1. 26-year old male has right groin pain after lifting a 50 lb box ...
2. A 20-year old male medical student vomits blood the night before the exam ...
3. A seven-week-old male infant has persistant vomiting ...
4. A 42-year-old mother of three has post-prandial, right upper quandrant pain ...
5. A 50-year old woman chokes at a restaurant. Thirty minutes later, while drinking coffee, she has severe left chest pain ...
6. A 47-year-old find a 3/4 cm lump in her left breast ...
7. A 70-year-old male presenting with melana ...
8. A 35-year-old woman complains of blood with bowel movements ...
9. A 25-year-old stabbed in right chest ...
10. A 25-year-old married female has mild nausea with right lower quadrant pain ....
11. A 72-year-old male with suddent back pain and leg weakness ...
12. A 63-year-old female has sudden left leg pain and her foot is cold ...
13. A 14-year-old boy has pain in the right testicle ...
14. A 72-year-old male with jaundice and pruritis ...
15. A 50-year-old woman with periumbilical crampy pain ...
16. An 18-year-old is elbowed in the face at a basketball game and has diplopia and a numb left check ...
17. A 57-year-old female has a 1 cm lesion in the right middle lobe on a routine CXr ...
18. A 20-year-old, struck by a line-drive during a baseball game, passes out 40 minutes later ...
19. A 40-year-old has epigastric pain radiating to the back ...
20. A 55-year-old has difficulty swallowing after 10 years of heartburn ...

26-year old male has right groin pain after lifting a 50 lb box ...

Differential Dx:

1. Inguinal hernia: 75% of all abdominal wall hernias, may be indirect (through inguinal ring) or direct (through Hesselbach’s triangle)
2. Muscle strain
3. Hydrocele: fluid collection within the tunica vaginalis or along the spermatic cord, often associated with inguinal hernias
4. Testicular torsion: twisting of the spermatic cord which cuts off blood supply to testis
5. Groin abscess
6. Epididymitis/orchitis: inflammation of the epididymis or testis, most commonly caused by reflux of urine due to obstruction, epididymitis may be caused by tuberculosis, orchitis is most commonly caused by mumps
7. Spermatocele: cystic accumulation of sperm in the epididymis (postero-lateral border of testis), etiology unknown
8. Varicocele: Dilated venous plexus along spermatic cord (90% of these are left-sided, though)

History

1. Describe pain. (onset/duration, quality, radiation, severity, timing) Hernias are painful with increased abdominal pressure, torsion is intermittantly painful – pain may be associated with activity, epididymitis/orchitis has gradual onset, muscle strain may be associated with certain activities/positions or may radiate down leg along involved muscle
2. History of previous groin pull/sports injury – these may take a long time to heal and be very suceptible to reinjury
3. History of testicular injury/infection – may predispose to groin abscess, epididymitis, orchitis
4. Urinary frequency, urgency or dysuria – suggest UTI – epididymitis/orchitis are often due to reflux of infected urine
5. Urethral discharge suggests an infective source – epididymitis/orchitis, groin abscess
6. Associated bulge in the groin? Reducible?
7. Worse with standing or increasing abdominal pressure? (coughing, straining, etc.)
8. Symptoms of bowel obstruction (nausea, vomiting, changes in bowel habits, distended abdomen) may indicate incarcerated hernia
9. Fever/chills – an infectious cause or a strangulated inguinal hernia may cause fever/chills

Physical Exam

Patient should be examined both in the supine and standing positions with and without the Valsalva maneuver.

1. Vitals: Look for fever
2. Look for swelling/erythema or mass in the groin area.
3. Palpate the groin area and the upper leg for tenderness.
4. Range of motion of leg – look for limited ROM or tenderness with movement
5. Palpate testicle for tenderness/masses – varicocele is “bag of worms”, abscess will have fluctuance, spermatocele is postero-lateral with usually well-defined borders)
6. Place fingertip in the scrotum and advance up to the inguinal canal to feel for hernia. Ask patient to strain or cough. If hernia is palpated, attempt to define the borders of the defect.
7. Hernia traveling from superolateral to inferomedial is likely an indirect inguinal hernia, hernia traveling from deep to superficial is most likely a direct inguinal hernia, hernia below the inguinal ligament is most likely a femoral hernia
8. An incarcerated hernia cannot be reduced
9. A strangulated hernia is suggested by pain out of proportion to physical exam findings, toxic appearance or persistance of pain after the reduction of the hernia
10. Transillumination for associated hydrocele

Diagnosis

1. Labs: CBC – elevated WBC?, Chem 10 – everybody gets this
2. Imaging: Can get color doppler to see blood flow to testis if torsion is suspected (but if there is a high suspicion, get to the OR because unless you can manually untwist it, torsion is a surgical emergency)
3. A hernia can be diagnosed clinically
4. Muscle injury can be diagnosed clinically

Treatment

1. Appropriate pain medication – for hernias give po pain meds (percocet) or IV (morphine), for muscle injuries can give injections of lidocaine/bupivicaine and possibly steroids to reduce swelling
2. If muscle injury – rest, ice, anti-inflammatories,
3. If hernia, attempt to reduce.
   • If not reducible, admit patient and consult general surgery for emergent repair.
   • If strangulated hernia is suspected, give antibiotics.
   • If reducible, refer patient to general surgery within 1-2 weeks for early repair, apply support to hernia (thrust undergarments), instruct patient to avoid activities that increase intraabdominal pressure
4. For any other infectious cause (epididymitis/orchitis, abscess), give appropriate antibiotics
5. If torsion, attempt to manually untwist/go to the OR
6. Spermatocele/varicocele – may manage with observation or surgery

Comments

An indirect inguinal hernia is a protrusion of bowel, omentum or other intraabdominal structure protrudes through the internal inguinal ring into the inguinal canal and through a patent processus vaginalis. The boundries of the inguinal canal are anteriorly – conjoint tendon, posteriorly – transversalis fascia, inferiorly – inguinal ligament (from anterior superior iliac spine to pubic tubercle).

A direct inguinal hernia protrudes through Hesselbach’s triangle, medial to the inferior epigastric vessels. The borders of Hesselbach’s triangle are the inferior epigastrics, the lateral border of the rectus and the inguinal ligament. Direct hernias are at decreased risk for incarceration but require more complex surgical repair.

Surgical repair is indicated for all inguinal hernias because the natural history of hernias is to enlarge which increases the risk of incarceration. Intraoperatively, the two nerves to be concerned with are the ilioinguinal nerve which runs on top of the spermatic cord and the genital branch of the genitofemoral nerve which runs in the spermatic cord. Cutting the ilioinguinal will cause numbness of the inner thigh/lateral scrotum and cutting the genital branch of the genitofemoral will cause numbness.

Femoral hernias are located inferior to the inguinal ligament. They are most commonly found in women. They are rare, but carry a very high risk of incarceration.

If a patient is a poor candidate for surgery, a truss may be used. (ball of rubber or fabric strapped over the defect) However, use of a truss increases scarring and risk of incarceration.

Return to the index of cases.

A 20-year old male medical student vomits blood the night before the exam ...

Differential Diagnosis: Upper GI bleeding

1. Esophageal: varices, ulceration, esophagitis, Mallory-Weiss tear, carcinoma, trauma, Boerhaave’s syndrome
2. Gastric: peptic ulcer, gastritis, angiodysplasia, gastric neoplasm, hiatal hernia, gastric diverticulum, pseudoxanthoma elasticum, Osler-Weber-Rendu syndrome
3. Duodenal: peptic ulcer, duodenitis, angiodysplasia, aortoduodenal fistula, duodenal diverticulum, duodenal tumors, carcinoma, Crohn’s disease
4. Biliary: hematobilia (penetrating injury to liver, hepatobiliary malignancy)

History

1. How much emesis?
2. 2. Describe emesis – bright red, coffee grounds, blood throughout vs. small amount of blood
3. Pain – epigastric?
4. Fever/chills?
5. Any history of similar episodes
6. If pain, is it relieved or exacerbated by food? (gastric ulcer pain is exacerbated by meals, duodenal ulcer pain is relieved by food)
7. Excessive consumption of caffeine or alcohol?
8. Smoking history (increases risk for ulcers) and alcohol use (increases risk for gastritis and esophageal varices)
9. History of drug use – aspirin, NSAIDs, steroids, H2-blockers for previously diagnosed problem
10. History of any GI problems or chronic GI conditions? (heartburn, GERD, previous ulcer, Crohn’s disease)
11. Weight changes, night sweats
12. Dysphagia – esophageal CA
13. Family history of GI problems? (Crohn’s disease, ulcerative colitis, GI cancers, etc.)
14. Family and social stressors – it is debatable whether or not stress can exacerbate ulcers or not.
15. Bowel habits and description of stool. (melena? Hematochezia?)

