Categorized by location of the tip of the tube.
Gastrostomy or PEG tube – terminates in the stomach
Jejunostomy – terminates in the stomach
PEG-J tube or GJ tube – terminates in both the stomach and the small intestine
PEG (Gastrostomy tubes)
Placed endoscopically, no surgical incision
Can temporarily keep stoma patent with a foley catheter. Need bolster to prevent further migration (can use 3 cm segment of another foley with hole in the middle to act as temporarily bolster if one is not available).
Replacing blindly must only be done on a mature stoma track (2-3 weeks) for possible complication of placing tube into peritoneal cavity. Stomach most likely adhered to abdominal wall by that time.
For clogged or leaking G-tubes without balloon that need to be removed, traction/countertraction should be enough force to squeeze the mushroom out of the stomach. Will likely hear or feel a pop.
Tintinalli recommends consulting the GI or surgeon initially before applying traction depending on the internal bolster.
If still unable to remove, can pull out the tube as much as possible and cut it at the skin to allow rectal passage. Have been reported cases of obstruction, though rare. Still better to consult surgeon prior to doing this.
Can verify placement with Gastrograffin (water-soluble, diatrizoate meglumine-diatrizoate sodium). Barium is contraindicated due to potential peritoneal contamination. Inject 20-30mL, take supine abdominal film 1-2 minutes after dye instillation to optimize gut visualization.
Irregular or rounded blotch with wispy edges or streamers suggests peritoneal leakage.
Entry site irritation: common, can be treated with silver nitrate at time of dressing change to prevent granuloma.
Large stomas: can cause leak. Though insertion of larger tube or firmer traction can be temporarily effect, this often results in further stoma enlargement. Need to replace to pliant soft tube or just remove to allow stoma to shrink. Large amounts of drainage can also be due to high residual volumes – consider checking for residuals after feeds and holding anything further until residual is < 100 mL.
Clogged tubes: can use roter-rooter type wire to drill the clog out. Using guidewire or needle is contraindicated. If unsuccessful, should inject with contrast with imaging to check tube integrity.
Placed surgically under general anesthesia, require a surgical incision and have surgical scar at insertion site.
Less likely to cause aspiration or reflux compared to PEG tubes.
If foley catheter used to replace dislodged J-tube stoma, DO NOT INFLATE BALLOON. Advance 20cm and keep in place.
Does not have balloon on end of it. Generally, jejunum is sutured to abdominal wall. If patient pulls it out, can just place tube back in place and then adhere it to the skin by suture or tape until surgeon sees it again. Needs to have been in place for at least 2-6 weeks though.
Roberts and Hedges, Expert Consult, 2013.
Tintinalli, Chapter 89, 2011.
Small Bowel Obstruction
Causes: adhesions (MCC), hernia, intussusception (lymphomas can be the leading point), lymphoma, stricture. Mesenteric defects can occur with marathon runners. If its caused by cancer, its usually metastasis (colonic, ovarian, pancreatic, gastric).
Nausea/Vomiting, abdominal distension. Dehydration due to decreased oral intake and decreased body uptake. Can get ischemic bowel from distention and increased intraluminal pressures causing ischemia.
Episodic pain, usually for a few minutes intermittently, though can be constant. The earlier and more sever the vomiting, the more proximal the obstruction. Complete obstruction causes inability to pass bowel movement or flatus, though partial bowel obstruction often associated with passage of stool and flatus. Mechanical obstruction early has high-pitched bowel sounds where as later in the course and in adynamic ileus will have diminished or absent bowel sounds.
Only need upright chest and abdominal X-ray. Can help confirm suspicion for obstruction, severe constipation, or free air. Will show multiple air-fluid levels (string of pearls, air-fluid levels, step-laddering). Looking for dilation > 2.5cm and presences of air-fluid levels differing > 5mm from each other. Sensitivity 80%, specificity 67-80%. Does not show point of twisting.
