Upper GI Flashcards

1
Q

Dysphagia

Definition

A
  • Subj sx of abnormal or difficulty swallowing
    • Can be related to strx or mobility/ fx disorder
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2
Q

Oropharyngeal dysphagia vs. Esophageal dysphagia

A
  • Oropharyngeal: functional impairment in initiation of swallowing
    • Typically results from systemic neuro or myopic conditions
  • Esophageal: fx or anatomical esophagus abnormality
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3
Q

Odynophagia

A

Pain w/swallowing

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4
Q

Globus sensation

A

nonpainful sensation of a lump, tightness, or fx in pharyngeal/cervical area

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5
Q

Associated symptoms w/Dysphagia

A
  • Heart burn
  • Wt. loss
  • Hematemesis
  • Anemia
  • Regurgitation of food particles, and
  • Respiratory symptoms
  • Dry mouth
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6
Q

Dysphagia PE

A
  • Thorough HEENT, neuromuscular including cranial nerves, cardiac, respiratory, signs of malnutrition/dehydration
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7
Q

Dysphagia Diagnostics: Modified Barium swallow

A

Assessment of oropharyngeal swallowing mech + aspiration risk (preferred → easier)

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8
Q

Dysphagia Diagnostics: Barium Swallow

A
  • Assess esophageal swallowing function
  • structural defects
  • esophageal wave propulsion + clearance; reflux
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9
Q

Dysphagia Diagnostics (3 others besides barium swallows)

A
  • CT Neck: Looking specifically for structural lesion or malignancy of neck impinging on swallowing function
  • Upper endoscopy: assessment of esophageal mucosa, structure, cellularity/pathology, malignancy, eosinophilic presence
  • Esophageal manometry: specifically measures relaxation of upper + lower esophageal pressures + pressure gradient of peristalsis in esophagus
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10
Q

Meds that cause dysphagia

A

Bisphosphonates, NSAIDs, K+, doxy/tetracycline

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11
Q

What to do if patient has acute symptoms of dysphagia?

A

UNABLE TO SWALLOW SOLIDS +/OR LIQUIDS → ED

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12
Q

GERD
Reflux

Definitions

A
  • Reflux: Retrograde movement of gastric contents from stomach to esophagus
    • Normal physiologic process
  • GERD: when esophageal mucosa unable to tolerate caustic gastric contents → chronic pathologic s/s in oropharynx, larynx, esophagus, respiratory tract
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13
Q

Barrett’s esophagus

Definition

A
  • Chronic exposure to gastric acid → esophageal cell changes
  • Small increased risk of developing esophageal cancer
  • If alarm features or risk of Barrett’s esophagus → upper endoscopy
    • Barrett’s for many years → higher risk for precancerous changes
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14
Q

CLASSIC GERD S/S

A
  • Asthma sx: Wheeze
  • Bloating, belching
  • Chronic cough, Chest pain
  • Dyspepsia, Dysphagia
  • Epigastric fullness
  • Retrosternal burning sensation (heartburn) – typically pos-prandial
  • Nausea
  • Water brash

Extra-esophageal sx:
- Sore throat, Hoarseness
* Symptoms exacerbated by anything that ↑ pressures on LESph: laying down, bending over, large meals
* **Can frequently mimic ischemic cardiac p! – RULE OUT 1ST **

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15
Q

GERD Objective Findings

A
  • Unremarkable
  • Teeth/dental erosions from gastric acid coughing up
  • Wheezing/signs a/w asthma
  • Epigastric tenderness/adb masses
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16
Q

GERD Pathophysiology

A

Motor abnormalities
* Decreased LES tone
* Transient LES relaxations (TLESR)
* Most common cause
* Effected by endogenous hormones, medications, foods, smoking, etoh, caffeine
* Impaired esophageal acid clearance
* Dry mouth is a risk factor
* Delayed gastric emptying
* Commonly related to DM or connectvive tissue disorders
Anatomical Factors
* Hiatal Hernia
* Obesity
* Pregnancy
* Also increased levels of circulating estrogen and progesterone decrease LES tone*

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17
Q

GERD Diagnostics

A
  • Can be made clinically w/classic sx + no alarm features or risk for Barrett’s
  • In pts w/atypical sxs, other differentials must be r/o
  • Labs:
    • CBC
    • IFOB/guiac (+/-)
    • H. pylori
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18
Q