Physical

1. Vitals – look for signs of hypovolemia (tachycardia, hypotension), fever – food poisoning
2. Cardiovascular – rales, JVD
3. Abdominal exam – look for any masses, epigastric tenderness, distension (obstruction) and peritoneal signs (perforation)
4. Rectal exam with hemoccult

Diagnosis

1. Labs: CBC (H/H), Chem 10 (look for electrolyte abnormalities secondary to vomiting), Coags
2. Imaging: EGD, colonoscopy if any associated symptoms of lower GI problems, could do UGI series, could do angiography to treat bleeding by embolization if other treatment efforts are ineffective

Treatment

1. FLUID RESUSCITATION (do this first if he looks acutely ill) – antecubital IV x 2 with BIG NEEDLES (16 G), LR or NS
2. Type and cross or type and screen depending on severity of bleeding
3. If he is still bleeding, stop the bleeding. (angiographic embolization, balloon tamponade of esophageal varices, ligation of bleeders, use of electrocoagulation/heat probe via endoscopy for PUD)
4. If you cannot stop the bleeding by any of the above, surgery is indicated.
5. Graham patch – omental patch over a perforated ulcer
6. Truncal vagotomy
7. 80-85% stop bleeding spontaneously
8. After acute event is over, consider H2 blocker therapy and use of antacids
9. If there is evidence of H. pylori, treat with antibiotics

Return to the index of cases.

A seven-week-old male infant has persistant vomiting ...

diff Dx

most likely causes

• pyloric stenosis – usually presents btwn 2wks and 2mo
• GERD – must make sure the baby is vomiting and not just spitting up
  • diagnose with barium swallow, pH probe, manometry
  • treat with Reglan, H2 blockers, PPI’s
  • do Nissen fundoplication if fail Rx treatment

possible causes

• intussusception – usually presents btwn 6mo and 2yo, look for “currant jelly” stool
• malrot/volvulus – diagnose with Barium swallow – shows cecum in abnormal place, doesn’t show typical “C” of duodenom
  • - very serious b/c can lead to necrotic gut, death
• Milk protein intolerance
• Hirschsprung’s Dx – unlikely (presents with constipation more than vomiting)
• SBO – due to hernia, malrot, foreign body (swallowed a toy), etc.
• Gastroenteritis, poisoning, over feeding

Unlikely causes

• Increased ICP – would likely be a mass b/c of the chronicity of Sx’s
• Inborn errors of metabolism – make sure child had newborn screening (i.e. was not born at home w/o medical care)
• Duodenal atresia/web, annular pancreas, hiatal hernia, adrenal insufficiency, uremia

Note: this really could be anything b/c kids present with non-specific Sx’s – so keep things like otitis media, pharyngitis, pneumonia, etc. in the back of your head

PYLORIC STENOSIS – likely b/c of age of child, sex of child (males have 4X risk) and chief complaint is classic for PS

History

• Vomiting – should be progressively increasing in size/strength over days until it is “projectile”
  • Is non-bilious, non-bloody and occurs after feeding
  • Baby is hungry! – very impt b/c kids aren’t hungry if they have an infection, obstruction, dying gut, etc.
• UOP and stool frequency should be decreasing with time b/c of decreased intake
• Baby should be afebrile, should not have diarrhea

PMH

Fam Hx

PSH

PE

Gen – can look sick or healthy depending on how quickly mom brought them in, may have lost weight, 10% have icterus

Vitals – afebrile, may be tachycardic b/c of hypovolemia (look for dry mucus membranes, poor cap refill), RR may be low b/c trying to hold on to acid

Abdomen – look for visible peristaltic waves

• Feel for “olive” – hard, round, moveable epigastric/RUQ mass - is diagnostic for PS

Workup

• Chem panel – should show high bicarb, low Cl, low K, metabolic alkalosis
• CBC – should be nL
• Paradoxical aciduria
• U/S – shows thick muscle, long pyloric channel
• Barium swallow – shows “string sign” or “double railroad sign” at pylorus

Treatment

• BEFORE SURGERY – must rehydrate! Use D5 1/2NS or D5 NS with up to 40 mEq/L of KCl depending on level of dehydration & alkalosis – at 1.5-2X maintenance rate until UOP is normal
• SURGERY: pyloromyotomy – open abdomen, make longitudinal incision along edge of pylorus to splay out hypertrophied muscle – do not enter lumen
• POST-OP – NPO for 12hrs, then slowly inc feeding over 24hrs, D/C in 1-3 days

Ddx for pediatric vomiting:

1. pyloric stenosis
2. Duodenal atresia
3. Gut malrotation
4. infection

Approach to Pt.

1. Hx and PE
   1. type of vomitus (i.e. bilious v. non-bilious)
   2. Projectile vomit ?, hunger post-emesis ?, is it progressive ?
   3. Is there dehydration present?
   4. Is there a palpable olive present?
2. Dx
   1. abdom Ultrasound (90% sensitive): elongated channel, thickened wall
   2. Radiograph: string sign, shoulder sign
   3. Chem 7/ CBC: hypochloremic metabolic alkalosis, r/o infection
3. Tx
   1. fluid correction
   2. IV fluid
   3. Ramstedt pyloromyotomy

Return to the index of cases.

A 42-year-old mother of three has post-prandial, right upper quandrant pain ...

DDx for RUQ pain

1. Biliary – cholelithiasis (stones in GB) choledocholiathisis (stones in common bile duct), cholecystitis (inflamed GB), cholangitis (inflamed bile ducts)
2. Liver – hepatitis, abscess, tumor
3. Stomach/duodenum – PUD, gastritis/gastroenteritis
4. Pancreatitis (classically more epigastric)
5. Appendicitis (esp. during pregnancy but classically more RLQ)
6. Non-abdominal – R. lower lobe pneumonia, MI
7. Kidney – nephrolithiasis, pyelonephritis

History

• The classic pain questions
  • Where? Well localized (parietal/peritoneal)? Poorly localized (visceral/organ pain)?
  • Quality? Dull, achy pain – visceral. Intermittent, crampy pain – obstruction, renal colic. Severe, explosive pain – perforation.
  • Radiation? To R. subscapula – biliary disease. To back – pancreatitis.
  • Duration? Surgical emergencies usually duration of few hours to a day
  • Onset? Post-prandial (fatty meal) – symptomatic cholelithiasis (biliary colic). Sudden – perforation, ischemia. Gradual – inflammation.
  • Better/worse? With eating?
• Similar episodes in past? (past workup and results)
• Hx gallstones or renal stones? High lipids?
• Surgical hx? (adhesions/obstruction, CA recurrence, etc.)
• Fevers/chills? Shaking chill – cholangitis with choledocholithiasis.
• GI symptoms? (N/V, diarrhea, constipation, hematemesis, hematochezia). More likely surgical if N/V comes on after pain and not the other way around. N/V and anorexia usually indicate acute inflamm.
• Urinary symptoms? (dysuria, hematuria, polyuria)
• Sxes of obstructive jaundice? (tea-colored urine, light-colored stools, pruritus)
• GYN hx? (last menses, sexually active, hx STDs, vaginal discharge)
• Alcohol? (pancreatitis)

Physical

1. General – Pt. fidgeting and unable to find comfortable position? (biliary colic). Pt. completely still? (peritonitis).
2. Vitals – febrile?
3. CV and Resp – RRR? CTAB?
4. Abdominal
   • Inspect. distended? voluntary guarding? (peritonitis)
   • Auscultate – BS?
   • Palpate starting away from location of pain. Localize pain. Palpable mass? Peritoneal signs (guarding, rebound tenderness)? Murphy’s sign?
5. Scleral icterus or jaundice?

Diagnosis

Cholelithiasis is #1 on the differential because it is the MC cause of RUQ pain, and this patient has most of the classic risk factors (Female, Fat, Fertile, Forties). Other supporting sxes/signs: N/V, pain worse after fatty meal. Potential complications that should also be worked up are cholecystitis, choledocholiathisis, and cholangitis. Fever + RUQ pain + jaundice (Charcot’s triad) = cholangitis.