CT scan is the diagnostic method of choice. Look for: bowel wall thickening > 3mm, submucosal edema, ascites, ‘target sign’ – alternating hypo/hyperdense layers indicating intussesception, ‘whirl sign’ from rotating small bowel mesentery from volvulus, ‘venous cut-off sign’ due to thrombosis. Finding transition point does not appear to make difference in emergent vs delay and sometimes has been off from intraoperative findings. No oral contrast: ACR recommends against it, Rating 9.
Abdominal US: More sensitive and specific than plain films for SBO. In one study, US was 75% sensitive (Suri, 1999). Ultrasound Podcast Video Tutorial. Jang, 2010 study: 10min teaching residents, found US to be 91% sensitive. Look for dilated loops of bowel in several quadrants (>2.5cm), looked for back and forth peristalsis.
With significantly elevated leukocytosis, consider bowel gangrene, abscess, or peritonitis. Also should check lactate for signs of ischemia as well.
Treatment: Closed-loop obstruction, bowel necrosis, and cecal volvulus usually require preoperative broad-spectrum antibiotics (Zosyn 3.375g / Unasyn 3g q6h). True mechanical obstruction requires surgery.
NG tube: not necessarily unless presence of severe distention or vomiting.
Large Bowel Obstruction
Causes: carcinoma (MCC, adenocarcinoma of the colon or rectum), fecal impaction, ulcerative colitis, volvulus (usually elderly, bedridden, psychiatric patients on anticholingerics or hx/o constipation), diverticulitis, intussuspection, pseudo-obstruction.
Hypogastric. Usually more constipation and gross distention.
Causes 5-6% of large bowel obstructions. Most often in inactive elderly, severe psychiatric or neurologic diseases. Usually due to severe constipation. Due to bowel segment twisting on mesenteric axis leading to luminal obstruction. Mortality 20% overall. Cecal volvulus is any age, commonly younger people, high mortality.
One of the few diagnosis that can be made on plain films (80% of the time), severely dilated single loop of colon in left abdomen, both ends in pelvis and bowel pointing superiorly (bent inner tube sign). Also can do barium enema which will show ‘bird’s beak’ deformity at point of twists, cut-off of contrast flow into proximal colon.
Treatment: Surgery for gangrenous bowel, usually can be reduced with sigmoidoscopy and rectal tube insertion (successful 85-95%), recurrence rate is 90% if reduction is not followed by colopexy
Occurs to some degree after most open abdominal operations. Other causes: peritonitis, trauma, ischemia, medications (opiates and anticholingerics), electrolyte disorders (hypokalemia). To differentiate SBO vs ileus in post-op patient, SBO usually have return of BMs prior to have symptoms where as ileus do not.
Treatment: conservative management including IV fluids and observation.
Ogilvie syndrome: mimics bowel obstruction, usually lower colonic obstruction. Very large dilated haustra in large intestines with little fluid/stool. RF: elderly, anticholingerics and TCAs. Colonoscopy is the treatment for decompression. Neostigmine infusion for refractory cases.
Diverticulosis thought to be due to increased intraluminal pressure due to American diet (low fiber, high fat, high carbs). Obesity and sedentary lifestyle are RF.
Diverticulitis due to erosion thru wall from thickened poop. Anaerobic bacteria: Bacteroides, Peptostreptococcus, Clostridium, Fusobacterium. GN rods such as E.Coli. (this was the reason for triple abx – GP, GN, Anaerobes: Amp/Gent/Flagyl).
Usually in the older population (>50yo), though it is trending in younger population, particularly male and obese. Recurrence rate 20-40%.
LLQ pain, fever, leukocytosis (45% will have normal WBC). 30% have diarrhea, 50% have constipation. N/V (60%), anorexia (40%), urinary symptoms (10% – due to adjacent inflammation). Tenderness only in LLQ + absence of vomiting + CRP > 50mg/L has a LR + 18 (Lameris, 2010).
CT preferred imaging study, though do not necessarily need if patient has prior hx and similar presentation. CT will recurrence if initial therapy does not improve symptoms. CT findings: retroperitoneal fat stranding (most sensitive); does not require contrast (IV or PO) for fat stranding (Tack, 2005), though can miss ischemia or abscess.
