Upper GI Flashcards
Dysphagia
Definition
- Subj sx of abnormal or difficulty swallowing
- Can be related to strx or mobility/ fx disorder
Oropharyngeal dysphagia vs. Esophageal dysphagia
- Oropharyngeal: functional impairment in initiation of swallowing
- Typically results from systemic neuro or myopic conditions
- Esophageal: fx or anatomical esophagus abnormality
Odynophagia
Pain w/swallowing
Globus sensation
nonpainful sensation of a lump, tightness, or fx in pharyngeal/cervical area
Associated symptoms w/Dysphagia
- Heart burn
- Wt. loss
- Hematemesis
- Anemia
- Regurgitation of food particles, and
- Respiratory symptoms
- Dry mouth
Dysphagia PE
- Thorough HEENT, neuromuscular including cranial nerves, cardiac, respiratory, signs of malnutrition/dehydration
Dysphagia Diagnostics: Modified Barium swallow
Assessment of oropharyngeal swallowing mech + aspiration risk (preferred → easier)
Dysphagia Diagnostics: Barium Swallow
- Assess esophageal swallowing function
- structural defects
- esophageal wave propulsion + clearance; reflux
Dysphagia Diagnostics (3 others besides barium swallows)
- 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
Meds that cause dysphagia
Bisphosphonates, NSAIDs, K+, doxy/tetracycline
What to do if patient has acute symptoms of dysphagia?
UNABLE TO SWALLOW SOLIDS +/OR LIQUIDS → ED
GERD
Reflux
Definitions
- 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
Barrett’s esophagus
Definition
- 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
CLASSIC GERD S/S
- 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 **
GERD Objective Findings
- Unremarkable
- Teeth/dental erosions from gastric acid coughing up
- Wheezing/signs a/w asthma
- Epigastric tenderness/adb masses
GERD Pathophysiology
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*
GERD Diagnostics
- 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
Common meds that REDUCE LESph tone:
DEFINITELY ON EXAM
- Anticholinergics
- BBs
- Benzos
- Bronchodilators
- CCBs
- Nitrates
- TCAs
- Theophylline
GERD Pharm meds
- 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
If patient has had GERD for > (5-10yrs)…
…+ 1 additional RF indicates need for upper endoscopy
GERD nonpharm modifications
- 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
How to R/O CARDIAC sxs for DX GERD?
- 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)
Barrett’s RFS
- 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
Pregnancy considerations GERD
- 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
GERD in elderly considerations
- 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
GERD alarm sxs
Not in lecutre?
- 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
GERD Treatment Recommendations (Stepwise) Mild
Mild
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*
GERD Treatment Recommendations (Stepwise) Severe
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
Safety Considerations: Long Term PPI usage
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
PPI Tapering education
- 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
PUD
Definition
- Erosion in either stomach or duodenum > 5mm AND penetrates into submucosa
PUD Causes
Most common?