Tests:

1. U/S gallbladder. Initial diagnostic study of choice for biliary tract disease. S& Sp about 95% for stones in GB. Not so good for stones in bile ducts (33% sens.) but can look for dilated ducts and distended GB. Also look for thickened GB wall > 3mm and pericholecystic fluid (acute cholecystitis),
2. CBC, LFTs (AST, ALT, alk phos, T. bili, d. bili), amylase/lipase
   • Fever and increased WBCs with left shift indicate acute inflammation (acute cholecystitis, normal labs for chronic)
   • abnl alk phos, bili, (maybe LFTs) indicate obstructive jaundice (choledocholithiasis)
   • abnl WBC, alk phos, and bili indicate cholangitis
   • abnl amylase/lipase indicate pancreatic disease.
3. Can confirm choledocholithiasis while in OR by cholangiogram (see treatment).
4. HIDA (hepatobiliary iminodiacetic acid) scan for cholecystitis, bile leak, choledochal cyst, and biliary dyskinesia (EF<35%)
5. ERCP (endoscopic retrograde cholangiopancreatography) for patients with jaundice. Evaluate stomach, duodenum, ampulla of Vater, pancreatic duct, and CBD. Diagnostic and therapeutic, any coagulopathies must be corrected beforehand.

Peptic ulcer disease is probably next on the list but less likely because of the description of the pain onset and location.

Duodenal ulcers – more common than gastric, usually 1st part of duod.

• Sxes/signs: burning or aching epigastric pain several hours after meal, N/V, anorexia, epigastric tenderness.
• Cxes: perforation (acute abd. signs, free air), hemorrhage (tachy, syncope, hematemesis), obstruction (crampy pain, N/V).

1. Upper GI series – barium swallow, GI tract up to duodenum examined for swallowing and peristaltic function, size, shape, flexibility, distensibility, ulcers, scars, strictures, etc.
2. Endoscopy (EGD) – Diagnostic (visualize ulcer, biopsy for H. pylori) and therapeutic (can control hemorrhage with a heater probe or bipolar coagulator)
3. Gastric acid analysis – sample of NG fluid, high basal acid output for ulcer (>4.0 mEa/hr) but even higher for Zollinger-Ellison syndrome (10x or more than normal)

Gastric ulcers - more common in men, elderly, usually along lesser curvature near transition zone.

• Sxes/signs: burning midepigastric pain relieved by food, may radiate to back.
• Tests: Upper GI and EGD. Must take biopsy samples of ulcers to rule out carcinoma (10% of gastric ulcers are CA with ulceration).

Treatment

Biliary disease

1. Symptomatic cholelithiasis à Cholecystectomy (usually lap.)
   • If suspect CBD stones (signs obstructive jaundice), perform intraop. cholangiogram to visualize blockage of CBD (dye injected through cystic duct and picture obtained by fluoroscopy).
   • If + stones, can remove operatively or by ERCP.
   • Cxes of lap chole: CBD injury, right hepatic duct/artery injury, cystic duct leak, biloma (can use HIDA to evaluate bile duct leak)
2. Acute cholecystitis à start IVF and ABX with or without NG tube. Within 3 days of sx onset, do chole. If > 3 days, wait for ABX to calm down inflamm. and do chole in 4-6 weeks.
   • Common bacteria – E. coli, K. pneumo, Strep. faecalis, Clost. welchii or perfr.
   • Cholecystostomy – for pt. with cholecystitis that is so inflamed that cholecystectomy is dangerous or pt. is too ill to tolerate it.
3. Choledocholithiasis: ERCP (or operative). Cut sphincter of Oddi, extract calculi, and place stent.
4. Cholangitis: IVF, ABX, and urgent removal of bile duct stones. MC bact. is E. coli.

Duodenal ulcers

Medical: H2 blockers (cimetidine), antacids, proton pump inhibitors (omeprazole), triple therapy for H. pylori (colloidal bismuth, amoxicillin or tetracycline, and metronidazole). Surgery indications: Intractability Hemorrhage Obstruction Perforation. Surgery: Vagotomy with antrectomy (Billroth I or II), vagotomy with drainage, Graham patch for perf. ulcer, oversewing the bleeding point and pyloroplasty for bleeding ulcer. (See Surgical Recall p. 233-237 for more details.)

Gastric ulcers

Similar medical. Similar indic. for surgery similar plus cannot r/o malignancy. Similar surgeries (See Recall p. 238-239).

Comments

Sources - Surgical Recall, NMS Surgery, Lawrence, and lecture

Cholelithiasis:

• Incidence in U.S. pop. about 10%.
• Types of stones: cholesterol (75%) and pigmented (25%). Pigmented more common with chronic hemolysis and cirrhosois.
• Cholelithiasis leads to cholecystitis (obstructed cystic duct causes GB inflamm.), or it leads to choledocholithiasis (stone passes through cystic duct to CBD), and choledocho. leads to cholangitis (bile duct infection secondary to CBD stones).

Return to the index of cases.

A 50-year old woman chokes at a restaurant. Thirty minutes later, while drinking coffee, she has severe left chest pain ...

Differential Diagnosis: Left chest pain

1. Things that kill: Acute MI / pneumothorax (from broken ribs) / PE
2. Aspirated foreign body
3. Esophogeal spasm/ Mallory-Weiss Syndrome / Boerhaave’s Syndrome
4. Hiatal hernia / GERD
5. Aortic dissection (unlikely) / angina

History:

1. Describe pain.
   • Onset. Known
   • Location. Known, but could confirm left versus substernal
   • Quality. Tight? Squeezing? Tearing? Dull? Sharp?
   • Radiation. MI: Radiating to shoulder/arm/jaw? Dissection: Back? GERD/Mallory Weiss/Boerhaave's: Substernal?
   • Duration. Known, but could confirm no twinges before acute onset, still going on or isolated timeframe
   • Other symptoms. MI: Nausea, vomiting, diaphoretic, palpitations? Hernia: dysphagia? Mallory-Weiss: epigastric pain, vomiting, hematemesis, esophageal pain after choking episode? Boerhaave’s: same as MW minus hematemesis? MI/PE/Boerhaaves/pneumo: dyspnea? GERD: heartburn?
   • And everyone’s favorite question, “Has this happened before,” leading quite nicely to
2. PMH: MI: HX angina/MI/CAD? GERD/hiatal hernia: heartburn/regurg/recurrent pneumonias (aspiration)? What was she eating when she choked (bones can shift and cause obstruction)?
3. PSH / FH should be non-contributory
4. Social HX: GERD: Smoker? Drinker? Fatty food eater? How much coffee?

Physical Exam:

1. General: Uncomfortable? Clutching chest? SOB? Obtunded?
2. Vitals: Tachy (almost certainly)? Tachypnic (probably)? O2 sat? Hypertensive (angina, dissection)? Hypotensive (extensive MI, large PE, tension pneumo)? Different in each arm (dissection)? Fever (probably too soon)?
3. Cardio: new onset murmur (MI)? RRR? Tender to palpation (broken ribs)?
4. Pulm: trachea in the midline (pneumo)? equal breath sounds bilaterally (pneumo, Boerhaave’s)? Pleural rub (PE)? Stridor (obstruction)? Sub Q / cervical emphysema (Boerhaave’s)? flail chest (fractured ribs)?

Diagnosis:

1. EKG ASAP. Looking for ischemic changes (T wave inversion, ST elevation/depression, Q waves)
2. CXR: pneumo? rib fx? widened mediastinum (dissection, Boerhaave’s)? radiolucent object (aspirated FB)?
3. Labs: send off AMI panel (CK-MB, CK, myoglobin, Troponin I) just because, ABG if you’re concerned about pneumo/aspirated FB/airway compromise
4. Bronchoscopy to look for aspirated FB
5. Still negative? EGD with biopsy if necessary (Boerhaave’s, MW, GERD), UGI (hiatal hernia), manometry, 24 hr. pH probe

Treatment:

1. Acute MI – ASA, fluids, anti-coagulate
2. Pneumo – chest tube
   • tension pneumo: dyspnea, JVD, tachy, chest pain, unilateral decreased breath sounds, trachea deviation is unlikely but emergency, needle thoracostomy
3. Aspirated FB: rigid bronchoscopy is both diagnostic and therapeutic, allows removal and ventilation
4. Mallory-Weiss: room temperature water lavage (90% stop bleeding)
5. Boerhaave’s: surgery within 24 hours to drain mediastinum, close perforation, place pleural patch; use broad spectrum ABX (3d gen ceph)
6. Hiatal hernia: most likely type I (sliding), majority of which are treated medically with antacids/H2 blockers/PPIs/lifestyle adjustments; refractory requires lap Nissen fundoplication (wrap fundus around LES) or other surgery options (see Recall p 260)
7. GERD: same medical options as hiatal hernia

Comments:

1. Mallory-Weiss Syndrome: post-retching longitudinal tear near GE junction of mucosa and submucosa (75% in stomach, 50% have hiatal hernia). Think alcoholics. Dx via EGD.
2. Boerhaave’s Syndrome: post emesis complete esophageal rupture most often posterior aspect above GE jxn (50% have GERD)
   • signs: Left pneumothorax, left pleural effusion, sub Q mediastinal emphysema, fever, tachy, tachypnic, neck crepitus, widened mediastinum
   • Mackler’s Triad: Emesis, lower chest pain, cervical emphysema
   • Hamman’s sign: mediastinal crunch/click (heart v. air filled tissues)
   • Mortality can be up to 33% if surgery delayed over 24 hours
3. GERD: 5-10% develop Barrett’s, 5-10% Barrett’s develop adenocarcinoma; 90% with Nissen have complete resolution
   • post-op cx: gas-bloat syndrome (no burping or vomiting), stricture, dysphagia, spleen injury, esophageal perf, pneumo
   • association with SLIDING HERNIA (type I): stomach and GE jxn in thorax, although this condition is most often asymptomatic
4. Aspirated FB: right mainstem bronchus is shorter/wider/less acute angle than left, ergo most objects wide up there in general; this does not mean our lady could not have something lodged in the left bronchus
   • Symptoms are fever, hemoptysis, dyspnea and chest pain when ldged beyond the carina
   • Classis acute presentation = coughing, wheezing, decreased breath sounds (preceeding aphonia, cyanosis, LOC and death)

Return to the index of cases.

A 47-year-old find a 3/4 cm lump in her left breast ...

Diff dx: breast cancer, fibrocystic changes, cyst, papilloma, lipoma, abscess, fat necrosis, phyllodes

History

• Location? (quadrant, distance from nipple)
• Onset, Timing, Duration for presence of lump
• Changes with respect to menstrual cycle (size, shape, pain)
• Is there pain associated with the lump?
• Features: shape, consistency (soft, firm, cystic, etc.), mobility, delineation (discrete, fixed)
• Recent breast injury?
• Discharge? (amount, color, smell, spontaneous or nonspontaneous)
• Nipple retraction?
• Skin changes? (discoloration, induration, erythema, dimpling)
• Breast size changes
• Axillary lumps or swelling, arm swelling
• Fever, chills, weight loss?
• Family history of breast or ovarian cancer?
• Past history of breast cancer or abnormalities? (if so, what kind of treatment was received)
• Age of menarche and menopause?
• Parity and age at first delivery
• Diet, alcohol, radiation exposure
• Symptoms that may be associated with metastasis: brain (changes in personality, hearing, sight, and/or memory), lung (SOB, cough, hemoptysis), bone (pain, fractures)
• Past and current medical conditions, surgeries, medications (including hormonal treatments), etc.

Physical exam

• Visual exam first: have patient sit with arms at her sides, raised over her head, pressing her hips, and leaning forward.
• Breast inspection: Size, symmetry, visible masses, shape changes (abnormal bulging), skin retraction, dimpling, flattening, ulceration or eczema, erythema, peau d’orange, increased vascularity.
• Areola and nipple inspection: size, shape (retraction?), symmetry, ulceration or eczema (think Paget’s), discharge (serous, bloody, milky, clear, etc; from single or multiple ducts), supernumerary nipples
• Palpation of cervical, supraclavicular, infraclavicular, and axillary nodes (location, size, shape, consistency, mobility)
• Palpation of breast, including areola

Diagnosis

Definitive diagnosis is biopsy (fine-needle aspiration cytology, large-needle core, or open). Initial steps that can be taken before biopsy are ultrasound to determine whether the mass is cystic or solid, and mammography. (I believe Dr. Shenk said he would do an FNA first, but most books say to do the imaging first.) Further evaluation: ER, PR status and metastasis work-up. Axillary dissection or sentinel node biopsy can help stage the cancer, determine prognosis, and determine a treatment plan. Axillary dissection or sentinel node biopsy can be done at the time of lumpectomy or mastectomy.

Treatment

• 1) Lumpectomy followed by radiation – for stage I or II. Contraindications: previous radiation, positive margins, collagen vascular disease, extensive DCIS
• 2) Modified radical mastectomy. Breast, nipple, areolar complex, and axillary nodes removed. Possible complications – lymphedema, infection, neural injury, skin flap necrosis, hematoma/seroma, phantom breast syndrome
• Adjuvant therapies: hormonal and chemo
• Tamoxifen – if ER are (+)
• Chemotherapy – in general, chemo is given if nodes test positive and/or the tumor is considered high-risk (larger than 1 cm?). Typical regimens: cyclophosphamide, methotrexate, 5’-FU OR cyclophosphamide, adriamycin, and 5’-FU.

Additional comments (from Surgical Recall)

• Mammography is more accurate in older women than in younger women.
• Indications for biopsy: persistent mass after aspiration, solid mass, blood in cyst aspirate, suspicious lesion on mammography, bloody nipple discharge, ulcer or dermatitis of nipple.
• TRAM flap is one option for reconstruction.
• LCIS is a risk factor for future development of either type of cancer in either breast while DCIS is a risk factor for development of infiltrating ductal carcinoma in that breast.
• Etc, etc, etc. Let me know if I made any mistakes or forgot anything!

Return to the index of cases.

A 70-year-old male presenting with melana ...

Diff dx of upper GI bleed (proximal to ligament of Treitz): peptic ulcers, portal hypertension (from varices or portal hypertensive gastropathy), Mallory-Weiss tears (lacerations of the gastroesophageal junction), vascular anomalies, gastric neoplasms, erosive gastritis, erosive esophagitis, aortoenteric fistula, hemobilia, pancreatic malignancy, pseudoaneurysm, Dieulafoy’s lesion (aberrant gastric submucosal artery), coagulopathy

Also need to rule out lower GI bleeding. For example, right-sided colon neoplasms may be a source of melena. 30% of melena is caused by lower GI bleeding (see case scenario #8 for lower GI bleeding)

History

• When did this begin?
• What does the stool look like?
• Does every bowel movement produce black, tarry stools? Has this happened before?
• Is there ever bright red blood in the stool as well?
• Recent history of frequent emesis? Do you ever vomit blood (hematemesis indicates upper GI bleed)?
• What does the vomit look like? (coffee grounds, bright red?)
• Are you experiencing abdominal pain? What does the pain feel like and where is it? Does anything make it feel better or worse? Relationship to meals?
• Is there associated bloating, excessive gas, diarrhea, constipation?
• What is your diet usually like?
• Weight loss, night sweats, fevers?
• Medications? (NSAIDs can aggravate ulcers, Pepto-Bismol can discolor stool, etc.)
• Alcohol use? Smoking?
• Past medical history (ulcers, liver disease, cirrhosis, portal hypertension)
• Past surgeries (aortic surgery – aortoenteric fistula can be complication, shunt surgery, etc.)
• Family history (liver disease, bleeding disorders)

Physical exam

• General: pale? diaphoretic? confused? malnourished?
• Vitals (look for evidence of hypovolemic shock): tachycardia, orthostatic hypotension
• Skin: delayed capillary refill? Stigmata of chronic liver disease? Abnormal pigmentation/lesions (Peutz-Jeghers, Kaposi’s sarcoma, telangiectasias, etc.)
• HEENT: scleral pallor, flat neck veins
• Chest: gynecomastia (liver disease), breast masses (metastasis)
• Abdomen: Distension, tenderness, rebound, masses, splenomegaly, hepatic atrophy (cirrhosis), evidence of ascites, dilated abdominal veins
• Extremities: edema
• Neuro: mental status, confusion, asterixis (hepatic encephalopathy)
• GU/Rectal: gross or occult blood, masses, testicular atrophy

Diagnosis

• Place NG tube – look for red blood or “coffee grounds”
• CBC with differential
• Prothrombin time with INR
• Chem 7
• Serum Cr, BUN, liver enzymes, type and cross (if necessary)
• Upper endoscopy, colonoscopy, stool culture, KUB
• Angiography, nuclear scan (these two reserved for massive bleeding)

Treatment

• The sequence of procedures for upper GI bleeding: 1) resuscitate if necessary 2) NG tube aspirate 3) endoscopy 4) arteriography
• If there is evidence of hemodynamic compromise, administer NS or LR and blood, if needed.
• Some sources of bleeding (varices, ulcers, angiomas, Mallory-Weiss tears) can be endoscopically treated by cautery, banding, or injection of sclerosing agents. If endoscopic treatment of acute variceal bleeding fails, then transvenous intrahepatic portosystemic shunts (TIPS) can be used.
• Octreotide can be given to temporarily reduce splanchic blood flow and portal blood pressures if the suspected source of bleeding is upper GI and there is evidence of portal HTN or liver disease.
• H2 blockers do not stop acute bleeding or the chance of rebleeding from ulcers. Large doses of PPIs will lower the risk of rebleeding in those with high-risk peptic ulcers.