Ultrasound: hypoechoic peridiverticular inflammatory reaction ‘Dome sign‘ , mural/peridiverticular abscess formation w/wo gas, bowel wall thickening > 4mm at point of maximal tenderness, presence of diverticula in surrounding segments.
Uncomplicated: inflammation of the diverticula. Complicated (10-20%): inflammation with: abscess, stricture, obstruction, fistula, or perforation. Hinchey stages: Stage I: small, confined pericolic/mesenteric abscess, Stage II: larger abscesses, often confined to pelvis; Stage III: perforated diverticulitis with large abscess; Stage IV: free perforation with fecal contamination of peritoneal cavity, generalized peritonitis.
Uncomplicated: Clear liquid diet (2-3d) + oral antibiotics. 70-100% success rate, specifically if uncomplicated confirmed with CT. Complicated: Admission, bowel rest, IV antibiotics.
Antibiotics: Outpatient (7-14d): Metronidazole 500mg q8h + Cipro 500mg q12h, or Levofloxacin 500mg qd or Clindamycin 300mg q6h or Bactrim DS q12 or Augmentin 875mg q12 or Moxifloxacin 400mg qd. Also Cefoxitin or Cefazolin + Metro. Single vs double agent regiments?: same efficacy (Kellum, 1992). Inpatient: Unasyn 3g q6h or Zosyn 3.35g q6h/4.5g q8 or Ertapenem 1g qd or Timentin 3.1g q6h or Moxifloxacin 400mg qd or Metronidazole 500mg q6h + Levofloxacin 750mg qd or Cipro 400mg q12h. Also Cefepime +Metro.
Most abscess Stage II or > 4cm require percutaneous drainage. Perforation has high mortality rate, consider emergent exploratory surgery. Stage III mortality rate 13%, Stage IV 43%.
No abx at all?: Chabok, 2012: CT-confirmed uncomplicated diverticulitis. Randomized into admission with IV fluids alone vs IV fluids + abx. 623 pts. No difference in hospital LOS (3d median), no statistical difference in complications (1.9% vs 1.0%, p=0.302), recurrent diverticulitis at 1y (16%). Though 10 from no-abx group crossed over into abx group due to increased pain.
Regardless, needs colonoscopy in 6 weeks after resolution due to CT scan unable to differentiate carcinoma.
No evidence backing cessation of seeds/nuts for prevention (Strate, 2008). Recommended high fiber diet for possible prevention.
Small fat-filled sacs near lining of colon. Can become inflamed due to torsion or venous thrombosis. Generally younger population (average 35yo). Presents with sharp pain with n/v, appears similar to appendicitis, normal labs. Usually benign, self-limiting course. Tx: pain management and f/u in 1 week.
8-12% lifetime risk, 2/3 before age 30. Caused by obstruction of appendix lumen usually by fecalith (MCC, found in 11-52% on pathology)
Classic: Anorexia with nonspecific abdominal symptoms. Periumbilical pain develops later with nausea w/wo emesis. Pain migrates to RLQ. 1/3 will have atypical symptoms.
McBurney’s point: 1/3 distance on a line traced superomedially from anterior superior iliac spine to umbilicus. Rovsing sign: palpation of LLQ worsens RLQ pain. Psoas sign: extension of R leg at the hip while pt lying on left side. Obturator sign: pain with internal and external rotation of the thigh at the hip. Adler’s sign: to differentiate appendicitis from tuboovarian pathology in RLQ: find point of maximal tenderness in supine position, then have pt roll onto left side and if pain shifts toward center, its tubo-ovarian.
LR: RLQ pain 7.3-8.4, rigidity 3.76, migration 3.18, pain before vomiting 2.76, psoas sign 2.38, fever 1.94. (Wagner, 1996)
Hyperbilirubemia on labs has higher chance of perforation when in the setting of appendicitis (Estrada, 2007).
UA can have blood or pyuria in it due to close proximity, though > 30 RBCs or > 20 WBCs more likely true urinary (Paulson, 2003)
Ultrasound (83-96% in experts hand): preferred initially in children and pregnant women. Looking for thickened, non compressible appendix > 6mm in diameter.