Common meds that REDUCE LESph tone:

DEFINITELY ON EXAM

A
  • Anticholinergics
  • BBs
  • Benzos
  • Bronchodilators
  • CCBs
  • Nitrates
  • TCAs
  • Theophylline
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19
Q

GERD Pharm meds

A
  • Antacids (neutralize gas pH)
  • H2 Blockers (inhibitor histamine 2 receptor on gastric parietal cells → lowering acid production)
  • PPIs (most potent) binding to + inhibiting ATPase pump
    • Best when taken 30 mins before 1st meal of day
    • More effective vs. H2 at healing erosive esophagitis
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20
Q

If patient has had GERD for > (5-10yrs)…

A

…+ 1 additional RF indicates need for upper endoscopy

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21
Q

GERD nonpharm modifications

A
  • Weight loss
  • HOB elevation in ppl w/nocturnal or laryngeal sxs (blocks or wedge)
  • Sitting up post meals + no meals 2-3 hrs prior to bedtime; no large meals
  • Selective dietary changes
    • Eliminate/cut down on caffeine, chocolate, spicy foods, food w/high fat content, carbonated beverages, peppermint, EtOH, No peppermint (lower tone)
  • Smoking cessation
  • Avoid tight fitting garments
  • Chewing gum or lozenges → salivation → neutralize refluxed acid → esophageal acid clearance
  • Adb breathing exercises to strengthen antireflux barrier to LES
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22
Q

How to R/O CARDIAC sxs for DX GERD?

A
  • Get worse w/exertion (going up stairs)
  • Cause dyspnea on exertion
  • Radiate to jaw/arm
  • EKG
  • GI cocktail: Omeprazole, Mylanta, Lidocaine (if it helps = GERD)
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23
Q

Barrett’s RFS

A
  • GERD 5 to 10yrs
  • Age > 50
  • Male sex
  • White race
  • Hiatal hernia
  • Obesity
  • Nocturnal reflex
  • Tobacco use (past or current)
  • 1st - degree relative w/ Barrett’s esophagus +/or adenocarcinoma
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24
Q

Pregnancy considerations GERD

A
  • Progesterone relaxes uterus smooth mm + LES
  • Heartburn (when 1st experienced): 52% 1st tri, 24% 2nd tri, 9% 3rd tri
  • Tends to recur in subsequent pregnancies
  • Sx therapy includes:
    • Multiple small meals, avoid lying down for 2-3hr after meals, elevate HOB @ night
  • Start w/ antacids → sucralfate → H2Ras → PPIs
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25
Q

GERD in elderly considerations

A
  • Highest risk of complications
  • Lower threshold for endoscopy
  • PPIs safe, but need to be mindful of Rx interactions, (Cyto P450 path) most common)
    • Major: WARFARIN (BLEED RISK)
    • Minor: Benzos, CCBs, theophylline
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26
Q

GERD alarm sxs

Not in lecutre?

A
  • New onset of dyspepsia in patient ≥ 60 years
  • Evidence of gastrointestinal bleeding (hematemesis, melena, hematochezia, occult blood in stool)
  • Iron deficiency anemia
  • Anorexia
  • Unexplained weight loss
  • Dysphagia
  • Odynophagia
  • Persistent vomiting
  • Gastrointestinal cancer in a first-degree relative
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27
Q

GERD Treatment Recommendations (Stepwise) Mild

Mild

A

Mild/Intermittent Symptoms
* Step Up Therapy
* Lifestyle/diet modifications then
* Fewer than 1 episode per week: PRN antacids
* Fewer than 2 episodes per week
* Stepwise therapy:
low dose H2 blockers x 2 weeks, if no improvement → standard dose H2 blockers for 2 weeks, if no improvement →
Once daily PPI
Successful treatment should continue for a minimum of 8 weeks*

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28
Q

GERD Treatment Recommendations (Stepwise) Severe

A

Severe/Frequent Symptoms OR Erosive Esophagitis on EGD
* Step Down Therapy → start with high dose then step down
* Lifestyle/diet modifications +
* Standard dose PPI x 8 weeks → Low dose PPI → H2 Blocker if intermittent symptoms