Return to the index of cases.

A second answer ...

Differential Dx: Upper GI bleeding, above the ligament of Treitz

1. Oral or pharyngeal lesions: swallowed blood from the nose or oropharynx Swallowed hemoptysis
2. Esophageal: varices, ulceration, esophagitis, Mallory-Weiss tear, carcinoma, trauma, Boerhaave’s syndrome (post emetic esophageal rupture)
3. Gastric: peptic ulcer-most common (including Cushing’s and Curling’s ulcers), gastritis, angiodysplasia, gastric neoplasms, hiatal hernia, gastric diverticulum, pseudoxanthoma elasticum, Osler-Weber-Rendu syndrome
4. Duodenal: peptic ulcer, duodenitis, angiodysplasia, aortoduodenal fistula, duodenal diverticulum, duodenal tumors, carcinoma of the ampulla of Vater, parasites, Crohn’s disease
5. Biliary: hematobilia (penetrating injury to liver, hepatobiliary malignancy, endoscopic papillotomy)

Hx:

1. Drug Hx: specifically aspirin, steroids, “blood thinners,” NSAIDS
2. prior GI or vascular surgery
3. Hx of GI diagnosis or bleeding
4. Hx smoking (increased risk of PUD)
5. Alcohol (gastritis, esophageal varices)
6. Symptoms of peptic ulcer
7. Associated diseases
8. Protracted retching and vomiting, hematemesis, coffe ground emesis (Mallory-Weiss syndrome)
9. Weight loss, anorexia, constitutional symptoms (carcinoma)
10. +/- hematemesis
11. color/character of stools
12. symptoms of hypovolemia (dizziness, diaphoresis), anemia (pallor, dyspnea, angina, exertional weakness)
13. pain-epigastric

PE:

1. vitals: tachycardia , hypotension, postural changes. A pulse increase of more than 20 bpm or a postural fall in systolic blood pressure greater than 10-15 mmHg usually indicates blood loss greater than 1L
2. Cardiorespiratory: murmurs (increased incidence of angiodysplasia in patients with aortic stenosis), rales, JVD
3. Abdominal: masses, tenderness, distension, ascites, auscultate for bowel sounds and bruits, look for liver disease (hepatomegaly, spenomegaly, abnormal vascular patterns, gynecomastia, spider angiomata, palmar erythema, testicular atrophy)
4. DRE: masses, strictures, hemorrhoids, occult blood, inspect stool for abnormalities (tarry, blood-streaked, bright red mahogany color
5. skin: jaundice (liver disease), ecchymoses (coagulation abnormality), cutaneous telangiectasia (Osler-Weber-Rendu), buccal pigmentation (Peutz-Jeghers syndrome) and other mucocutaneous changes (Ehlers-Danlos syndrome)
6. evidence of metastatic disease (cachexia, firm nodular liver)

Stabilization:

1. Ringer’s lactate or NS. 16 G or larger peripheral IV x2
2. type and cross

1. Labs: CBC, Chem 10 (BUN/Cr ratio >36 suggests UGI bleed, BUN elevated due to absorption of blood by the GI tract), LFTs, Coags (exclude bleeding disorder), amylase
2. chest, abdominal x-ray.
3. ECG (r/o myocardial ischemia and severe anemia)
4. insert NG tube: if blood from upper GI-bright red blood clots or coffee ground guaiac + aspirate. If negative, does not r/o upper GI bleed-could have subsided, or could be bleeding from duodenal bulb w/o reflux into stomach. Note bile in aspirate.
5. endoscopy: if Diagnostic-treat, can also be therapeutic
6. if endoscopy is non-diagnostic and bleeding is inactive, do upper GI series
7. if endoscopy is non-diagnostic and bleeding is active, do angiography: can be therapeutic- vasoconstrictors, autologous clots, or Gelfoam emboli can be administered intraarterially to occlude bleeding vessel. Drawbacks-need high bleeding rate to be diagnostic (>0.5 ml/min), allergic rxn to contrast.

Tx:

1. correct bleeding abnormalities with FFP or vit K if coagulopathic, platelets if thrombocytopenic
2. H2-antagonists, omeprazole, sucralfate, antacids for PUD or gastritis. After endoscopic Tx of PUD, high dose omeprazole reduces risk of recurrent bleed. Treat H. pylori w/ MOC, AMO, or ACO (A-ampicillin, m-metronidazole, o-omeprazole)
3. Octreonide: for variceal bleeding. decreases portal flow by direct vasoconstrictive effect and indirectly by inhibition of glucagon.
4. Vasopressin: variceal bleeding. Only temporizing
5. endoscopy: sclerotherapy or ligation for bleeding varices. injection therapy (saline, epi), bipolar electrocoagulation and heater-probe therapy effective for bleeding PUD.
6. balloon tamponade: severe bleeding from esophageal varices.
7. radiologic modalities: localized infusion vasopressing, autologous clots, foreign coagulating substances (Gelfoam) in bleeding vessel during arteriography
8. surgery: refractory and recurrent bleeding and site known, about 10% need surgery Graham patch-omental patch over perforated ulcer Truncal vagotomy-resect 1-2 cm of vagal trunk w/ drainage procedure-pyloroplasty, antrectomy, gastrojejunostomy (pylorus won’t open) Biliroth I-truncal vagotomy, antrectomy, and gastroduodenostomy Biliroth II-truncal vagotomy, antrectomy, gastrojejunostomy
9. 80-85% stop bleeding spontaneously

Return to the index of cases.

A 35-year-old woman complains of blood with bowel movements ...

Differential Dx: Lower GI bleeding, below the ligament of Treitz

1. Small intestine: ischemic bowel disease (mesenteric thrombosis, embolism, vasculitis, trauma), small bowel neoplasm (leiomyoma, carcinoid), hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), meckel’s diverticulum and other small intestine diverticula, aortoenteric fistula, intestinal hemangiomas (blue rubber-bleb nevi, intestinal hemangiomas, cutaneous vascular nevi), hamartomatous polyps (Peutz-Jeghers syndrome-intestinal polyps, mucocutaneous pigmentation), infections of small bowel (tuberculous enteritis, enteritis necroticans), volvulus, intussusception, lymphoma of the small bowel, Kaposi’s sarcoma, irradiation ileitis, AV malformation, IBD, polyarteritis nodosa, pancreatoenteric fistulas, Henoch-Schonlein purpura, Ehlers-Danlos syndrome, SLE, amyloidosis, metastatic melanoma.
2. Colon: carcinoma (esp left), diverticular disease-most common, IBD, ischemic colitis, polyps, vascular abnormalities (angiodysplasia, vascular estasia), radiation colitis, infectious colitis, aortoenteric fistula, lymphoma, hemorrhoids, anal fissure, trauma, foreign body, solitary rectal/cecal ulcers, sterocoral ulcer, long-distance running.

Hx:

1. Drug Hx: specifically aspirin, steroids, “blood thinners,” NSAIDS
2. prior GI or vascular surgery
3. Hx of GI diagnosis or bleeding
4. Hx smoking/alcohol
5. Associated diseases
6. Weight loss, anorexia, constitutional symptoms (carcinoma)
7. +/- hematemesis
8. color/character of stools
9. symptoms of hypovolemia (dizziness, diaphoresis), anemia (pallor, dyspnea, angina, exertional weakness)
10. Family Hx of colon cancer

PE:

1. vitals: tachycardia , hypotension, postural changes. A pulse increase of more than 20 bpm or a postural fall in systolic blood pressure greater than 10-15 mmHg usually indicates blood loss greater than 1L
2. Cardiorespiratory: murmurs (increased incidence of angiodysplasia in patients with aortic stenosis), rales, JVD
3. Abdominal: masses, tenderness, distension, ascites, auscultate for bowel sounds and bruits, look for liver disease (hepatomegaly, spenomegaly, abnormal vascular patterns, gynecomastia, spider angiomata, palmar erythema, testicular atrophy)
4. DRE: masses, strictures, hemorrhoids, occult blood, inspect stool for abnormalities (tarry, blood-streaked, bright red mahogany color
5. skin: jaundice (liver disease), ecchymoses (coagulation abnormality), cutaneous telangiectasia (Osler-Weber-Rendu), buccal pigmentation (Peutz-Jeghers syndrome) and other mucocutaneous changes (Ehlers-Danlos syndrome)
6. evidence of metastatic disease (cachexia, firm nodular liver)

Stabilization:

1. Ringer’s lactate, IV x2
2. type and cross

Dx:

1. Labs: CBC, Chem 10, Coags (exclude bleeding disorder)
2. ECG (r/o myocardial ischemia and severe anemia)
3. Chest and abdominal x-ray
4. Flexible sigmoidoscopy: helps Dx anal disease, colitis, diverticulitis, neoplasms in lower colon
5. colonoscopy: if sigmoidoscopy not diagnostic and bleeding appears colonic-useful for AV malformations, colitis, neoplasms, intussusception.
6. barium enema: not initial therapy-precludes other diagnostic modalities. Can be therapeutic to bleeding from diverticular disease or intussusception.
7. Radionucleotide scan: Technetium 99 pertechnetate (Meckel scan) tags acid-secreting cells (gastric mucosa), for active bleeding
8. Radiolabeled RBC scan more sensitive for blood loss at rate of .1 ml/min or intermittent blood loss due to longer half-life.
9. angiography: for active bleeding. can be therapeutic- vasoconstrictors, autologous clots, or Gelfoam emboli can be administered intraarterially to occlude bleeding vessel. Drawbacks-need high bleeding rate to be diagnostic (>0.5 ml/min), allergic rxn to contrast.