CT: IV may not be needed. One study with unenhanced CT was 95% sens and 100% spec. A systemic review showed 93% sensitivity. If CT equivocal, 30% still have true appendicitis (Daly, 2005). ACR Appropriateness recommendations leave it up to institutional preference, though give CT without contrast a 7 rating.
Using Samuel’s Pediatric Score (PAS), one study placed children into low, moderate, or high risk. If low, they were discharge with f/u (no appys found). In high risk, all had appy in OR. Moderate risk were either admitted with most have ultrasound. 33 of 119 had positive US, positive OR. 5 with negative US were found later to have appy. Only 13 of the 196 kids had CT scans. (Saucier, 2014). PAS points: Anorexia, Nausea or Vomiting, Migration of pain, Fever > 100.5, Pain with cough, percussion, or hopping (2 points), RLQ tenderness (2 points), WBC > 10, Neutrophils > 75%.
Alvarado Score: 10 point scale; modified to take out left shift now. One ED study looking at score < 4 can rule out? 29% still had appendicitis. 50% spec, 70% sens (Meltzer, 2013). Alvarado points: Migratory right iliac fossa pain, Anorexia, Nausea/Vomiting, Fever > 99.5, Tenderness in right iliac fossa (2 points), rebound tenderness in right iliac fossa, leukocytosis (2 points).
Same rate of appendicitis as general population.
Do ultrasound first; if equivocal, get surgeon involved for MRI vs CT vs diagnostic lap. Fetal loss at lap appy 6%, WORSE than open appy; though fetal loss greatest in complex/perforated appy. Fetal loss same for simple appendicitis as the ‘negative’ appy group. (Walsh, 2007). Tetrogenic exposure threshold: 5 rads (<1% risk). CT appy protocol in first trimester 2.4 rads vs 3 rads in second/third. Still 99% chance nothing will happen with the fetus.
Can consider MRI without gadolinium (crosses placenta) in first trimester pregnancy.
Call surgeon, make NPO, start antibiotics.
IV antibiotics: Uncomplicated: Unasyn 3g or Cefoxitin 2g or Ertapenem 1g or Moxifloxacin 500mg + Cefuroxime 1.5g/Cefazolin 1g/Cipro 400mg/Levofloxacin 750mg. Complicated: Imipenem 500mg or Meropenem 1g or Doripenem 500mg or Moxifloxacin or Zosyn or Metro 500mg + Aztreonam 2g/Cefepime 2g/Cipro 400mg/Levofloxacin 750mg.
Non-surgical tx: 5 non-US trials: about 70% did not need surgery up to 1 year. 46% reduction in complications. Limitations: small size, no CT done, varied criteria for ‘rescue’ surgery. (Ericksson, 1995) (Styrud, 2006) (Hansson, 2009) (Malik, 2009) (Vons, 2011).
Vons, 2011: 239 pts diagnosed by CT. Augmentin vs surgery. Rate of peritonitis at 30d: Surgery 2% vs Augmentin 8%. In abx group, 12% had surgery within 30d & another 22% within a year.
Recent research shows promise with Tenofovir (HIV medication). Recent study showed it actually reversed cirrhosis changes in patients given it for 5 years. (Marcellin, Lancet 2013)
Coagulation in End Stage Liver Disease
Liver synthesizes both anti and pro-coagulation cascade so because both are decreased in liver disease, actually evens out. INR useless (only useful for warfarin use). There is no single test to determine coagulation affect in liver disease (PT, PTT, bleeding time, etc).
Systemic complication of liver dx. Transient and reversible neuro and psychiatric manifestations. Poor prognostic indicator
Symptoms: mild neuro disturbance, forgetfulness, nystagmus, asterixis – flapping hand tremor, agitation, seizures, ultimately coma
Causes: Gi bleed, infection, noncompliance, dehydration, hepatorenal syndrome. Colon flora creates ammonia – goes into liver and gets converted and excreted in urine. With cirrhotic, pathway inhibited and ammonia floating around. Cerebellum and basal ganglia pick it up and cause abnormalities and disturbance in neuro transmission
Level of ammonia tends to be elevated – poorly correlates with grade of hepatic encelopathy. Little clinical value. Need to diagnosis CLINICALLY.