Acid suppression therapy should be discontinued EXCEPT in patient with Barrett’s Esophagus or severe erosive esophagitis → Maintenance PPI therapy

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29
Q

Safety Considerations: Long Term PPI usage

A

Overuse can change stomach medium + can facilitate growth of bacteria
* C. difficile diarrhea (mechanism unclear)
* ↑ risk of pneumonia, likely d/t decreased gastric acid secretion – easier colonization UGI tract

  • Malabsorption – Mg, Ca, Vit B12, Iron
  • Atrophic Gastritis, kidney disease, drug-induced lupus
  • Large study showed long-term use of PPI a/w osteoporosis + hip fractures, although this is now in question; however, still FDA labeling on fracture risk
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30
Q

PPI Tapering education

A
  • After at least 3 months symptom free on PPI, may taper
  • Cut dose by half every week
  • Once on lowest dose for one week, may stop
  • Do not reduce or discontinue if patient has Barrett’s Esophagitis
  • Patients receiving 4-8 wk treatment for acute duodenal or gastric ulcers do not require taper, nor do those being treated for H. pylori
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31
Q

PUD

Definition

A
  • Erosion in either stomach or duodenum > 5mm AND penetrates into submucosa
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32
Q

PUD Causes
Most common?

A
  • H. Pylori responsible for 60% of PUD in US
    • Causes increased acid secretion
    • Increases inflamm
    • Downregulates mucosal defense system
  • NSAIDs (4x inc risk)
  • Smoking
  • EtOH
  • Genetics
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33
Q

PUD clinical manifestations

A
  • 70% asymptomatic
  • Gnawing or burning epigastric pain
  • Bloating, abd fullness, nausea, early satiety, GERD
  • Establish relationship w/eating
    • Duodenal: Pain worse 2-5hrs post eating
    • Gastric: Pain worse soon after eating
  • Nocturnal pain relieved w/food, antacids
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34
Q

PUD Objective Signs

A
  • Hx should assess for prior Hx of H. pylori, NSAID use, RFs, alarm features
  • PE normal
    • +/- epigastric tenderness
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35
Q

PUD confirmation of eradication

A
  • Confirmation should be performed on all pts treated for H. Pylori d/t abx resistance
    • Should be performed at least 4wks after completion of abs treatment
    • Can use either urea breath test, stool antigen test or endoscopy based testing
    • DO NOT use serologic testing; does not distinguish between past + present
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36
Q

PUD diagnostics

Non-invasive testing (test & treat category)

A

only if < 55 + no alarm sx
* Active or hx of PUD
* Dyspepsia
* Gastric MALT lymphoma
* Consider before starting chronic NSAID therapy
* ? Unexplained iron deficiency

37
Q

PUD Diagnostics

Invasive testing - Endoscopy

A
  • > 55
  • Alarm sx: Unexplained wt loss, Progressive dysphagia
  • Odynophagia
  • Recurrent vomiting
  • FMHx of GI cancer
  • GI bleeding
  • Anemia
  • Jaundice
  • Abd mass
    ** Endoscopy is not indicated for sole purpose of determining H. Pylori status**
38
Q

H. Pylori noninvasive Tests

A

Urea breath testing (UBT):
* Highly sensitive and specific
* Cannot be used if any PPI, bismuth or abx use in the last 2 weeks
* False negatives may be seen with bleeding ulcers
* Expensive

Stool antigen assay – best in COVID setting
* Less expensive vs. UBT + slightly less affected by PPI use
* Still recommend avoidance of PPIs, bismuth or abx for 2 weeks
* POC test not as sensitive but lab based testing equal to urea breath test
* Can be used for diagnosis and confirmation of eradication

Serology
* ELISA test to detect H. Pylori IgG
* Inexpensive
* Not accurate (85% sensitive and 79% specific)
* Does not determine between active and past infection
* Not affected by PPI, bismuth, antibiotic use
* Not generally recommended

39
Q

PUD Pharm meds

A
  • Clarithromycin, Metronidazole (metallic taste)
  • Metronidazole: Peripheral neuropathy, seizures, vomiting w/EtOH; DO NOT DRINK
  • Clarithromycin: N/V, abd p!, prolonged QT
  • Amoxicillin: diarrhea, allergic reaction – skin rash
40
Q

