalized malaise
- Inflamed anterior appendix produces localized RLQ pain
- Retrocecal appendix may cause dull abdominal ache
- Appendix tip in the pelvis may cause urinary frequency, dysuria or rectal symptoms such as tenesmus (urgency to have bowel movement) and diarrhea
***There are NO physical findings taken alone or in concert that can definitively confirm a diagnosis of appendicitis!
- in early appendicitis, PE may be unrevealing
- Rectal exam may be helpful when the appendix is recto-cecal
- In women a pelvic exam is a must!!! But it is difficult to differentiate between adnexal tenderness (ovary/fallopian tube) and appendicitis
COMMONLY DESCRIBED PHYSICAL SIGNS
⦁ McBurney’s point - RLQ pain/tenderness
⦁ Rovsing’s sign - pushing on LLQ causes RLQ pain
⦁ Psoas sign—associated with a rectocecal appendix (resisted leg raise)
⦁ Obturator sign—associated with a pelvic appendix
⦁ Rebound tenderness
⦁ Abdominal guarding
The McBurney point is an anatomical landmark located 1/3 (3-5 cm) of the distance from the right anterior superior iliac spine to the umbilicus.
The most sensitive sign for appendicitis is pain at McBurney’s point
A positive obturator sign - pain on passive flexion + internal rotation of hip = indicative of appendicitis.
Pain on active hip extension constitutes a positive psoas sign, which is indicative of acute appendicitis.
A ruptured appendix results in peritonitis that presents with guarding and rebound tenderness.
first - early = visceral pain - central abdominal pain
later = somatic pain - RLQ pain - McBurney’s point
Pain referral in early appendicitis usually involves the T10 dermatome at the level of the umbilicus - as an inflamed appendix stimulates visceral afferent nerves at the T8-T10 level of the spine, causing periumbilical pain
As inflammation process continues, more local somatic fibers become irritated, focusing pain more to RLQ
LAB FINDINGS
⦁ Mild leukocytosis—WBC > 10,000 and a left shift
⦁ elevated CRP
⦁ Women of child bearing age = pregnancy test
⦁ dehydration / fluid + electrolyte imbalances
MODIFIED ALVARADO SCORE - Diagnostic Criteria ⦁ Migration of pain to RLQ (1 point) ⦁ Anorexia (1 point) - lack or loss of appetite ⦁ Nausea or vomiting (1 point) ⦁ Tenderness in RLQ (2 points)* ⦁ Rebound tenderness in RLQ (1 point) ⦁ Fever > 37.5 C˚ (99.5 F˚) (1 point) ⦁ Leukocytosis > 10,000 (2 points)*
- Score 4 or less = unlikely appendicitis; work up for other dx
- Score > 4 = further work up for appendicitis
DIAGNOSIS
⦁ **Abdominopelvic CT WITH CONTRAST ** = oral and IV contrast = preferred study
- CT without contrast is acceptable - imaging not always required - if high clinical suspicion for appendicitis using Alvarado scale
⦁ ULTRASOUND
- (Test = preferred first choice, then do CT if US is inconclusive)
- Imaging of choice for children < 14 or pregnant women, or if CT cannot be done within 3 hours
- ultrasound can be done at bedside
TREATMENT
- pain meds **
- IV fluids / rebalance electrolyte
- NPO
⦁ ** Appendectomy! **
- preop antibiotics = cephalosporin (cefazolin) or unasyn (ampicillin sulbactam) + metronidazole (flagyl)
- postop antibiotics if perforated appendix - until no longer febrile
Laparotomy vs Laparoscopy
Approach depends on:
⦁ Confidence of diagnosis
⦁ History of prior surgery
⦁ Patient’s age—laparoscope easier on the elderly
⦁ Gender
⦁ Body habitus—Laparoscope generally easier to do on the obese patient
⦁ Skills of the surgeon
laparoscopy = safer, less expensive, and shorter recovery time Laparoscopy = lower rate of wound infections, less pain on post-op day 1, shorter duration of hospital stay, and shorter duration of return to bowel function....
however, laparoscopy = also higher rate of intra-abdominal abscess, longer operative time, and higher operative + in-hospital cost
NEPHROLITHIASIS
KIDNEY STONE or RENAL CALCULI or UROLITHIASIS
men affected more often than women
initial presentation = 30s - 50s
prevalence increases with age
5 major stone types ⦁ calcium oxalate = most common*** ⦁ calcium phosphate ⦁ struvite (form staghorn calculi) ⦁ uric acid ⦁ cystine (genetic)
Kidney stones form when solutes in the urine precipitate out and crystallize
These stones form most commonly in the kidney, but can also form in the ureter, bladder and urethra
Urine = water (solvent) and particles (solutes). When the solutes become too concentrated in the solvent (supersaturated), they precipitate and form crystals, and can then act as a NIDUS - where more solutes can deposit so crystal gets bigger
MOST COMMON STONE TYPE = CALCIUM OXALATE = form brown/black crystals = radiopaque on xray (shows up as white on xray)
= more likely to form in acidic urine
- Excessive vitamin C may cause calcium oxalate nephrolithiasis.
- avoid grapefruit juice!!!
85% of patients with kidney stones form CALCIUM STONES (either phosphate or oxalate)
Calcium Phosphate = dirty white in color, and are also radiopaque on xray (shows up as white on xray)
= more likely to form in alkaline urine
- uric acid stones also often have a calcium component
only CALCIUM + STRUVITE stones appear on KUB - are radiopaque
- other stones (uric acid / cystine) don’t
- stone formation thought to be from supersaturation of solutes or lack of enough solvent (dehydration)
- stones form in interstitium; get extruded at renal papilla
Same patients may have more than one stone type at a time
RISK FACTORS FOR STONES ⦁ Decreased fluid intake*** ⦁ Hypercalcemia / Hypercalciuria ⦁ Areas of high humidity ⦁ Elevated temperatures ⦁ Incidence greater in the summer months ⦁ Sedentary lifestyle ⦁ High protein and salt intake ⦁ Genetic factors –particularly with calcium stones
CROHNS DISEASE is an inflammatory bowel disease associated with kidney stones.
Hypercalcemia = can be due to increased absorption in GI tract, or increased resorption (breakdown of bones) or hyperparathyroidism (hormonal)
Hypercalciuria = impaired renal tubular reabsorption of calcium from urine
Hyperoxaluria = can be due to defect in liver metabolism, genetic defect with increased oxalate excretion, or oxalate-rich diet (rhubarb, spinach, chocolate, nuts, beer)
Uric Acid Stones = red-brown in color, radio-lucent (won’t show up on xray - transparent)
- Uric Acid –> Urate + Na –> Monosodium urate crystals
- Uric acid = a breakdown product of purines, so a diet rich in purines = risk factor for uric acid stones (seafood - shellfish / anchovies), red meat, organ meat, alcohol. Can also cause gout / gouty arthritis
Struvite stones = composite mixed of magnesium + phosphate + ammonium. Also called INFFECTION stones. Stones form when bacteria - Proteus - use Urease enzyme to split urea into CO2 + ammonia.