Grade 2: lethargy, gross intellectual impairment, asterixis – ADMISSION
Grade 3: somnolence, amnesia, bizarre behavior, nystagmus/clonus
Grade 4: stupor to unconscious, comatose, dilated pupils. HIGH mortality
Tx: Eliminate precipitating event. Remove excess ammonia – lactulose ORAL (non absorbable sugar and changes pH of gut – ammonia charged and can’t get absorbed. SE: electrolyte abnormalities and dehydration). Abx: neomycin (ototoxicity/nephrotoxicity) & rifaximin. Supportive care. Low protein diet / Probiotics. Flumazenil – blocks GABA, pt temporarily wakes up and goes back to asleep – able to check in ICU to see how patient is doing
Gallstones MCC – 60%. Alcohol second MCC. Other causes: I GET SMASHED: Idiopathic, Gallstones, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hypertriglyceridemia (3rd MC, 10%, probably need to check level on most patients) calcium/parathyroid, ERCP, Drugs. Parasites is MCC worldwide.
Trypsin activation within the pancreas with autodigestion, inflammatory markers initiated.
Epigastric pain, radiating into upper quadrants, back. Usually pain increases over 30 minutes until its constant. Pain worse with laying flat. Nausea/vomiting. Fever is severe cases. Cullen sign: periumbilical ecchymoses and Turner sign: ecchymoses in the flanks – indicate retroperitoneal/intraabdominal hemorrhage – severe necrotizing pancreatitis. ARDS can occur with severe pancreatitis. Large pleural effusions can be related to pancreaticopleural fistula with pseudocyst. Pleural effusion good indicator of severe pancreatitis.
Lipase 3x upper limit of normal. Lipase stays elevated longer than amylase – better sensitivity for delayed presentations. Recurrent disease can have normal levels. Level does not predict severity either. Need 2 of the 3: HPI/exam consistent with pancreatitis, lipase > 3x upper limit, and CT findings. Need to check all first time pancreatitis for upper abdominal ultrasound for GS pancreatitis – even the alcoholics.
Colon cutoff sign: colonic gas stops at splenic flexure due to spasm from pancreatic exudate. CT best test for diagnosis. Abscess don’t usually form until >15 days after initial event.
Ranson criteria: terms severity of pancreatitis. 5 points determined on admission (age>55, WBC>16k, Glucose >200, LDH>350, AST>250) and 6 obtained 48 hours after (Decrease in hemocrit by 10%, fluid sequestration >6L, calcium level <8, PaO2 <60, BUN>5 after hydration, base deficit >4). APACHEII used as well for severity. CT Severity Index is better predictor of severity than Ranson.
Treatment: supportive/conservative. Hydration (start at 2L, need 4L likely by the 6-12 hour mark, can check with serial hemocrits – LR > NS), pain control (ok to do oral over IV). Newer recommendations are to start fluids/food early, recommend low-fat food – NPO no longer recommended unless unable to. If elevated bili, GI consult for urgent ERCP in the next day or so. Pseudocysts that are large, symptomatic or complicated can be treated by endoscopic ultrasound (usually GI service).
Inflammation of the gallbladder. Acute cholecystitis is bacterial invasion. Biliary colic is constant RUQ lasting 2-6 hrs and then resolving. Acute calculus cholecystitis occurs with absence of gallstones (RF: elderly, critical ill, burns, trauma, major surgery, TPN, DM, immunosuppression, childbirth). Silent gallstones: 1-4% per year of causing symptoms, 10% by 5 years, 20% by year 20. Sludge can form into gallstones or can completely resolve – no methods to prevent sludge.
Cholangitis is ascending infection due to obstructing stone.