Tx:

1. correct bleeding abnormalities with FFP or vit K if coagulopathic, platelets if thrombocytopenic
2. radiologic modalities: localized infusion vasopressing, autologous clots, foreign coagulating substances (Gelfoam) in bleeding vessel during arteriography
3. surgery: 10% require surgery. segmental bowel resection for massive or recurrent bleed. Ex lap w/ or w/o small intestine enteroscopy for massive bleed and w/o localization. Total abdominal colectomy w/ primary anastamosis of ileum to rectum as last resort.
4. 80-90% stop bleeding spontaneously

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A 25-year-old stabbed in right chest ...

Primary Survey

A: Airway and C-spine stabilization: if speaking-airway intact. Other ways to establish airway: chin lift, jaw thrust, oral/nasal airway, endotracheal intubation, cricothyroidotomy

B: Breathing:

EXAM: inspect for air movement, respiratory rate, cyanosis, tracheal shift, JVD, asymmetric chest expansion, accessory muscle use, open chest wound. Auscultate (breath sounds), percussion (hyperresonance or dullness), palpate (subcutaneous emphysema, flail segments)

TREAT: (all possible with stab wound to chest) Pneumothorax: esp tension pneumo: dyspnea, JVD, tachypnea, anxiety, pleuritic chest pain, unilateral or decreased or absent breath sounds, tracheal shift away from affected side, hyperresonance on affected side-immediately decompress w/ needle thoracostomy in 2nd intercostal space, midclavicular line. Follow w/ tube thoracostomy in anterior/midaxillary line in 4th intercostal space Open pneumo: sucking chest wound: +/- intubation w/ positive pressure ventilation, chest tube, occlusive dressing over defect Flail chest (2 separate fractures in 3 or more consecutive ribs): moves paradoxically, usually w/ underlying pulmonary contusion. Intubate with PEEP Cardiac tamponade: Beck’s triad: hypotension, muffled heart sounds, JVD, also tachycardia, shock, pulsus paradoxus, Kussmaul’s sound. Definitive Dx: echocardiogram. Treat with immediate IV fluid bolus, paracardiocentesis and surgical exploration Hemothorax: hypotension, unilaterally decreased or absent breath sounds, dullness to percussion, CXR. Treat with volume, chest tube (cell saver), removal of the blood. Emergent thoracotomy if >1500 cc of blood on initial chest tube placement or >200 cc bleeding/hr.

C: Circulation: palpate pulses, HR, BP, peripheral perfusion, urinary output, mental status, capillary refill (<2 seconds), skin-cold, clammy=hypovolemia). Treat external bleeding with direct pressure. 2 large bore peripheral IVs for fluid (LR).

D: Disability: Neurologic: GCS, pupils, motor/sensory

E: Exposure and Environment: disrobe, keep warm environment to prevent hypothermia

Secondary Survey

• Trauma films: x-rays c-spine, chest, pelvis.
• Labs: CBC, Chem 10, amylase, LFTs, lactic acid, coags, type and cross, UA
• Complete physical exam and history if able to obtain.
• Specific work-up for stab wound to chest: Chest tube or subxiphoid window-if blood returns, then sternotomy to assess for cardiac injury.

Other injuries specific to this patient not mentioned above:

1. Great vessel injury: widened mediastinum on CXR, apical pleural capping, loss of aortic contour/KNOB/a-p window, depression of left mainstem bronchus, NG tube/tracheal deviation, pleural fluid, elevation of right mainstem bronchus. R/O w/ thoracic arch aortogram or spiral CT of the mediastinum.
2. Consider abdominal injury w/ penetrating injury to the thorax (diaphragm extends to the nipples in men on full expiration): tenderness, guarding, rebound, distension. CT (when stable), FAST exam (ultrasound-Focused Assessment with Sonography for Trauma), DPL (diagnostic peritoneal lavage) both when unstable.

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A 25-year-old married female has mild nausea with right lower quadrant pain ....

diff dx:

• intestinal – appendicitis, Crohn’s/UC, SBO (think of ABC’s), Meckel’s divirticulitis/volvulus, enteritis, incarcerated hernia, Ca
• ob/gyn – ectopic pregnancy, ruptured ovarian cyst, torsion of ovarian cyst, salpingitis, tubo-ovarian abscess, Mittelschmerz (pain w/ ovulation), endometriosis, PID
• renal – stones, pyelonephritis, Ca, cystitis
• vasc – leaking AAA
• pulm – right lower lobe pneumonia
• psoas abscess, trauma, cholecystitis
• if pain is “not really” in RLQ – could be biliary dx, pancreatits, PUD, etc.

APPENDICITIS

History

• Pain – where did it start? Usually starts around umbilicus and then moves to RLQ
  • Quality? Usually starts vague and become more specific
  • Severity? Increasing from mild to bad as it moves from umbil to RLQ
• Nausea/vomiting – usually happens after onset of pain
• PO intake – almost always decreased - the “hamburger sign” should be negative (“If I gave you a hamburger (or whatever their favorite food is), would you eat it?”)
• Fever – often present, usually mild – high fever indicates perforation
• To r/o other Dz’s:
  • Chron’s/UC – ask about personal/family Hx
  • Perf PUD: hx of PUD? Reflux?
  • SBO – previous abdom surgery? Hernia? Fam hx of GI Ca?
  • Enteritis – diarrhea?
  • Ob/gyn diseases – ask about LMP, sexual activity, use of birth control, Hx of similar Sx’s, Hx of STDs, vaginal d/c, ab-nL menstrual sx’s
  • Renal – incontinent? Urgency? Dysuria? Hematuria?
  • AAA – “tearing” pain?
  • Pneumonia – dyspnea? Cough?

PMH:

Ask about conditions mentioned above in “to r/o other Dz’s”

PSH:

Hx of previous abdom surgery puts SBO higher on list

Diagnosis

PE:

• General: appear to be in pain
• Abdomen: pain at McBurney’s point (1/3 from ASIS to umbilicus), decreased/absent BS, +/- rebound tenderness, look for peritoneal signs (rebound tenderness, rigidity, etc) b/c indicates perf.
• Resp – r/o pneumonia
• Pelvic – may cause pain, use to r/o ob/gyn diseases
• Signs: Rovsing’s – palpating LLQ causes pain in RLQ
  • Psoas – pain on extension of R hip
  • Obturator – pain on passive rotation of flexed R thigh

Labs:

• CBC – high WBC with a left shift
• U/A – to r/o pyelo, renal stones
  • Mild hematuria and pyuria are common with appendicitis (therefore a (+)U/A does not r/o appendicitis)
• For r/o-ing other Dz’s: get beta-HCG

Imaging:

• CXR – to r/o pneumonia
• KUB: see fecalith in 5%, sentinel loops, scoliosis towards L b/c of pain, loss of psoas shadow, loss of preperitoneal fat stripe, air indicates perforation
• U/S: can show noncompressible appendix, fecalith, would show evidence of other Dz’s in the differential
• CT: fat stranding, inflamed looking appendicitis, would show evidence of other Dz’s in the differential

Treatment

• If non-perf: replace F&E’s, do appendectomy (open or laprascopic), give IV Abx for 24hrs (2nd/3rd generation cephalosporin – usually Cefoxitin or piperacillin/flagyl)
• If perf: replace F&E’s, do appy (must drain all pus, culture the fluid) – usually leave wound open to close by 2nd intention, give IV Abx for 5-7days
• If appendix looks normal during surgery: look for Meckel’s, Crohn’s, intussusception, ob/gyn diseases
• If appendiceal abscess is seen: drain the abscess, give Abx, do appy in 6-8wks

Other

#1 surgical emergency, 7% of people get it, 20% false negative rate is acceptable

Return to the index of cases.