- the ammonium makes the urine more ALKALINE –> allows magnesium, ammonium and phosphate to form jagged STAGHORN CALCULI
- dirty white in color
- radiopaque on xray
- risk factors = VUR, UTIs*** and obstructive uropathy
Cystine stones - yellow or light pink in color. more rare type of stone = radiolucent under xray
Xanthine stones = also a byproduct of purine breakdown (in addition to uric acid)
- also red-brown in color, like uric acid stones, and are radiolucent too
MC risk factor for kidney stones = DECREASED FLUID INTAKE
Citrate and Magnesium lower calcium levels, and inhibit crystal growth / aggregation. so for calcium stones = may have hypercalcuria, hyperoxaluria, hypocitraturia and hypomagnesemia
SIGNS / SYMPTOMS ⦁ dull / localized flank pain (mid to lower back) ⦁ constant sharp pain ⦁ hematuria ⦁ fever ⦁ N / V ⦁ pain radiates to groin ⦁ increased urgency / frequency with decreased urine volume
- pain is caused by dilation, stretching and spasm of ureter from stone
- pain is typically worse at UPJ (ureteropelvic junction), down the ureter and UVJ, but subsides at bladder
The most common site for renal calculi is the ureteropelvic junction (between kidney + ureter)
Kidney stones may become caught as they cross the PSOAS MAJOR = muscle that can most likely be used to localize the patient’s internal pain
- UA with culture = may have microscopic or gross hematuria (Most pts experience hematuria); but could still be a stone with no hematuria present
- Urine pH (normal = 5.8-5.9)
⦁ pH < 5.5 = uric acid or cystine stone
⦁ pH 5.5-6.8 = calcium oxalate or phosphate stone
⦁ pH > 7.2 = struvite stone - Pregnancy test
- CBC
- CMP
METABOLIC EVALUATION OF STONES
- strain urine to catch stones for analysis
- complete metabolic evaluation required for recurrent stone formers (or family hx)
⦁ serum PTH, calcium, phosphate, uric acid, electrolytes, creatinine, BUN
⦁ 24 hour urine collection = volume, pH, calcium, uric acid, oxalate, phosphate, sodium, citrate
DIAGNOSIS OF KIDNEY STONES
⦁ NONCONTRAST ABDOMINOPELVIC CT** = MC initial diagnostic test **
⦁ Urinalysis - may show microscopic or gross hematuria
⦁ Ultrasound (can detect hydronephrosis and sometimes stones) - used if CT is contraindicated
⦁ KUB = can only detect large radiopaque stones (calcium oxalate / phosphate / struvite)
⦁ IV Pyelography = used to be gold standard - determines the extent of obstruction + severity
Gold standard = CT - noncontrast abdomen/pelvic**
The use of IV contrast will obscure visualization of the stone within the urinary tract and is therefore not the diagnostic test for a presumed kidney stone.
most painful part of kidney stone passage = ureter
TREATMENT FOR KIDNEY STONES
- ACUTE THERAPY- for stones < 5 mm = 80% chance of spontaneous passage within hours
⦁ IV fluids
⦁ Pain Meds = Ketorolac/Toradol or Diclofenac/ Voltaren (NSAID) or Morphine IV
⦁ Antiemetic = Metoclopramide/Reglan IV
- can give alpha-1 blocker (Tamsulosin/Flomax - causes dilation) to help pass stone
- stones at the URETEROVESICULAR JUNCTION (narrowest point of urinary tract) + ureteropelvic junction may make passage of stones difficult
- if the pain is under control, stable, and there are no signs of infection, the patient can be discharged and followed-up as an outpatient**
PREVENTION (50% will experience recurrence)
⦁ increased fluid intake
⦁ decreased protein + sodium intake
⦁ ** Potassium Citrate ** to reduce stone formation
⦁ HCTZ to reduce CALCIUM stone formation
** Citrate or Sodium Bicarb ** prevent uric acid stones
WHEN KIDNEY STONES BECOME A MEDICAL EMERGENCY
= any obstructing stone with an associated infection***
WHEN TO ADMIT THE PATIENT WITH KIDNEY STONES
⦁ intractable nausea/vomiting or pain
⦁ obstructing stone with signs of infection (emergency!)
REASONS FOR UROLOGICAL CONSULT FOR KIDNEY STONES
⦁ evidence of urinary obstruction*
⦁ urinary stone with associated flank pain*
⦁ anatomic abnormalities or solitary kidney**
⦁ concomitant pyelonephritis or recurrent infection
THERAPEUTIC INTERVENTION IS NEEDED WHEN:
⦁ failure to pass stone in 4 weeks
⦁ fever, intolerable pain, persistent N / V
SURGICAL TREATMENT = for stones > 7mm = 20% chance of spontaneous passage
⦁ ESWL = extracorporeal shock wave lithotripsy = used to break up larger stones that are less likely to pass spontaneously. May need multiple treatments to reduce size of stone
⦁ Ureteroscopy with/without stent placement = used to provide immediate relief to an obstructed or at-risk kidney
⦁ Percutaneous Nephrolithotomy (PNL) = most invasive = used for LARGE STONES (> 10mm), struvite or if less invasive techniques fail. Incision made in back, stone removed via tube
Percutaneous nephrolithotomy is currently the primary surgical intervention of choice for struvite stones.
ACUTE CHOLECYSTITIS
= Acute inflammation of the gallbladder
MC CAUSE = gallstone lodged in cystic duct
stones = MC made up of cholesterol
MC in women than men
Prevalence increases with age
Higher in Native American population
4 F’s = FERTILE + FAT + FORTY + FERTILE = classic patient
Bile is made in the liver, stored in the gallbladder
the hepatic ducts descend and meet with the cystic duct to form the common bile duct
- the pancreatic duct and the common bile duct drain into the duodenum through Ampulla of Vater via Sphincter of Oddi
PATHOPHYSIOLOGY
1) gallstones present in gallbladder
2) person eats food
3) In small intestine, the I cells in duodenum/jejunum secrete CCK (cholecystokinin) into blood –> makes its way into the gallbladder –> signals gallbladder to secrete bile to aid in digestion of food
4) the gallbladder contracts –> gallstone gets lodged in cystic duct
5) flow of bile is blocked by gallstone in cystic duct
- -> builds up in gallbladder
6) Gallbladder continues to squeeze / contract, but is blocked, and CCK continues to trigger gallbladder to secrete bile. Gallbladder gets stretched –> irritation of nerves in gallbladder + cystic duct –> pain!