Generally RUQ pain with radiation into back, shoulder. Can also cause pain in LUQ. Some symptoms develop at night with peak in symptoms at midnight to 1am. Not necessarily with meals. Colic should only last about 5 hours. If >, consider cholecystitis/pancreatitis. Murphy sign has highest sensitivity for diagnosing acute cholecystitis. WBC > 10k is 63% sensitive, CRP sensitive in 97%. Mirizzi syndrome (compression of common hepatic duct from impacted stone on cystic duct – external squeeze). US only 94% sensitive for cholecystitis.
Ultrasound findings: gallbladder wall >3mm, pericholecystic fluid. >5 is more predictive of cholecystitis. Consider ascites, pancreatitis, heart failure, alcoholic hepatitis as causes for incidental wall thickening.
HIDA (hepatobiliary imilodiacetic acid cholescintigraphy) looks at GB function. Looks for biliary dyskinesia (<35% EF). Morphine can interfere with result.
Treatment: biliary colic can be outpatient surgery. Acute cholecystitis require laparoscopic cholecystectomy. ERCP for CBD stones. All narcotics can increase biliary pressure and induce spasm of Oddi. Antibiotics: third generation cephalosporin + flagyl or fluoroquinolone + flagyl. Zosyn for severe cases.
Obstruction + Infection. Causes: choledocholithiasis, biliary stricture, compression caused by malignant. Charcot triad: fever, jaundice, RUQ pain. Reynolds pentad: AMS, shock, fever, jaundice, and pain. Tx: Abx, hydration, GI/surgery consult.
Longer milder symptoms. US can show porcelain gallbladder.
SBO due to impaction from large gallstone at terminal ileum. Gallstone usually enters from biliary-duodenal fistula. Usually pneumobilia. Morbidity/mortality high.
Tintinalli, Seventh Edition, Chapter 82: Pancreatitis and Cholecystitis
EMRAP, December 2017
Peptic Ulcer Disease
Lesions > 5mm: ulcers; Lesions < 5mm: erosions. Most common in gastric antrum and duodenal bulb. Duodenal ulcers > gastric ulcers. Gastric ulcers caused by NSAIDs or H.pylori 90% of the time. Also consider Crohns or Zollinger-Ellison as well.
H.pylori: GN bacilli, associated with lower socioeconomic status. Secretes urease enzyme that produces ammonia to protect bacteria. Test IgG ab ELISA for H.pylori – antibodies can remain for up to 1 yr after tx. Urease assay tests for enzyme – urease breath tests – checks for active infection and check for cure rate. False negative rate with current use of PPI/abx/bismuth. Need to hold for 1-2 weeks.
NSAIDs: endogenous prostanglandin synthesis. Enteric coated doesn’t matter. Risk factors: steroid use, anticoagulants, older age. NSAID-gastric ulcers more likely to cause hemorrhage/perforation. Usually painless, not necessarily dyspepsia. Even if you d/c NSAIDs, ulcers can be present up to 1 year later.
Zollinger-Ellison: 0.1% of peptic ulcers, gastrin-producing endocrine tumor of pancreas/duodenum. Associated with multiple ulcers and diarrhea. Elevated gastrin level. Dx: secretin stimulation test or elevated fasting gastric acid output.
Gastric ulcer pain 5-15min after oral intake, relieved with fasting. Duodenal ulcers relieved temporarily by eating, returns 1-2 hours afterward – also pain can occur at night.
Endoscope: Used primarily in significant dyspepsia, acute GI bleeding, fecal occult blood, abdominal pain of unclear etiology.
H2 blockers: inhibit basal and food-induced acid secretion, renal dosing required. Most effective when given between dinner and bedtime.
PPI: require acid for activation so effective when taken before or with meal and in absence of other antisecretory drugs.
Misoprostol: prostanglin analong that inhibits acid secretion. Can cause diarrhea/spontaneous abortion.
Sucralfate: mucosal protectant.
H.pylori treatment: Triple therapy: clarithromycin 500mg BID, amoxicillin 1g BID, PPI BID for 10-14 days. 4 therapy: Bismuth, tetracycline, flagyl, and PPI for PCN allergy patients.