GI bleed, ascites, peritonitis, and obesity

bleeding proximal to the ligament of treitz where blood can accumulate fast and is irritating to the stomach

upper GI bleeding

what can hematemesis indicate

moderate to severe upper GI bleeding

what can coffee-ground emesis indicate

limited upper GI bleeding, may have already stopped actively bleeding

how does blood that moves through the GI tract emerge

emerges as melena (black/ tar like stool from digested blood, 50-100ml blood loss) or hematoschezia (bright red blood from rectum)

if you have hematochezia that isnt from the rectum and is from upper GI bleed what can that mean

indicated blood loss over 1000ml (often self limited but fatal in 4-10%)

what is the biggest cause of upper GI bleed

peptic ulcer disease

ligament that connects diaphragm to the duedenum

ligament of treitz

bleeding proximal to ligament of treitz =

upper GI bleed

bleeding distal to ligament of treitz =

lower GI bleed

other causes of upper GI bleeds

portal HTN (esp w liver disease), mallory weiss tears, vascular anomalies, erosive gastritis/esophagitis, gastric neoplasms

upper GI bleed sx

nausea, vomiting bright red blood or coffee grounds, abdominal discomfort

maybe: melena or blood in stools, cause related sx, pallor, diaphoresis, fatigue due to large blood loss

labs for upper GI bleed

anemia from possible chronic blood loss (acute blood loss will not be reflected in labs until 2-3hrs)

possible H. pylori, liver pathology

definitive dx and tx in most upper GI bleed cases

EGD

upper GI bleed tx

assess hemodynamics and stabilize first (if SBP under 100, HR over 100, or postural hypotensive that indicates moderate/severe blood loss requiring stabilization)

2 large bore IVs w blood products and IV fluids

correct any coagulopathies

EGD initial intervention of choice for dx and tx ca[abilities of upper GI bleeding after stabilized

also do endoscopic variceal litigation within 12hrs

proton pump inhibitors, abx in pts w bleeding varicies (octreotide if bleeding esophageal varicies)

where do 95% of lower GI bleeds originate

in colon

which is more common, upper or lower GI bleeds

upper (lower also lower morbidity)

what do lower GI bleeds often present w

hematochezia (blood on toilet paper, mixed w stool or dripping into toilet w stool, or massive bowel movement consisting of all blood)

prognosis for lower GI bleeds

spontaneous stopping 75%, mortality less than 4%

do we admit upper GI bleed pts

yes

most common cause of lower GI bleeds

diverticulosis

other causes of lower GI bleeds

neoplasms, polyps, IBS, ulcerative colitis, anorectal disease (hemorrhoids, fissures, ulcers), ischemic colitis (pts w coronary artery disease, PVD, or embolic risk factors)

lower GI bleeds sx and physical exam findings

report of bright red blood from rectum

digital rectum exam w frank blood or positive fecal occult blood test

anoscope can possibly visualize the source of bleeding from teh hemorrhoid or rectal bault

maybe: pallor, sweating, fatigue from bld lodd, abdominal discomfort

lower GI bleeds tx

assess hemodynamics and stabilize first (if SBP under 100, HR over 100, or postural hypotensive that indicates moderate/severe blood loss requiring stabilization)

2 large bore IVs with blood products and IV fluids

correct any coagulopathies

if you have a pt w hematochezia who is stable what is the next dx test to do

colonoscopy

if you hace a pt w hematochezia who is stable and the colonoscopy doesnt find the cause what do we do next to dx

EGD

if you have a pt w hematochezia who is not stable what do we do

stabilize first (possible surgery) and then EGD once stable

if you have a pt w hematochezia who is not stable what do we do ifthe EGD doesnt find the source

colonoscopy

how to prevent upper and lower GI bleeds

consider omeprazole to erduce bleeding for pts at risk of ulcers who are taking NSAIDS long term

all pts w esophageal varices should be on beta blocker

preventitive EVL in pts w contraindications to beta blockers

pathologic accumulation of fluid in peritoneal cavity

ascites

normal ascites

accumulation of up to 20ml in women during period

most common pathological cause of ascites

portal hypertension from liver disease

other patho causes of ascites

infectious (TB, called bacterial peritonitis), intra-abdominal malignancy, inflammatory disorders of peritoneaum, ductal disorders (chylous, pancreatic, biliary)

risk factors for ascites

liver disease, alc, blood transfusions, tattoos, injection drug use, hepatits or jaundice at birth