7) Bile remaining in Gallbladder for prolonged time becomes an IRRITANT –> gallbladder mucosa starts secreting mucus + inflammatory enzymes –> inflammation / distention / more pressure –> RUQ pain
8) May start to have some bacterial growth in gallbladder (MC = E. Coli, Others = Klebsiella, Enterococci, Bacteroides fragilis, clostridium)
9) Bacteria can start invading through gallbladder wall –> peritonitis –> Rebound tenderness
10) bacterial invasion –> triggers immune response –> leukocytosis + neutrophils
SUMMARY: 90% of acute cholecystitis cases = caused by GALLSTONES
- trapped bile becomes concentrated and causes irritation + pressure build-up in gallbladder
- -> can lead to bacterial infection
- -> can lead to perforation
- usually follows a large or fatty meal
SYMPTOMS ⦁ Pain - initially MID EPIGASTRIC ⦁ Pain then moves to RUQ - dull / achy pain ⦁ precipitated by fatty foods / large meal ⦁ Pain may radiate to scapula or shoulders ⦁ Nausea / Vomiting ⦁ Anorexia ⦁ Fever* (often low-grade) ⦁ Rebound tenderness ⦁ Guarding ⦁ Enlarged, palpable gallbladder ⦁ Murphy's sign = positive!
Murphy’s Sign: Patient exhales, then apply deep pressure to RUQ, will have severe pain upon inhalation
- when taking a deep breath, the diaphragm expands downwards and pushes gallbladder down
- if pressure is in place after exhalation, then upon inhalation when diaphragm contracts downwards, the gallbladder is pinned in place –> PAIN! –> patient will quickly stop breathing in further
+ Boas sign = referred pain to the right subscapular / right shoulder area due to phrenic nerve irritation
(vs Kehr’s sign = referred pain to LEFT subscapular area due to phrenic nerve irritation, but seen with splenic rupture instead)
1 of 2 things can happen
1) gallstone moves back into gallbladder on its own –> resolves cholecystitis = happens in majority of cases!
= Biliary Colic (RUQ pain, but no fever / WBC, no jaundice)
2) stone doesn’t fall back into gallbladder, and pressure continues to build up due to increased mucus / bacteria / WBCs
–> pressure can eventually cause gallbladder to start compressing on blood vessels supplying gallbladder with blood –> no blood / oxygen supply –> ischemia –> gangrenous cell death
- gallbladder walls may also weaken due to pressure + bacteria –> RUPTURE –> sharp pain, and if left untreated, could cause sepsis
- if gets this bad = patient may need cholecystectomy
COMPLICATIONS OF ACUTE CHOLECYSTITIS
⦁ chronic cholecystitis
⦁ mucocele
⦁ empyema
⦁ Mirizzi’s Syndrome = gallstone also obstructs hepatic duct –> jaundice
⦁ Perforation
⦁ Gallbladder - Duodenal fistula formation (allows gallstones to cause gallstone ileus at terminal ileum) –> gastric outlet obstruction
⦁ Choledocholithiasis (formation of gallstone in common bile duct)
⦁ Cholangitis (from choledocholithiasis –> infection)
⦁ Pancreatitis (if gallstone moves down to obstruct pancreatic enzymes from getting through pancreatic duct to duodenum
⦁ Obstructive jaundice (bile backflow to liver due to stone in common bile duct)
DIAGNOSIS
⦁ HIDA = GOLD STANDARD TEST
⦁ Ultrasound = best initial test
⦁ CT = alternative to ultrasound + can detect complications
Ultrasound - can detect stones, stone sludge, and mucus buildup in gallbladder or cystic duct
- if stone is lodged in common bile duct though = a lot more difficult to see on ultrasound
- includes murphy’s sign test
HIDA SCAN (cholescintigraphy) = Most Specific!
- radioactive tracer = attached to HIDA (acid) and injected into patient
- HIDA is taken up by hepatocytes and gets excreted into the bile
- can watch tracer drain down hepatic ducts and into gallbladder + common bile duct; will see if obstruction is present
- if cholecystitis present = will not see gallbladder
LABS
⦁ CBC = leukocytosis with left shift (excess neutrophils)
⦁ may have slightly elevated bilirubin (direct)
- can get Alk Phos, Lipase / amylase, LFTs to check for pancreatitis / choledocholithiasis / cholangitis
⦁ would have elevated Alkaline Phosphatase (ALP)
⦁ would have elevated AST / ALT (liver) - AST = 10-40
- ALT = 7-56
⦁ would have elevated total bilirubin (0.3-1.0) (increased direct or conjugated bilirubin) (liver)
(direct = 0.1 - 0.3) (indirect = 0.2-0.8)
⦁ would have elevated Lipase / Amylase (pancreas)
ALP (20-140) = an enzyme found high in liver + bile ducts, so when bile backs up and increases pressure on the ducts in the liver, liver cells lining the ducts can get damaged –> release ALP
Lipase (0-160)= enzyme secreted by pancreas that hydrolyzes fats. When pancreas is inflamed or damaged –> elevated Lipase (lipase more sensitive than amylase)
Amylase (40-140) = enzyme also secreted by pancreas that digests carbs (starch –> sugars). When pancreas is inflamed or damaged –> elevated Amylase
TREATMENT
- NPO
- IV fluids
- Pain meds (NSAIDS or narcotics)
- antibiotics (Ceftriaxone + Metronidazole)
⦁ Laparoscopic Cholecystectomy
⦁ emergency surgery may be necessary if gangrene, perforation, ischemia, pancreatitis, inflammation of common bile duct occurs
Early cholecystectomy is generally preferred, best done during the first 24-48 hours following symptoms
- laparoscopic preferred over open
Prophylactic cholecystectomy for asymptomatic cholelithiasis is generally not recommended
ANAL FISSURE
- painful linear split, tear or crack in anal mucosa
- initially only involves the epithelium, but may involve the full thickness of the mucosa if left untreated
- one of the most common causes of anal pain + anal bleeding
MC cause of anal bleeding
ETIOLOGY - usually from trauma to the anal canal low fiber diet --> constipation --> passage of large, hard stools, or other anal trauma ⦁ defecation ⦁ straining ⦁ constipation
Anal fissures are believed to result from laceration by a hard / large stool or from frequent loose stools
Caused by:
⦁ hard stool passage (constipation)
⦁ hyperactive sphincter
⦁ disease process (e.g., Crohn’s disease)
The fissure may cause internal sphincter spasm, decreasing blood supply and perpetuating the fissure
- anal fissures most commonly occur in the 12 o’clock or 6 o’clock area (superiorly or inferiorly) = vertical
horizontal fissures = more associated with Crohns or HIV
- MC @ POSTERIOR MIDLINE*
- because of the relatively unsupported nature and poor perfusion of the anal wall in that location.