A 72-year-old male with sudden back pain and leg weakness ...

Differential Diagnosis

• ruptured AAA
• lumbar disc herniation (includes cauda equina syndrome)
• spinal epidural abscess
• traumatic spinal cord injury, traumatic injury to musculature surrounding SC
• vertebral fx w/ minimal trauma due to degenerative disease, osteoporosis, osteomalacia

this is likely a AAA rupture, or possibly a traumatic injury. the others are unlikely. since there are other trauma presentations on the list, I'm assuming this will turn out to be a AAA. note: the leg sx's are due to a hematoma impinging on nerves and/or decreased blood supply to legs

History

• what were you doing when the pain started?
• any hx of trauma? - directly to area or compressing cord
• describe the pain - "tearing" could indicate AAA dissection
• ever been diagnosed with a AAA? how big is it (the bigger it is, the more likely to rupture)?
• other possible sx's to ask about include: abdominal pain, syncope, vomiting, pain in groin
• ever have similar sx's before? - would point to disc herniation, degenerative disease

PMH:

• risk factors: COPD, HTN, Marfans, Ehlers-Danlos, male, elderly, atherosclerosis
• DM is risk factor for rupture
• hx of HTN, angina, MI all increase mortality

Fam Hx:

social hx:

PEM

• signs include pulsatile abdominal mass (usually in LUQ), tenderness, hypotension are classic triad
• others are paralysis, flank mass, abdominal bruit
• other sx's of hypotension - looking ill, mental impairment, cold skin, pallor, weak pulses, LOC, tachycardia, poor cap refill, poor UOP, tachypnea, low pulse pressure

Workup

• first: start 2 large bore IVs and pour fluid in, get blood and send for type and screen (plus labs below if Pt is hemodynamically stable)
• labs: WBC>10, Hct<32
  • look at BUN and creatinine for sx's of renal failure
• if Pt is very hemodynamically unstable: straight to OR
• if Pt is mildly hemodynamically unstable: do U/S or Doppler then to OR emergently
• if Pt is hemodyn. stable: get nonenhanced and enhanced CT of chest/abd/pelvis
  • CT shows hyperintensity in soft tissue around aorta, indistinct aortic wall, thinning or fracture of calcified aortic wall segment, contrast extravastation into psoas or retroperitoneum, "crescent sign" indicates hematoma in wall of aorta
• could also get MRI - especially in Pt where contrast induced nephropathy is a concern
• angiography is almost never used

Treatment

• all symptomatic AAA's are operated on (asymptomatic's >5cm too)
• operation: open abdomen with large midline incision, also prepare both groins for femoral access
  • clamp aorta above then below the AAA
  • open the aneurysm
  • sew graft into aneurysm
  • sew wall over graft
  • close

Return to the index of cases.

A 63-year-old female has sudden left leg pain and her foot is cold ...

Differential Diagnosis Acute arterial occlusion

1. Thrombosis
2. Embolization
3. Traumatic/iatrogenic
4. Aortic dissection
5. Phlegmasia cerulea dolens
6. Graft thrombosis

History

1. How long ago did the pain start?
2. Any history of claudication (pain in legs with walking) or rest pain (pain in dorsum of foot at rest)?
3. History of A-fib or recent MI? (possible causes of an embolus)
4. Any evidence of cerebral or visceral embolization?
5. Risk factors for PVD (smoking, DM, HTN, family history, high cholesterol)
6. Cardiac history: MI, angina, CHF, arrhythmias
7. Renal history: any history of renal insufficiency (this is important if you want to do angiography)
8. Surgical history: any previous vascular surgery
9. Any problems with easy bleeding (e. g. bleeding excessively after dental procedures)
10. Any problems with excessive clotting

Physical Exam

1. Vitals: irregular heartbeat (e. g. A-fib)
2. Vascular: PULSES!!! (the point at which you cannot feel a pulse helps indicate where the occlusion is), capillary refill (blanching suggests possible retrieval of capillary bed), decreased temperature of left foot?, pallor of foot?, possible tenderness over affected artery
3. Neurologic: pain or parasthesia of foot, paralysis of foot, sensation to light touch lost early, decreased motor function is lost later… this is more worrisome
4. Musculoskeletal: Rigor suggests skeletal muscle death

Diagnosis

1. Labs: CBC, Chem 10, PT, PTT
2. Cardiac: CXR, EKG
3. Vascular: Do ABIs, Angiography if there is time – presence of collaterals suggests chronic disease, MRA is an alternative in patients who cannot tolerate contrast

Treatment

1. If the diagnosis of an acute occlusion is made, you must go to the OR for thrombectomy or embolectomy
2. UNLESS the extremity is clearly nonviable. In this situation, administer heparin and wait for nonviable tissue to demarcate itself and proceed with amputation.
3. Can give Dextran (decreases electronegativity of RBCs and slows propogation of thrombus)
4. Can give Mannitol (both Dextran and Mannitol will draw fluid back into vasculature and hemodilute blood)
5. If distal extremity has been ischemic for more than 4 hours, you may have to perform a fasciotomy to prevent compartment syndrome
6. Post-operatively, get an echocardiogram to look for a thrombus.
7. Consider long-term anti-coagulation
8. If there appears only to be acute arterial occlusion without danger to the distal extremities, you may attempt thrombolytic therapy instead of emergent surgery (streptokinase, urokinase)

Comments

Know the 6 Ps for acute arterial occlusion: Pain, Pallor, Parasthesias, Paralysis, Pulselessness, Poikilothermia (change in temperature)

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A 14-year-old boy has pain in the right testicle ...

Ddx for Pt. :

1. testicular torsion
2. epididymitis
3. tumor w/ hemorrhage (unlikely, but…)

1. Hx and PE
   1. localization of pain, duration of pain
   2. Is nausea/vomit present?
   3. What is presentation of scrotum?
   4. Was there strenuous activity involved that precipitated pain?
   5. Fever?
   6. Is there loss of cremasteric reflex?
   7. Is there hx of undescended testes?
   8. Is there inguinal pain?
2. Dx
   1. U/A (unremarkable in torsion)
   2. CBC (unremarkable in torsion)
   3. Afebrile
   4. Color Doppler U/S (sensitivity of 85-100%)
   5. Surgical exploration
3. Tx
   1. manual detorsion whle awaiting surgical exploration
   2. lateral detorsion during surgical exploration.

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A 72-year-old male with jaundice and pruritis ...

Differential Diagnosis:

Jaundice

1. Hemolytic -- less than 80% unconjugated bilirubin Hemolytic anemia (Differential diagnosis)
   • Reduced bilirubin uptake: Gilbert's syndrome, severe congestive heart failure and drugs.
   • Reduced bilirubin conjugation: Crigler-Najjar syndrome, breast milk jaundice.
2. Hepatocellular Mainly conjugated bilirubin

1. Acute liver diseases
   • Infectious hepatitis
   • Drugs: alcohol, paracetamol, halothane, MAO inhibitors
   • Poisons: amanita phalloides, aflatoxin, carbon tetrachloride, tetracyclines
   • Wilson's disease.
2. Chronic liver diseases
   • Chronic viral hepatitis
   • Chronic autoimmune hepatitis
   • Drugs: methyl dopa, isoniazide, ketoconazole, nitrofurantoin.
   • Alpha - 1 antitrypsin deficiency
   • Wilson's disease

1. Obstructive Mainly conjugated bilirubin
   1. Intrahepatic
      • Biliary cirrhosis
      • Sclerosing cholangitis
      • Viral hepatitis
      • Congenital: Dubin-Johnson syndrome, Rotor syndrome
   2. Extrahepatic
      • Cancer of pancreas
      • Stone
      • Biliary stricture
      • Sclerosing cholangitis

Pruritus (overlapping with jaundice)

History and PE

History may suggest either obstructive or hepatocellular disease and may indicate an underlying malignancy

Presence of light-colored stools and dark tea-colored urine indicates extrahepatic biliary Obstruction; if sharp or severe pain also, suggests a benign etiology for the jaundice (biliary stones). In contrast, patients with malignancies (pancreatic carcinoma) generally have dull, vague, or insignificant abdominal pain, in addition to a history of marked weight loss. Pruritus is believed to be caused by high tissue concentrations of reabsorbed bile acids and if often present in patients with obstructive jaundice