- 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
PUD clinical manifestations
- 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
PUD Objective Signs
- Hx should assess for prior Hx of H. pylori, NSAID use, RFs, alarm features
- PE normal
- +/- epigastric tenderness
PUD confirmation of eradication
- 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
PUD diagnostics
Non-invasive testing (test & treat category)
only if < 55 + no alarm sx
* Active or hx of PUD
* Dyspepsia
* Gastric MALT lymphoma
* Consider before starting chronic NSAID therapy
* ? Unexplained iron deficiency
PUD Diagnostics
Invasive testing - Endoscopy
- > 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**
H. Pylori noninvasive Tests
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
PUD Pharm meds
- 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
PUD Considerations in Elderly
- 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)
PUD considerations > 50
- 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
Cholecystitis
- 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
Cholecystitis Etiologies
Cholelithiasis, Choledocholithiasis, Cholangitis Definitions too
- 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
Cholecystitis Clinical Manifestations
- RUQ pain or epigastric area
- Radiating pain to R shoulder or back
- Worsens after eating
- N/V
Cholecystitis Objective Findings
- **(+) 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
Cholecystitis Diagnostics
Labs
- 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
Cholecystitis Diagnostics
Imaging
- **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
Cholecystitis Pharm interventions
- IV fluids
- Pain management
Cholecystitis Nonpharm management
- 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
Common complication with cholecystectomy
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
Cholecystitis Risk Factors
- 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
Cholecystitis pregnancy + elderly considerations
- Be aware of ↑ likelihood of gallbladder disease during pregnancy & postpartum period
- In elderly pts, sometimes difficult to DX; complications more likely; cholecystectomy mortality rate ↑
Pancreatitis
Definition
- Can be acute or chronic inflamm
- Digestive enzymes attack pancreatic tissues → swelling
- Leading cause of hospitalization among digestive system diseases
Acute pancreatitis
Definition
- Disorder of exocrine pancreas + A/w cell injury w/local + systemic inflamm responses
- Inflamm range from milld edema → necrosis
- Life threatening
Chronic Pancreatitis
Definition + Risks
- 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
Most common causes of pancreatitis
And list of other causes
NOT ABCS
-
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
ABCs of Acute Pancreatitis
- 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
Pancreatitis clinical manifestations
- N/V
- Acute onset of epigastric pain → back, worse w/movement
Pancreatitis Objective Findings
- ↑ 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 (+)
Pancreatitis Labs
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
Acute pracreatitis pharm treatments
1st line tx: IV hydration, pain control
* Meperidine
* Ketorlac
* Ondansetron
Early TPN
Chronic Pancreatitis pharm treatments
- Pancreatic enzyme supplements w/every meal (creon)
Pancreatitis nonpharm treatments
- 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
Pancreatitis Patient Education
- Lifestyle modifications
- EtOH misuse: D/C
- Control ↑ TG
- Lipid lowering meds
- Eat small, low-fat meals of carbs + proteins
Pancreatitis pregnancy considerations
- Diagnostics – don’t delay diagnosis + tx as delay can ↑ maternal = newborn morbidity + mortality
- Care by obstetrician well-versed in high-risk pregnancies
Abdominal / inguinal hernia
Definition
- Protrusion of abd viscera through abnormal opening in mm wall
Hernia types
Reducible, Irreducible/incarcerated, strangulated
- Reducible: structure returns abd cavity
- Irreducible/ incarcerated: structure does not return to abd cavity
- Strangulated: interrupted blood flow to structure that has herniated
Hernia Etiologies
- 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)
Diagram of hernia locations
Most common hernia sites
- 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
Epidemiology of hernia types
Which one has high risk of strangulation?
- 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.
Inguinal Hernia - indirect
Definition
- 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
Inguinal hernia - direct
Definition
- 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
Femoral hernia
Definition
- 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
Obturator Hernia
Definition
- 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
Clinical manifestations for
Inguinal, femoral, umbilical, obturator hernia
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
Hernia RED FLAGS
Red flags
* Painful to palpation
* Erythema
* Ulceration
* Febrile patient
* Abdominal pain
* Bloating
* N/V
DO NOT TRY TO REDUCE A STRANGULATED HERNIA
Hernia Physical Exam
- 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
Indirect inguinal hernia objective findings
- Higher up
- Insert finger into inguinal canal → palp for bulge → bear down
- Hernia comes down inguinal canal + touches fingertip
Direct inguinal hernia objective findings
- Insert finger through inguinal canal → bear down → palp for bulging
- Hernia bulges anteriorly + pushes side of finger forward
Femoral Hernia Objective findings
(Aka what to do if it’s a femoral hernia)
- Hernias become strangulated (high risk) → refer to surgeon
Umbilical Hernia Objective Findings
- Pt lies supine → bear down → palp mass at umbilicus
- Have pt sit up + watch for protrusion of umbilical or ventral mass
Obturator Hernias Objective findings
- 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
Hernia Differentials
- 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
Hernia Diagnostics
- 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)
Treatment plan for all abdominal hernias
REFER, either electively or emergently
Is watchful waiting appropriate for hernia treatment?
Male + pregnant pts
- 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
General Treatment plan for hernias
- 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
Patient education: Hernias
And F/U
- 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