often seen in little kids who are constipated
very common in infants
CLINICAL PRESENTATION
⦁ severe tearing rectal pain during defecation
⦁ causes patient to refrain from having a bowel movement, leading to more constipation
⦁ mild hematochezia - BRIGHT RED BLOOD (blood on stool or toilet paper)
⦁ may/may not have mucoid discharge
PHYSICAL EXAM
- confirmed by visual inspection of the anus
⦁ acute = looks like cracks in the epithelium
⦁ chronic = fibrosis + development of skin tags**
- may see ** SENTINEL PILE ** = Thickened mucosa/skin at the distal end of an anal fissure that is often confused with a small hemorrhoid
pain intensity = less with chronic fissures
TREATMENT
- 80% resolve spontaneously
- 1ST LINE = supportive measures ⦁ fiber supplements ⦁ increased water intake ⦁ stool softeners ⦁ sitz baths ⦁ analgesics ⦁ laxatives ⦁ petroleum jelly
o 2nd line
⦁ 0.4% nitroglycerin ointment (glyceryl nitrate)
- topical vasodilator - improve blood flow to area to help heal
- BID x 6-8 weeks.
⦁ SE = headaches** + dizziness (hypotension)
- another = Nifedipine or Diltiazem ointment (CCB)
- Botox - inject into enteral anal sphincter to relax anal sphincter - lasts about 3 months
o ** DEFINITIVE = INTERNAL ANAL SPHINCTEROTOMY ** - remove internal anal sphincter = if conservative tx fails
⦁ risk = minor fecal incontinence
Patient will present as → a 45-year-old man with severe RECTAL PAIN when he DEFECATES, lasts for several hours and subsides until the next bowel movement. He has been CONSTIPATED for the past 6 months and when he does have a bowel movement the stool is covered with BRIGHT RED BLOOD. A sentinel pile is noted on physical exam.
CHOLELITHIASIS
Cholelithiasis = Gallstones (stones in gallbladder)
GALLBLADDER
- stores bile that is produced in the liver
- foods high in fat cause the duodenum / jejunum’s I cells to release CCK, which stimulates the gallbladder to contract and squeeze bile into the duodenum
- the bile emulsifies the fat to make it easier to absorb
Function of Gallbladder = store + concentrate bile until the time comes to release bile into small intestine
COMPOSITION OF BILE ⦁ 70% bile salts + acids ⦁ 10% cholesterol ⦁ 5% phospholipids ⦁ 5% proteins ⦁ 1% bilirubin - others = water / electrolytes / bicarb
Bile salts + acids = products of cholesterol metabolism
GALLSTONES
= round, solid stones found in gallbladder
- made from components of bile, so are categorized depending on what they’re made of
MC GALLSTONE = CHOLESTEROL STONES (75-90%)
⦁ can also have bilirubin stones (pigmented stones)
MC stone = cholesterol stones
- cholesterol precipitates out of bile and forms stone
- but stones are rarely completely made out of cholesterol - usually mostly cholesterol and then small parts of other particles
ETIOLOGIES OF STONE FORMATION
1) bile becomes super saturated with cholesterol –> precipitates out to form stones
2) not enough bile salts / acids + phospholipids to keep cholesterol in solution –> precipitates out
3) gallbladder stasis - can cause cholesterol to separate out of solution –> precipitates out
Bilirubin stones = occur when too much bilirubin in solution –> precipitates out and joins with calcium (electrolyte in bile) –> allows it to be seen on xray (RADIOPAQUE)
Would think that pigmented stones in gallbladder are made from conjugated (direct) bilirubin, but it is actually made up on unconjugated bilirubin!
While the vast majority of bilirubin in bile is conjugated (like 99%), there is still a small % of UCB in bile
- thought to form from non-bacterial / non-enzymatic hydrolysis of conjugated bilirubin (CB) into UCB
CB vs UCB
⦁ Conjugated = Unconjugated + Glucuronic acid
⦁ Conjugated = water soluble
⦁ Unconjugated = lipid soluble
- UCB probably likes to bind with calcium –> form stones
Bile salts usually bind to calcium to keep them from binding to UCB
- hemolysis –> UCB –> CB –> Bile
- if hemolysis is increased, UCB will be increased, CB will be increased.
- if increased CB in bile in gallbladder –> more will be hydrolyzed into UCB –> more chances of UCB binding to calcium to form stones
STONES
⦁ Cholesterol (90%) vs Pigmented (10%)
⦁ Black stones = ** HEMOLYSIS ** or ETOH cirrhosis
⦁ Brown stones = bacterial infections / parasitic infections - increased in Asian population due to parasite
RISK FACTORS ⦁ Women MC ⦁ Estrogen / OCP - estrogen increases cholesterol stone formation ⦁ Obesity ⦁ Fertile ⦁ rapid weight loss - rapid weight loss --> drop in lipids --> increased risk of gallstones
(Fat, female, forty, and fertile) OCP’s, chronic hemolysis, cirrhosis, infection, rapid weight loss, IBD, TPN, fibrates, increased triglycerides
= 4 F’s = Female / Fat / Fertile / Forty
Hypercholesterolemia = NOT a risk factor, but Hyperlipidemia is
COMPLICATIONS OF GALLSTONES ⦁ Cholecystitis ⦁ Pancreatitis ⦁ Ascending Cholangitis ⦁ Choledocholithiasis ⦁ Gallstone ileus
Gallstone ileus can develop from a cholecysto-enteric fistula
FIBRATES
Cholesterol gallstones are a biliary adverse effect associated with fibrates, especially when given with bile acid resins.
SYMPTOMS
⦁ MC = Asymptomatic
- until causes a blockage somewhere (biliary colic / cholecystitis / ascending cholangitis / pancreatitis / etc.)