PUD Considerations in Elderly

A
  • Age independent predisposing factor in GI bleeding
  • Risk increases significantly > 65 yrs + further > 75 yrs
  • UGI bleed dramatic event w/ high mortality
  • NSAID use highest cause followed by H. Pylori
  • Cox-2 inhibitors (though not as high risk, not without risk)
  • Low dose ASA (risk doubles)
41
Q

PUD considerations > 50

A
  • Unexplained or gradual drop in Hgb—think of GI bleeding
  • Gradual = usually asymptomatic
  • Avoid NSAID use
  • If must use:
    • Lowest dose for shortest amount of time
    • Prescribe gastroprotective drug concomitantly; PPI best choice
  • Long term considerations
    • Consider testing for & tx H. Pylori if NSAID tx will be > 3 mos
42
Q

Cholecystitis

A
  • Inflamm of gallbladder
  • Can be w/calculous or w/o
  • More serious complications may occur when gallstone passes out of cystic duct + into common bile duct
43
Q

Cholecystitis Etiologies

Cholelithiasis, Choledocholithiasis, Cholangitis Definitions too

A
  • Gallstones can block tube (cystic duct) leading out of gallbladder → cholecystitis
  • Bile buildup can → inflamm
  • Bile duct problems, tumors, serious illness, infection (E. coli, enterococcus, Klebsiella, Enterobacter)
  • More serious complications may occur when a gallstone passes → cystic duct → common bile duct

Cholelithiasis
* Appearance of gallstones w/in gallbladder or cystic duct
* Choledocholithiasis – common bile stones
* Cholangitis – inflamm of common bile duct – via bact infxn

44
Q

Cholecystitis Clinical Manifestations

A
  • RUQ pain or epigastric area
  • Radiating pain to R shoulder or back
  • Worsens after eating
  • N/V
45
Q

Cholecystitis Objective Findings

A
  • **(+) Murphy’s sign **: tenderness to RUQ palpation
  • Distended gallbladder
  • Jaundice (choledocholithiasis, I.e. gallstones in the common bile duct)
  • Bile duct obstruction → turn yellow
  • ↑ fever & chills if septic
46
Q

Cholecystitis Diagnostics

Labs

A
  • CBC – Leukocytosis
  • LFTs – ALT, AST normal or mildly elevated
    • ALKphos + bilirubin elevated w/CBD obstruction or cholangitis
  • Serum pancreatic enzymes (amylase + lipase) – mildly elevated
  • Pregnancy test
47
Q

Cholecystitis Diagnostics

Imaging

A
  • **1st line Abd U/S (practical) **– not contraindicated in preg
  • Can’t determine if stone passed out of gallbladder → bile duct
  • Look for thickening of gallbladder wall - acute
  • HIDA scan
  • CT scans: if unclear picture
  • MRCP: for current choledocholithiasis in pts w/acute cholecystitis; noninvasive for evaluating intrahepatic + extrahepatic bile ducts
48
Q

Cholecystitis Pharm interventions

A
  • IV fluids
  • Pain management
49
Q

Cholecystitis Nonpharm management

A
  • Hospitalization usually necessary: observation
  • Cholecystectomy most widely used therapy when s/s arise from gallstones
    • Pts do well post surgery, w/no difficulty w/digesting food, despite lacking gallbladder to help
    • Laparoscopic cholecystectomy preferred
  • Open procedure if ↑ inflamed gallbladder
  • Stones in bile duct can frequently be removed w/ERCP
50
Q

Common complication with cholecystectomy

A

Bile duct injury is most common complication of laparoscopic cholecystectomy
* Can have post-surgical diarrhea
* D/t ↑ bile acid entering large intestine causes laxative effect
* Usually resolves but can treat w/immodium or cholestyramine

51
Q

Cholecystitis Risk Factors

A
  • Female sex
  • Overweight
  • Adv age > 40
  • Pregnancy
  • Hx of “crash diets” w/rapid weight loss
  • Meds: estrogens, thiazides, fibrates, anabolic steroids
  • FMHx, HiTGs
  • Spinal cord injury
  • Hx of gastric bypass surgery
  • DM
  • Crohn’s disease
  • Alcoholic + biliary cirrhosis
  • Hyperparathyroidism
52
Q