ascites clinical presentation

increasing abdominal girth (may become taunt), abdominal dullness (early satiety, SOB), signs of infection, portal hypertension, chronic liver disease, or malignancy, distended abdomen, maybe fluid wave

how do we confirm ascites dx

abdominal ultrasound

when is abdominal paracentesis indicated for ascites

for initial onset, pts w cirrhosis for sx relief, or dx bacterial peritonitis

what can abdominal paracentesis cause

iatrogenic bacterial peritonitis or damage/perforate organs

clear, yellowish, honey colored fluid on abdominal paracentesis

normal

cloudy fluid on abdominal paracentesis

infection

milky fluid on abdominal paracentesis

chylous

bloody fluid on abdominal paracentesis

trauma or malignancy

if you do an abdominal paracentesis for ascites pt and their WBC is over 500 or their polymorphonuclear cells are over 250 what does that mean

bacterial infxn

if you do abdominal paracentesis for your ascites pt and you see more lymphs than polymorphonuclear cells what does that mean

viral, TB or malignancy

serum albumin: ascites albumin gradient (SAAG) over 1.1 indicates

portal hypertension

serum albumin: ascites albumin gradient (SAAG) under 1.1 indicates

nonportal hypertension

imaging for ascites

abdominal U/S: to confirm ascites and find best pocket for drainage, often used real time

CT: used to identify masses

laparoscopy: direct visualization and biopsy of suspected malignacy

ascites tx

tx underlying cause

1st line gneral tx of ascites in pts w cirrhosis is Na restriction and diuresis with spironolactone and maybe furosemide

symptomatic relief by paracentesis (“theraputic paracentesis”)

trans jugular intrahepatic portosystemic shunt or liver transplant can be considered in refeactory cases w cirrhotic cause

infection of ascitic fluid with no apparent intra-abdominal source of infxn (translocation of enteric bacteria form gut)

spontaneous bacterial peritonitis

what is the most common cause of spontaneous bacterial peritonitis

enteric gram negative organisms (e.coli, K. pneumonia)

20-30% of pts w chronic liver disease will develop _____

spontaneous bacterial peritonitis

spontaneous bacterial peritonitis clinical presentation

fever, abdominal pain, ascites, abdominal tenderness

maybe: abdominal skin erythema, rebound abdominal tenderness and positive heel tap, altered mental status

spontaneous bacterial peritonitis labs

paracentesis is required to rule it out

ascited polymorphonuclear cells count over 250 is presumed spontaneous bacterial peritonitis

culture and gram stain

blood culture

spontaneous bacterial peritonitis empiric tx

start empiric therapy in pts w ascities who have one or more: temp over 100F, abdominal pain/tenderness, change in mental status, polymorphonuclear cells over 250

IV 3rd gen cephalosporins (cefotaxime, ceftriaxone) for 5-10days

IV albumin improves mortality and protects from renal failure

discontinue non-selective beta blockets bc they inc risk of hepatorenal failure

how do we prevent spontaneous bacterial peritonitis

long term prophylactic abx should be given to all survivors of spontaneous bacterial peritonitis because high recurrence rates

excessive accumulation of body fat, with BMI over 30

obesity

causes of obesity

energy imbalance (caloric intake exceeds expenditure)

genetic, environmental, behavioral factors

hormonal dysregulation (leptin resistance, insulin resistance)

chronic low grade inflammation and altered gut micro-organisms

ways to dx obesity

BMI, waist circumference to assess central obesity, clinical hx and physical

BMI categories

less than 18.5 = underweight

18.5-24.9 = normal

25- 29.9 = overweight

30-34.9 = class 1 obesity

35-39.9 = class 2 obesity

40-49.9 = class 3 obesity

complications of obesity

cardiovascular (HTN, coronary artery disease)

metabolic (T2D, dyslipidemia)

respiratory (obstructive sleep apnea)

others (osteoarthritis, some cancers, depression)

obesity lifestyle tx

caloric deficit and balanced nutrition, at least 150min/week of physical activity

behavioral therapy and counseling

first line obesity pharm tx (indicated for BMI 30+ or 27+ w comorbidities)

subcutaneous tirze[atide or semaglutide/ liraglutide

when is bariatric surgery indicated

for BMI 35+ or 30+ w comorbidities

second line obesity pharm tx (indicated for BMI 30+ or 27+ w comorbidities)

phentermine- topiramate

naltrexone - buproprion

orlistat (dec fat digestion)

lorcaserin ± liraglutide

avoid phentermine in pts w cardiovascular disease or uncontrolled HTN