Cholelithiasis = gallstones WITHOUT inflammation of gallbladder
Most cases are ASYMPTOMATIC. Majority of patients found to have incidental gallstones will remain asymptomatic
Biliary colic = cardinal symptom of gallstones = due to TEMPORARY obstruction of cystic duct by a gallstone. Pain occurs as gallbladder contracts against the obstruction
BILIARY COLIC = Classically presents as RUQ pain that begins abruptly, continues in duration, resolves slowly lasting 20 min to several hours = TEMPORARY, is associated with nausea and precipitated by fatty foods and large meals
Most likely PE findings with cholelithiasis = Physical examination and laboratory findings without abnormalities, just a hx of post-prandial biliary colic with N/V
WILL THEN CAUSE
⦁ RUQ pain
⦁ sharp / cramping or dull
⦁ may radiate to back or below shoulder blade
⦁ N / V
⦁ worse with fatty / greasy or large meals
⦁ occurs within minutes following meals
Murphy’s Sign - RUQ pain with palpation on inspiration
Boas sign—referred right subscapular pain of biliary colic
DIAGNOSIS
⦁ best initial test = ULTRASOUND
- cholesterol stones CANNOT be seen on xray (RADIOLUCENT)
Ceftriaxone is a major cause of biliary sludge. The mechanism of biliary sludge formation during ceftriaxone therapy appears to be the propensity of ceftriaxone to bind calcium and form insoluble crystals in bile in the gallbladder, resulting in biliary sludge or frank stones
LABS = NORMAL***
TREATMENT
⦁ asymptomatic = observe
⦁ symptomatic = CHOLECYSTECTOMY - definitive
medications that may dissolve gallstone = Actigall / Ursodiol (Ursodeoxycholic acid) = if asymptomatic or for prevention
SE OF BILIARY OBSTRUCTION
- lack bile –> malabsorption of fat
- -> can lead to malabsorption of fat-soluble vitamins (ADEK)
Vitamin K deficiency ⦁ easy bruising ⦁ mucosal bleeding ⦁ melena ⦁ defective in coagulation
BILIRUBIN
- erythrocytes (RBCs) = made in bone marrow
- start out as erythroblasts –> reticulocytes –> erythrocytes
erythrocytes (RBCs) contain hemoglobin, which carries oxygen around via blood vessels to tissues in body
When RBCs are damaged or reach lifespan of 120 days, macrophages (spleen + bone marrow) break down RBCs to release hemoglobin molecule
Hemoglobin = split into
⦁ Heme
⦁ Globin
Globin = protein –> broken down into amino acids –> enter the blood to be reused for erythropoiesis
Heme is broken down into
⦁ unconjugated bilirubin and
⦁ iron
Iron re-enters circulation, and is reused for erythropoiesis again
The unconjugated bilirubin is not recycled, and needs to be removed from the body as it is toxic
- the unconjugated bilirubin = has a yellow pigment
- unconjugated bilirubin is lipid soluble –> so when in the blood, it requires a protein to carry it around (Albumin))
ALBUMIN carries unconjugated bilirubin to the liver for further metabolism
Liver also has its own macrophages (Kupffer cells) which break down old / damaged erythrocytes into heme + globin. Globin reused, heme broken down into iron + unconjugated bilirubin. Iron also reused for erythropoiesis.
So Liver now has unconjugated bilirubin, both from albumin transport of broken down RBCs around the body, as well as from its own macrophages that break down RBCs.
In Liver, unconjugated bilirubin + glucuronic acid is converted into conjugated bilirubin (direct)
Conjugated bilirubin = now water soluble
- is excreted from liver with bile –> transported to both small intestine as well as to gallbladder for storage. Goes through hepatic ducts and cystic duct to gallbladder, and through common bile duct to small intestine
IN LARGE INTESTINE
- the conjugated bilirubin converted into UROBILINOGEN by intestinal bacteria
- urobilinogen = lipid soluble (requires protein)
⦁ 10-15% of urobilinogen binds to albumin and is re-entered into the blood
⦁ remaining 85-90% of urobilinogen is quickly converted by intestinal bacteria into STERCOBILIN (brown) = what gives feces its brown color
The Urobilinogen that was re-absorbed into the blood (via albumin) = carried back to liver via portal system
⦁ half is entered back down hepatic ducts with bile
⦁ half is entered into kidneys –> urobilin –> excreted via urine (gives urine its yellow color)
CHOLELITHIASIS VS CHOLECYSTITIS VS CHOLEDOCOLITHIASIS VS CHOLANGITIS
Low severity –> high severity
Cholelithiasis > Cholecystitis > Choledocolithiasis > cholangitis
BILIARY TREE
- left + right hepatic duct drains from liver
- cystic duct drains from gallbladder
- hepatic ducts + cystic duct connect to form common bile duct
- common bile duct then connects with pancreatic duct to both drain into small intestine
CHOLELITHIASIS
⦁ stone formation in gallbladder (gallstones)
⦁ *** key = colicky pain - waxes / wanes - sometimes have cramps, then disappear = CLASSIC FOR CHOLELITHIASIS
⦁ Worse with fatty foods
- bile needs to be released by gallbladder with fatty / greasy meals
⦁ RUQ pain
⦁ Diagnosis = RUQ Ultrasound = always the answer! - see acoustic shadowing
⦁ Treatment = elective cholecystectomy
- don’t have to remove gallbladder unless symptomatic
CHOLECYSTITIS
⦁ inflammation of gallbladder + cystic duct due to cystic duct obstruction
⦁ MC due to cholelithiasis
⦁ MURPHY’S SIGN
⦁ constant pain (vs colicky pain - stones)
- pain due to gallbladder contracting against an obstruction
⦁ FEVER / LEUKOCYTOSIS
⦁ Dx: 1st line = RUQ Ultrasound
- Gold standard = HIDA scan
- can gallbladder take up dye?
- may have elevated leukocytes (leukocytosis), elevated Alkaline Phosphatase, elevated total bilirubin, and elevated AST/ALT
⦁ Tx = cholecystectomy (non-elective)
CHOLEDOCOLITHIASIS
⦁ common bile duct obstruction with stone
⦁ JAUNDICE - due to back up of bilirubin - no way for drainage
⦁ ** DILATED HEPATIC BILE DUCTS **- 2 hepatic bile ducts become dilated due to backed up bile
⦁ Dx + Treatment = ERCP
- both a scope as well as can remove stone
(MRCP = only diagnostic, cannot remove stones)
⦁ no fever / no leukocytosis, some proximal inflammation, but relatively no pain
- ERCP = definitive
- can try RUQ US
CHOLANGITIS (ASCENDING CHOLANGITIS) ⦁ choledocholithiasis + infection ⦁ stone is lodged in common bile duct - backed up fluid --> causes infection --> inflammation ⦁ CHARCOT'S TRIAD = always 1) fever 2) jaundice 3) RUQ pain ⦁ may have REYNOLD'S PENTAD 1) fever 2) jaundice 3) RUQ pain 4) Hypotension 5) altered mental status - patient may be going into shock ⦁ Diagnosis = RUQ ultrasound ⦁ DEFINITIVE TX = EMERGENT ERCP**** - patient could go into shock and die! - broad spectrum abx: like pip-tazo
BILIARY LEAK
⦁ post-cholecystectomy
GALLSTONE ILEUS
Rigler triad of gallstone ileus:
⦁ pneumobilia (air in the biliary tract)
⦁ low small bowel obstruction with distended small bowel loops
⦁ an impacted gallstone in the terminal ileum
HEMORRHOIDS
- dilated veins of the hemorrhoidal plexus (venous plexus) in the lower rectum
- engorgement of venous plexus
The venous plexus in it’s normal state is a cushion that helps with stool control. Becomes pathological when swollen or inflamed.