Cholecystitis pregnancy + elderly considerations

A
  • Be aware of ↑ likelihood of gallbladder disease during pregnancy & postpartum period
  • In elderly pts, sometimes difficult to DX; complications more likely; cholecystectomy mortality rate ↑
53
Q

Pancreatitis

Definition

A
  • Can be acute or chronic inflamm
  • Digestive enzymes attack pancreatic tissues → swelling
  • Leading cause of hospitalization among digestive system diseases
54
Q

Acute pancreatitis

Definition

A
  • Disorder of exocrine pancreas + A/w cell injury w/local + systemic inflamm responses
  • Inflamm range from milld edema → necrosis
  • Life threatening
55
Q

Chronic Pancreatitis

Definition + Risks

A
  • Inflamm cause chronic damage to gland – fibrosis, calcification, + ductal inflamm
  • Slow progression over years
  • Related to XS EtOH
  • Smoking ↑ risk
  • More common in AMAB pts
  • Lead to panc. Failure
  • Exocrine: stop producing enzymes → dietary fat + protein poorly digested → oily stools
  • Endocrine: no insulin prod → DM
56
Q

Most common causes of pancreatitis

And list of other causes
NOT ABCS

A
  • Gallstones – AFAB pts
    • Cause obstruction in bile duct build-up of enzymes causing tissue damage
  • EtOH – AMAB pts
  • HLD TGs > 1000
  • Infxns: mumps, HIV
  • Meds: thiazide diuretics + furosemide
  • ERCP procedure
  • Heredity
  • Cystic fibrosis, DM, celiac, high calcium
  • Idiopathic
  • Malignancy
57
Q

ABCs of Acute Pancreatitis

A
  • Alcohol, autoimmune disorders, arteritis
  • Biliary, blunt trauma
  • Congenital – pancreas divisum (ducts don’t join up)
  • Drugs or meds
  • ERCP, eosinophilia
  • Formations – primary + metastatic tumors
  • Genetic - mutations
  • HLD, hypercalcemia
  • Idiopathic, infectious – HIV, IBD
58
Q

Pancreatitis clinical manifestations

A
  • N/V
  • Acute onset of epigastric pain → back, worse w/movement
59
Q

Pancreatitis Objective Findings

A
  • ↑ HR, RR, + temp
  • Low skin turgor, dry mucous membranes (dehydrated)
  • Diaphoretic
  • HoTN
  • Tender abd w/diminished bowel sounds
  • Mild rigidity w/o rebound tenderness
  • Jaundice possible
  • Cullen sign (+)
  • Grey Turner sign (+)
60
Q

Pancreatitis Labs

A

Amylase
- Rises w/in 6-12hrs + returns to normal w/in 3-5d
- 3x value of upper limit

Lipase
- Rises w/in 4-8hrs, peaks at 24hrs, returns to normal w/in 8-14d
- Rises earlier + lasts longer
- Useful in pts who present later, + more sensitive vs. amylast in pts w/this d/t EtOH
- Lipase 3x upper limit of normal

  • Am:Li > 5 = EtOH
  • Am:Li > 3x = gallstone
  • CBC w/diff = ↑ WBC
  • Hct ↑ = necrosis
  • CMP (electrolytes, BUN, HFTs)
  • Serum Hcg for pts w/uterus of childbearing age
  • Fasting lipids for TGs
61
Q

Acute pracreatitis pharm treatments

A

1st line tx: IV hydration, pain control
* Meperidine
* Ketorlac
* Ondansetron
Early TPN

62
Q

Chronic Pancreatitis pharm treatments

A
  • Pancreatic enzyme supplements w/every meal (creon)
63
Q

Pancreatitis nonpharm treatments

A
  • NPO
  • Refer/Hospitalize!
    • Hospitalize for 3-7d if responsive to conservative therapy

Need to address underlying cause
* ERCP – address bile duct narrowing/ obstructions
- ERCP: x-ray + endoscope
* Cholecystectomy
* Pancreatectomy (chronic)
* Low-fat diet + enzyme supplements help control pain in reducing pancreas stimulation
* EtOH + smoking cessation
* May need to drain pseudocyst