The pectinate line (dentate line) is a line which divides the upper two thirds and lower third of the anal canal
⦁ Internal hemorrhoids = superior hemorrhoid vein proximal to the dentate line (above dentate line)
⦁ External hemorrhoids = inferior hemorrhoid vein distal to the dentate line (below dentate line)
CAUSES/RISK FACTORS OF HEMORRHOIDS - basically anything that would cause the veins to become engorged from valsalva maneuver -> increased venous pressure ⦁ repeated straining during defecation -Constipation ⦁ pregnancy ⦁ frequent heavy lifting ⦁ obesity ⦁ prolonged sitting ⦁ cirrhosis with portal hypertension
hemorrhoids = very common, especially during pregnancy and after childbirth
CLINICAL PRESENTATION
- often asymptomatic, or may simply protrude
INTERNAL VS EXTERNAL HEMORRHOIDS
o External Hemorrhoids
⦁ perianal PAIN** - aggravated with defecation
⦁ NO BLEEDING (may cause minor bleeding if ulcerate)
⦁ painful/purplish swelling - worse if thrombosed
- External hemorrhoids receive SOMATIC innervation from the INFERIOR RECTAL branch of the PUDENDAL nerve = why they are painful when thrombosed
o Internal Hemorrhoids
manifest with bleeding after defecation
⦁ BRIGHT RED BLOOD on stool or toilet paper
⦁ PAINLESS unless thrombosed (usually not tender or palpable)
⦁ rectal itching
⦁ mucous discharge
Internal hemorrhoids receive VISCERAL innervation and therefore are NOT PAINFUL
INTERNAL HEMORRHOIDS ARE CLASSIFIED
- Grade I = no prolapse, just prominent blood vessels
- Grade II = prolapse upon bearing down, but spontaneously reduces
- Grade III = prolapse upon bearing down, and requires manual reduction
- Grade IV = prolapsed + cannot be manually reduced - may strangulate
again…
grade I = no prolapse
grade II = prolapse but spontaneous reduction
grade III = prolapse - requires manual reduction
grade IV = prolapse - cannot be reduced
COMPLICATIONS =
⦁ Strangulation
Strangulated hemorrhoids occur when protrusion and constriction occlude the blood supply. They cause pain that is occasionally followed by necrosis and ulceration.
⦁ Ulceration
⦁ Anemia
⦁ portal pyemia (abscess in portal vein –> sepsis)
DIAGNOSIS
⦁ visual inspection = external or protruding internal
⦁ DRE
⦁ fecal occult blood testing
⦁ anoscopy = for painless/bleeding hemorrhoids
- sigmoidoscopy or colonoscopy in patients with hematochezia to r/o colon cancer / etc.
Rectal bleeding should be attributed to hemorrhoids only after more serious conditions are excluded (ie, by sigmoidoscopy or colonoscopy).
TREATMENT
- 1st line = symptomatic treatment (like with fissures)
⦁ increased fiber diet
⦁ increased fluids
⦁ stool softeners**
⦁ laxatives
⦁ warm sitz baths**
⦁ topical rectal corticosteroids / analgesic ointments may be used for pruritus and discomfort
(steroids / analgesics = not used for internal hemorrhoids because not painful!)
⦁ NSAIDS for pain with external hemorrhoids
- PRAMOXINE = local anesthetic used for analgesia and antipruritic effects
- 2nd line tx = BANDING
- if conservative treatment not working
- if debilitating pain or strangulation
- if prolapsing grade 2 + grade 3 internal hemorrhoids
⦁ rubber band ligation = cuts off blood supply to hemorrhoid, they die and fall off
⦁ sclerotherapy
⦁ infrared coagulation
** RUBBER BAND LIGATION = 1ST LINE FOR GRADE 2 and 3 HEMORRHOIDS **
- 3rd line tx = surgical - hemorrhoidectomy
⦁ excision (and clot evacuation) of an external thrombosed hemorrhoid
⦁ stapled hemorrhoidectomy for prolapsing internal hemorrhoids
If thrombosed external hemorrhoid = EXCISION!
HEMORRHOIDECTOMY = FOR GRADE 4
Patients with external hemorrhoids will present with → significant pain, but no bleeding.
CI for hemorrhoidectomy = CROHNS!
THROMBOSED HEMORRHOID TX = EXCISION**
Patient with internal hemorrhoids will present as → a 43-year-old who has recently noticed bright red blood on the toilet paper when he wipes. He denies any fatigue, decreased exercise tolerance, abdominal pain, or maroon-colored or black, tarry stools. He has no family history of colon cancer. He has never had a colonoscopy.
ACUTE MESENTERIC ISCHEMIA
Mesenteric Ischemia = insufficient blood flow to the small intestine –> ischemia
CAUSES OF ISCHEMIA
⦁ thrombus (A-fib, MI)
⦁ embolus (atherosclerosis)
** MC due to occlusion **
** case = will often have patient with A-fib, MI or CHF
- could also be tumor, intussusception, hernia, volvulus that compresses on vasculature and occludes blood flow
A complication of volvulus and intussusception is small bowel ischemia where arteries that supply the small intestine becomes compressed.
NON-OCCLUSIVE CAUSES
⦁ shock (decreased blood flow)
⦁ cocaine (vasospasm)
MC ARTERY = ** PROXIMAL SUPERIOR MESENTERIC ARTERY **
The artery that branches off the aorta and supplies most of the small intestine is the superior mesenteric artery.
The 3 major mesenteric arteries branching off of the abdominal aorta are the celiac, superior mesenteric and inferior mesenteric arteries that supply the foregut, midgut, and hindgut, respectively.
The superior mesenteric artery supplies blood to the distal duodenum to the proximal 2/3 of the transverse colon
The inferior mesenteric artery supplies the distal 1/3 of the transverse colon to the upper portion of the rectum and is the smallest mesenteric vessel. The splenic flexure is considered a watershed area and is more susceptible to ischemia during poor arterial flow due to inferior mesenteric ischemia.
- splenic flexure = corner between transverse + descending colon
(hepatic flexure = corner between ascending + transverse colon)
The celiac artery supplies blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen
This lack of perfusion causes bowel ischemia + potentially necrosis if left untreated
Usually, the first layer of the intestine damaged in gastrointestinal ischemia or infarction is the MUCOSAL LAYER.