64
Q

Pancreatitis Patient Education

A
  • Lifestyle modifications
    • EtOH misuse: D/C
    • Control ↑ TG
    • Lipid lowering meds
    • Eat small, low-fat meals of carbs + proteins
65
Q

Pancreatitis pregnancy considerations

A
  • Diagnostics – don’t delay diagnosis + tx as delay can ↑ maternal = newborn morbidity + mortality
  • Care by obstetrician well-versed in high-risk pregnancies
66
Q

Abdominal / inguinal hernia

Definition

A
  • Protrusion of abd viscera through abnormal opening in mm wall
67
Q

Hernia types

Reducible, Irreducible/incarcerated, strangulated

A
  • Reducible: structure returns abd cavity
  • Irreducible/ incarcerated: structure does not return to abd cavity
  • Strangulated: interrupted blood flow to structure that has herniated
68
Q

Hernia Etiologies

A
  • Congenital/acquired
  • pregnancy
  • frequent stooping
  • acites
  • mm atrophy
  • trauma
  • dysfunctional CT r/t malnutrition
  • long-term steroid use
  • recurrent Valsalva (BPH, straining at urination, heavy lifting)
  • Chronic cough (COPD, asthma, GERD, smoking)
69
Q

Diagram of hernia locations

A
70
Q

Most common hernia sites

A
  • Ventral - epigastric, umbilical, spigelian, parastomal, most incisional
  • Groin - direct & **indirect inguinal & femoral **
    • most common; we will be spending the most time on these. 75% of hernias are inguinal.
  • Pelvic - sciatic, obturator, perineal
  • Flank – protrude through weakened areas of back musculature; superior and inferior lumbar triangle hernias
71
Q

Epidemiology of hernia types
Which one has high risk of strangulation?

A
  • Indirect inguinal: most common in both sexes; 60% of all hernias.
    • More common in infants < 1 year old & in males 16-20 years old
  • Direct inguinal-less common; occurs most often in men > 40; rare in women. Incidence increases with age. Acquired.
  • Femoral-least common; 10% of all groin hernias; more common in women. Usually seen later in life. Acquired.
  • Though uncommon, 40% present as emergencies.
  • Umbilical-very common in newborns & infants up to 1 year; often resolves in infants up to age 2. More common in women; often missed, obscured by subcutaneous fat. F/U w/surgeon
    • **High risk of strangulation and mortality due to risk of colonic entrapment **
  • Obturator – rare but serious; more common in elderly women; incidence increases with age. Acquired.
72
Q

Inguinal Hernia - indirect

Definition

A
  • Etiology – congenital; patent processes vaginalis
  • Incidence decreases with age
  • Location – lateral side of spermatic cord
  • Protrudes through internal inguinal ring, lateral to inferior epigastric artery
  • Can contain sac of peritoneum, omentum, or bowel
  • Medium likelihood of strangulation

Indirect inguinal hernia passes through the inguinal canal or the groin

73
Q

Inguinal hernia - direct

Definition

A
  • Etiology – acquired, weakness in the posterior floor
  • Incidence increases with age
  • Location – directly forward thru posterior wall of the inguinal canal
  • Protrudes through external inguinal ring, medial to inferior epigastric area
  • Can contain periorbital fat, bowel, peritoneal sac
  • Low likelihood of strangulation

A direct inguinal hernia shows a bulge from the posterior wall of the inguinal canal

74
Q

Femoral hernia

Definition

A
  • Incidence: more common in women, later in life
  • Location: femoral canal, fossa ovalis – medial to the femoral pulse
  • More common on the right side
  • Protrudes through femoral ring, medial to femoral sheath, which containes femoral artery
  • Likelihood of strangulation – high; nearly half of patients are unaware of their femoral hernia before strangulation occurs; groin pain and tenderness may be absent
75
Q

Obturator Hernia

Definition

A
  • Rare
  • Women affected > men 6:1, likely due to larger, more triangular obturator canal
  • R side more common
  • BL hernias & concurrent femoral hernias are rare but documented
  • Greatest incidence in patients in their 70s and 80s weighing < 40 kg
  • Decreased muscle and fat
  • 1/3rd of pts have history of previous attacks
  • Watch for symptoms of bowel obstruction, present in greater than 80% of cases
76
Q

Clinical manifestations for
Inguinal, femoral, umbilical, obturator hernia

A

Inguinal Hernia
* Pain w/straining
* Pt feels bulging in groin area/scrotal pain & swelling – scrotal hernia
* May also describe sensation as “dragging”
* Inguinal swelling w/o pain

Femoral Hernia
* Can have severe pain, but sometimes not

Umbilical hernia
* Periumbilical pain, may be severe; consider umbilical hernia for periumbilical pain

Obturator hernia
* Often no symptoms until acute onset of N/V
* Dull, cramping, abd pain
- Can be intestinal obstruction, recurrent

77
Q

Hernia RED FLAGS

A

Red flags
* Painful to palpation
* Erythema
* Ulceration
* Febrile patient
* Abdominal pain
* Bloating
* N/V

DO NOT TRY TO REDUCE A STRANGULATED HERNIA

78
Q

Hernia Physical Exam

A
  • Male patient stands to start
    • R hand = pt R side
    • L hand = pt L side
  • Invaginate loose scrotal skin w/index finger
  • Off note – not able to in women
    • Need to palpate mass or painful area
79
Q

Indirect inguinal hernia objective findings

A
  • Higher up
  • Insert finger into inguinal canal → palp for bulge → bear down
  • Hernia comes down inguinal canal + touches fingertip
80
Q

Direct inguinal hernia objective findings

A
  • Insert finger through inguinal canal → bear down → palp for bulging
  • Hernia bulges anteriorly + pushes side of finger forward
81
Q

Femoral Hernia Objective findings
(Aka what to do if it’s a femoral hernia)

A
  • Hernias become strangulated (high risk) → refer to surgeon
82
Q

Umbilical Hernia Objective Findings

A
  • Pt lies supine → bear down → palp mass at umbilicus
  • Have pt sit up + watch for protrusion of umbilical or ventral mass
83
Q

Obturator Hernias Objective findings

A
  • Usually not palpable externally but sometimes tender mass w/pelvic or rectal exam
  • (+) Howship-Romberg sign
    • Groin pain radiating down medial thigh w/EXT, ABD, or IR d/t compressed obturator nerve; knee pain relieved w/flexion
    • Indicator that the obturator nerve is irritated
84
Q

Hernia Differentials

A
  • Inguinal adenopathy-enlarged, palpable inguinal lymph nodes
  • Abd lesion
  • Incarcerated hernia - hernia that cannot be reduced
  • Strangulated hernia-blood supply of incarcerated contents is interrupted; gangrene may quickly ensue
  • Important to differentiate btwn diastasis vs. hernia
85
Q

Hernia Diagnostics

A
  • Usually DX on clinical exam, often not needed
    1st line: Abd U/S
    2nd line: Abd CT scan; Abd MRI; herniography (INJ contrast; subsequent x-ray imaging – invasive + rarely needed)
86
Q

Treatment plan for all abdominal hernias

A

REFER, either electively or emergently

87
Q

Is watchful waiting appropriate for hernia treatment?

Male + pregnant pts

A
  • For male pts: for inguinal hernias if hernia is reducible + not affecting pt’s ADL d/t pain or ROM
  • Pregnant pts: groin swelling can be caused by self-limiting round ligament varicosities
88
Q

General Treatment plan for hernias

A
  • For asymptomatic patients with risk factors such as female sex, femoral hernia, scrotal hernia, recurrent hernia, surgery is advised
  • For symptomatic inguinal and femoral hernias, surgery is recommended
  • For incarcerated/strangulated hernias, surgery is recommended urgently/emergently
    AKA REFER TO SURGERY
  • Surgery
  • Can be laparoscopic (more $$$; shorter recovery, can be open)
  • Open (less $$$; longer recovery)
  • Strangulated or necrotic hernia – bowel resection
89
Q

Patient education: Hernias
And F/U

A
  • Give guidance prior to surgery, recovering time
    • To walking – same day for local and general
    • To working – 10-21d if undemanding; 2-4 wks for more physically demanding work
    • No effect on sexual function
  • Follow-up: As indicated; often patients have post-op pain; refer back to operating surgeon after a few weeks