HALLMARK SYMPTOMS
⦁ severe abdominal pain that is out of proportion to their physical exam
⦁ Nausea / Vomiting
⦁ Bloody stools - bloody diarrhea
Bloody diarrhea = caused by
- damage to small intestine is caused by both tissue hypoxia + reperfusion injury
1) hypoxia –> tissue ischemia + necrosis
2) reperfusion injury = if tissue that has been damaged is reperfused => oxidative stress, and causes even more damage caused by neutrophil activation –> releases free radicals + buildup of toxic byproducts after periods of ischemia - this damage leads to sloughing of cells + blood into intestinal lumen –> blood in stool
DIAGNOSIS
o Labs
⦁ increased WBC (with increased bands = immature WBCs)
⦁ metabolic acidosis
⦁ elevated lactate
o Imaging
⦁ ** CT Angiography = definitive*** (without contrast)
⦁ Xray = thumb-printing sign = due to thickened bowel walls from bowel wall edema - initial test
⦁ Colonoscopy
Pneumatosis Intestinalis = air within bowel wall = indicates severe disease
TREATMENT ⦁ ** SURGICAL REVASCULARIZATION ** = angioplasty with stenting or bypass - surgical resection if bowel not salvageable ⦁ fluids ⦁ antibiotics ⦁ anticoagulation (heparin) or urokinase thrombolytic ⦁ emergency surgery in severe cases
Patient will present as → a 71-year-old male with a history of atrial fibrillation with a sudden onset of severe abdominal pain occurring 10 minutes after eating. Physical exam findings are relatively benign, and the patient has only minimal pain with palpation of the abdomen. Stool guaiac is positive and blood tests reveal leukocytosis with an elevated lactate and LDH.
CHRONIC MESENTERIC ISCHEMIA
- same pathophysiology of ischemic bowel disease caused by MESENTERIC ATHEROSCLEROSIS of the GI tract
Atherosclerosis –> inadequate perfusion, especially at the SPLENIC FLEXURE (inferior mesenteric artery) during POST-PRANDIAL STATES
SYMPTOMS
⦁ ** Chronic dull abdominal pain * that is WORSE AFTER MEALS
⦁ Weight loss (due to anorexia / fear of eating)
Postprandial epigastric pain usually within the first hour after eating
Pain will resolve in 2-3 hours
“Mesenteric angina”
Usually will present as recurrent cramping with postprandial pain in a patient with a history of PVD, smoker or DM
DIAGNOSIS
⦁ ** CT angiography = gold standard **
⦁ Xray = initial test
TREATMENT
⦁ bowel rest
⦁ surgical revascularization (angioplasty with stenting or bypass
ISCHEMIC COLITIS
ischemic colitis is the result of mesenteric ischemia
MC due to systemic hypotension or atherosclerosis that involve the superior + inferior mesenteric arteries ==> that leads to ischemia of bowel
MC Location = “watershed” areas with decreased collaterals = Splenic flexure + Rectosigmoid junction
SYMPTOMS
⦁ severe abdominal pain
⦁ MC = LLQ pain (splenic flexure / rectosigmoid jnct)
⦁ ** BLOODY DIARRHEA ** (sloughing of colon)
DIAGNOSIS
⦁ Colonoscopy
- see segmental ischemic changes in areas of low perfusion
(would be CT Angiogram to diagnose mesenteric ischemia, but colonoscopy if specifically diagnosing ischemic colitis)
TREATMENT
⦁ revascularization - restore perfusion + observe for signs of perforation
PLUMMER-VINSON SYNDROME
Paterson-Brown-Kelly syndrome
The triad of
⦁ 1) iron deficiency anemia
⦁ 2) dysphagia - due to cervical esophageal webs
⦁ 3) glossitis
Classically affects CAUCASIAN FEMALES aged 30-60
This syndrome must be recognized early - is a risk factor for SCC OF THE ESOPHAGUS
Dysphagia (trouble swallowing) occurs due to development of esophageal webs
- Dysphagia is typically post-cricoid
** Esophageal Webs ** = thin membranes of mucosal or submucosal tissue that protrude out and obstruct the esophagus ==> can lead to dysphagia
Glossitis = inflammation of the tongue; often related to nutritional deficiencies. “red and shiny” due to inflammation and loss of lingual papillae
Iron deficiency anemia - microcytic hypochromic anemia - usually occurs due to bleeding or poor nutrition
Iron deficiency anemia may manifest as glossitis, cheilosis, and plummer-vinson syndrome. May have weakness and dysphagia with iron-deficiency anemia
HIGHER RISK OF DEVELOPING SQUAMOUS CELL CARCINOMA OF THE ESOPHAGUS
LABS / DIAGNOSIS
⦁ decreased MCV (< 80% = microcytic anemia)
⦁ elevated RDW (> 11.5 - 14.5)
*** iron deficiency anemia if microcytic but elevated RDW
RDW = RED CELL DISTRIBUTION
- The RDW test shows the difference in size between the smallest and largest red blood cells in a sample
- RDW test results may be higher if more cells are larger or smaller than normal
- In iron deficiency anemia or B12 / folate deficiency = cells are smaller (microcytic) or larger than usual (macrocytic)
⦁ High RDW and low MCV = iron deficiency / microcytic anemia.
⦁ High RDW and high MCV = B-12 or folate deficiency / macrocytic anemia
TREATMENT
⦁ iron supplementation
⦁ mechanical widening of the esophagus
- these generally provide an excellent outcome
- Nowadays, this syndrome has become extremely rare.
In Plummer-Vinson syndrome, the symptoms of dysphagia may improve with correction of iron deficiency anemia if there are no advanced esophageal webs.
DIVERTICULOSIS
Diverticulosis = merely describes the presence of diverticula
condition of having diverticula of the colon, which are outpouchings of the colonic mucosa and submucosa through weaknesses of muscle layers in the colon wall
** MC CAUSE OF LOWER GI BLEED **
NOT INFLAMED!!!
(inflamed = diverticulitis)
USUALLY ASYMPTOMATIC*****
however…diverticulosis is the MC cause of acute lower GI BLEEDING***
MC LOCATION = SIGMOID COLON
- a common place for increased pressure
Prevalence increases with age
⦁ 5% under age 40
⦁ 30% at age 60
⦁ 65% at age 85
Etiology
⦁ low intake of dietary fiber*
⦁ constipation
⦁ obesity (weak association)***
⦁ high intake of fat or red meat (weak association)
⦁ Lack of vigorous exercise may also be a risk factor
PATHOPHYSIOLOGY
Diverticula = pouch that forms along the walls, like a cave
- usually talking about colonic diverticula (large intestine), but can happen in small intestine, esophagus, etc.
4 layers of intestines ⦁ mucosa ⦁ submucosa ⦁ muscularis ⦁ serosa
- sometimes, the diverticula contains all 4 layers of intestinal wall (true), sometimes just mucosa and submucosa poke through muscular layer (pseudo/false) and is then covered by the serosa (excludes muscle layer)
most of the time, diverticula = false, or pseudo
(only involve mucosa + submucosa)
ETIOLOGY = thought to be from high pressures in the large intestine that push on the intestinal wall to form these pouches
Diverticulosis is caused by chronic, intermittent, increased intraluminal pressure at a point of weakness in the muscular layer of the colon wall where blood vessels (vasa recta) enter the tissue.
- thought that the smooth muscle contractions of the large intestine are exaggerated in patients with diverticula, to where there are abnormal contractions for digestion/peristalsis, creating uneven pressures throughout the lumen, leading to outpouching in the areas of really high pressures
Diverticula are MC in the Sigmoid Colon
- due to LaPlace’s law of inverse relationship between diameter and pressure. As the diameter of the lumen gets smaller, pressure increases. The sigmoid colon = smallest lumen diameter = highest pressures
Diverticula also tend to form in areas where the muscle layer is weaker = in areas where the blood vessels traverse through the muscle layer. When the diverticula forms, which excludes the muscle layer, the blood vessel is only separated from the lumen by the mucosa, and is therefore easily ruptured with injury –> rectal bleeding –> blood in stool (hematochezia)
- this bleeding is usually PAINLESS (ddx: internal hemorrhoid)
RISK FACTORS
⦁ low fiber diet –> constipation –> increased stress/pressure –> diverticula
⦁ diet high in fatty foods + red meat –> associated with increased risk of diverticula
⦁ Marfan’s + Ehlers Danlos = without strong CT present, diverticula can form
IF SYMPTOMATIC = DIVERTICULAR DISEASE
⦁ chronic constipation alternating with diarrhea
⦁ some pts may c/o cramping, bloating, abdominal distention, flatulence**, and irregular defecation
⦁ may have painless rectal bleeding
- However, it is unclear if these symptoms are attributable to the underlying diverticulosis or to coexistent IBS
PHYSICAL EXAM
⦁ Usually normal
⦁ may have LLQ tenderness (sigmoid)
- Palpable sigmoid and descending colon
DIAGNOSIS ⦁ Often discovered incidentally ⦁ CT + contrast = MC**** ⦁ can also do barium enema => xray ⦁ routine colonoscopy
**Among all patients with diverticulosis, 70% remain asymptomatic. 15-25% develop diverticulitis, and 5-15% develop some form of diverticular bleeding
CBC to check for anemia (if severe bleeding)
vitals: severe diverticulosis –> hypovolemic shock
TREATMENT - Prevent symptoms ⦁ high fiber diet / fiber supplements ⦁ at least one bowel movement per day ⦁ avoid seeds / nuts
- Complications
⦁ Diverticulitis
⦁ Diverticular bleed
Diverticulosis = usually asymptomatic - mostly found incidentally via colonoscopy or CT when looking for something else
- sometimes stomach pain
- sometimes blood in stools
Diverticulosis will present as → a 63-year-old male who is being evaluated in the ED for an episode of painless bright red blood per rectum for two hours.
DIVERTICULITIS
DIVERTICULITIS
- inflamed diverticula = swelling + inflammation of diverticulum in the intestinal wall
CAUSES
⦁ lodged fecaliths (fecal matter) - become inflamed, but not very common
⦁ most commonly thought to occur due to EROSION of the diverticular wall from high luminal pressures
- the erosion and inflammation is what causes PAIN, MC in LLQ (sigmoid colon)
MC causes = E. coli + Bacteroides fragilis
The primary process is thought to be erosion of the diverticular wall by increased intraluminal pressure or inspissated stool within a diverticulum
DIVERTICULITIS = NOT associated with rectal bleeding, as the blood vessels become SCARRED from inflammation
- Bleeding = more associated with diverticulosis
COMPLICATIONS ⦁ fistula ⦁ abscess / infection ⦁ intestinal obstruction ⦁ colonic stricture ⦁ perforation
- inflammation + focal necrosis ensue –> can result in perforation
⦁ a small tear in a diverticulum OR perforation of colonic diverticulum - can then cause intra-abdominal infection (or body might wall it off as an abscess)
Colovesical fistula, a fistula between the colon and bladder, can develop as a complication of diverticulitis, presents with stool or air (pneumaturia) in the urine.
SIGNS/SYMPTOMS OF DIVERTICULITIS ⦁ aching abdominal pain ⦁ Usually LLQ (sigmoid) pain ⦁ alternating diarrhea + constipation **** ⦁ flatulence ⦁ hematochezia *** ⦁ N/V ⦁ low grade fever** ⦁ palpable mass ⦁ abdominal distention / bloating ** ⦁ stool occult blood ⦁ mild to mod leukocytosis** ⦁ ***Moderate/Severe generalized tenderness is indicative of free perforation + peritonitis
Diverticulitis presents with fever, pain in the left lower quadrant of the abdomen, and leukocytosis.
diverticula often contain small vessels; when blood vessels rupture, diverticula will bleed –> hematochezia
rebound tenderness = indicates more mod/severe case - indicative of perforation + peritonitis
rebound tenderness is basically automatically a surgical case - get CT scan
DIAGNOSIS
⦁ ** CT with contrast ** = test of choice
- No barium enema or colonoscopy in initial stages - risk of perforation!!!!
- Plain abdominal films - to rule out free air (perfed diverticulum), ileus, or obstruction
⦁ see increased soft tissue density within pericolic fat, secondary to inflammation
⦁ see colonic diverticula
⦁ bowel wall thickening
⦁ soft tissue masses representing phlegmons and pericolic fluid collections, representing abscesses
TREATMENT
o OUTPATIENT
- clear liquid diet - advance diet with symptomatic improvement
- analgesia - acetaminophen, tramadol (treat with pain meds, no opioids)
- Empiric antibiotics
⦁ Cipro
⦁ Bactrim + Metronidazole
⦁ Uptodate = Cipro + Metronidazole or Augmentin
==> ABX + PCP f/u
INPATIENT
- as a general rule, those who are admitted = elderly (anyone over 65 according to heather), immunosuppressed / immunocompromised, those with significant comorbidities, and those with high fever (102) or significant leukocytosis should be hospitalized
- IV fluids
- NG tube (if ileus)
- IV Abx for anaerobes + gram negative bacteria
⦁ Ceftriaxone (1-2g q24hrs)
⦁ Ampicillin (2 g IV q6hrs)
⦁ gentamicin (1.5 to 2 mg/kg IV q8 hrs), and metronidazole (500 mg IV every 8 hrs)
⦁ Imipenem/cilastin (500 mg IV every 6hrs)
⦁ Piperacillin-tazobactam (3.375 g IV q6hrs)
- Follow up with barium enema or colonoscopy
- Surgery - to drain abscess, or can do temporary or permanent colostomy
(ex: if patient returns to the ER after being in the ER for a few days, with worsened symptoms = need to broaden abx coverage to cover for nosocomial infections, particularly pseudomonas (pip-tazo, cipro)
Diverticulitis will present as → a 67-year-old man with a long history of constipation presents with steady left lower quadrant pain. Physical exam reveals low-grade fever, mid-abdominal distention, and lower left quadrant tenderness. Stool guaiac is negative. An absolute neutrophilic leukocytosis and a shift to the left are noted on the CBC.