The presence of a nontender, palpable gallbladder with jaundice suggests malignant disease, such as carcinoma of the pancreas (Courvoisier’s law)

Labs

• CBC/Chem 7
• Serum amylase elevated in acute cholecystitis and acute cholangitis, but marked elevations suggest acute pancreatitis.
• LFTs
• LDH/haptoglobin- to r/o a hemolytic cause (LDH up, hapto down)
• unconjugated or indirect bilirubin increases in hemolytic disorders, whereas direct or conjugated fraction is elevated in extrahepatic obstruction or cholestasis.
• alk phos increases as a result of overproduction in conditions that cause extrahepatic biliary obstruction, or less commonly, from cholestasis resulting from a drug reaction or primary biliary cirrhosis…also higher in hepatitis and bone disease, use heat stability to differentiate the two
• if GGT up, also indicates that the source of elevated alk phos is biliary tract
• if increase in alk phos greater than increase in AST/ALT, biliary obstruction and converse is true in hepatitis
• may also want to check out PT, often prolonged in pts with obstructive jaundice due to malabsorption of vit K

Imaging

• AXR to look for stones, air (probably not that helpful) 0U/S may see stones, but probably not, also look at bile ducts, possible fluid collection, gall bladder, liver, pancreatic mass
• HIDA scan to look at bile flow
• CT if suspect pancreatic mass/liver lesion/look at dilation of ducts
• ERCP if want to stent, look for pancreatic duct obstruction, perform sphincterotomy

Treatment

• Choledocholithiasis: elective cholecystectomy (if no cholangitis) and extraction of stones from common duct with ERCP, tx clotting abnormalities, sphincterotomy
• Pancreatic CA- Whipple (poor prognosis)
• GB cancer- wedge resection of GB fossa and liver bed and regional LND (poor prognosis)
• Bile duct stricture- stent placement with ERCP, anastomosis to jejunum
• Hemolytic anemia- figure out the cause and treat it
• Hepatitis- look it up, you’re all relatively bright

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A 50-year-old woman with periumbilical crampy pain ...

Differential Diagnosis (of periumbilical pain)

• Intestinal: small bowel obstruction or gangrene, early appendicitis
• Vascular: mesenteric thrombosis, dissecting aortic aneurysm
• Pancreatic: pancreatitis
• Metabolic: uremia, DKA
• Trauma
• Gyn causes?

H&P

Recent surgery (suggests adhesions and SBO or paralytic ileus)

anorexia, nausea, vomiting, and peritoneal signs- guarding, muscle spasm, rebound tenderness, obturator and psoas signs, low-grade fever (high grade if perf). (suggest appendicitis)

weight loss, postprandial abdominal pain-“intestinal angina”, pain out of proportion to physical exam, possible diarrhea and vomiting abdominal bruit, heme-positive stool (suggest acute mesenteric ischemia)

abdominal pain+palpable abdominal mass+hypotension (suggest dissecting AAA)

epigastric tenderness, hx of gallstones, diffuse abdominal tenderness, decreased bowel sounds (suggest acute pancreatitis)

if also weight loss, steatorrhea (suggest chronic pancreatitis)

trauma (suggests trauma, duh)

Labs/Imaging

• CBC/Chem 7/type and screen/urinalysis- often see lyte disturbances in proximal SBO
• AXR to look for obstruction (would see air/fluid levels and distended loops of small bowel), see calcifications in aorta which may suggest AAA
• spiral CT if suspect appendicitis (see periappendiceal fat stranding, large diameter and periappencieal fluid; also good to evaluate aorta
• A-gram if AAA suggested, also good to rule out mesenteric ischemia
• U/S can be used to evaluate pancreas, AAA

Treatment

Obviously, it depends on the individual cause because they’re all completely different. Briefly:

• Appendicitis (most likely): IV fluids, preop Abx (anaerobic coverage, usually cefoxitin) Lap or open appy, if perforated, drain pus and culture, continue preop abx for 3-7 days (use triples-amp/gent/clinda), leave wound open
• AAA/pancreatitis/mesenteric ischemia/trauma/others-call your doctor

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An 18-year-old is elbowed in the face at a basketball game and has diplopia and a numb left check ...

DDx: trauma-induced diplopia and numbness

1. Orbit floor (blow-out) fractures – most common
2. Ruptured globe
3. Traumatic optic neuropathy
4. Retrobulbar hemorrhage

Hx:

• Patients may relay a history of the eye being struck by an object larger than the diameter of the orbital entrance. Fists, balls, or car dashboards are examples.
• Patients may have no complaints. However, they may complain of vision loss or diplopia. The double vision is often vertical and worse with attempted up or downgaze.
• Numbness (hypoesthesia) of the cheek and gum on the affected side may be present. Ecchymoses, ptosis (droopiness of the eyelid), and swelling around the eye may be noted.
• The examiner should obtain a past ocular history to assess whether any loss of vision or diplopia is due to the present accident or was established prior to this incident.
• Other significant aspects include a review of systems (eg, history of diabetes, vascular disease, or hypertension; headache and other neurologic complaints), as well as a past surgical and medical history.

Physical:

• Visual acuity and pupils should be evaluated to ensure that no loss of vision or traumatic optic neuropathy has occurred.
• The examiner should evaluate extraocular movements and document any restriction or palsy.
• A complete slit lamp evaluation and measurement of intraocular pressures should be performed.
• Most posterior segment injuries can be ruled out with a dilated funduscopic examination.
• The physical findings may involve only periorbital edema and ecchymosis; however, more severe cases may demonstrate limited vertical movement, enophthalmos, ptosis, and possibly proptosis.
• Unusually severe orbital edema may be associated with more severe fractures and can cause proptosis. Once the edema has subsided (usually 1-2 wk), enophthalmos may be present.
• Limited vertical movement may be due to entrapment of the perimuscular fascia of the inferior rectus in the fracture site. However, traumatic palsy of the third nerve branch to the inferior rectus also may cause decreased extraocular movements. If a question exists, forced duction testing may differentiate between the two conditions.

Diagnosis:

• Imaging Studies: For the majority of orbital fractures, the imaging study of choice is CT scan. A CT scan with axial and coronal views is optimal. Ask for thin cuts (2-3 mm) with specific attention to the orbital floor and optic canal.
• Procedures: Forced duction testing may be performed to confirm that limited extraocular movements are due to restriction of the inferior rectus muscle instead of third nerve branch palsy. Testing should be performed after the orbital edema subsides, usually 10 days to 2 weeks after the trauma.

Treatment:

• Medical Care: When orbital edema is severe, steroids may be used to decrease orbital edema. However, most cases do not require any medical intervention. In addition, most cases are managed on an outpatient basis. Patients should be advised to avoid strenuous activity and nose blowing for several weeks after the injury to prevent orbital emphysema and possible visual compromise.
• Surgical Care: The criteria for surgical intervention in blowout fractures are controversial; however, 3 general guidelines exist for surgical intervention.
  1. Diplopia due to limitation of upgaze and/or downgaze with a positive forced duction test and radiologic confirmation of an orbital floor fracture is an indication of entrapment of the inferior rectus or the perimuscular tissues surrounding the inferior rectus. If diplopia is still present 10-14 days after trauma, a need for release and repair is indicated. Diplopia may be present initially after trauma but may resolve as the neuropraxia and/or orbital edema subsides.
  2. Enophthalmos of greater than 2 mm 10-14 days after trauma is cosmetically significant and is an indication for surgery. Orbital edema that is present initially may mask any enophthalmos. Therefore, measurements must be rechecked once the orbital edema has subsided. This usually occurs 10 days to 2 weeks after injury.
  3. A fracture involving one third or more of the orbital floor usually leads to a cosmetic and/or functional deformity. If left unattended, these fractures tend to result in significant enophthalmos.

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A 57-year-old female has a 1 cm lesion in the right middle lobe on a routine CXr ...

The solitary pulmonary nodule initially detected on chest radiograph represents a common clinical problem. Patients are typically (though not always) asymptomatic, and the nodule is often found on a routine or screening radiograph.

The major question following detection of a solitary pulmonary nodule is whether the lesion represents a benign or a malignant process, especially primary lung cancer. While it is preferable not to subject a patient to a surgical procedure for removal of a benign lesion that may not need therapy, it is probably even more important to resect a localized non-small cell primary lung cancer, which often has an excellent prognosis following surgical resection.

The differential diagnosis and general diagnostic approach to the patient with a solitary pulmonary nodule is presented here.

DIFFERENTIAL DIAGNOSIS — The causes of solitary pulmonary nodules are best classified initially into the major categories of benign and malignant (show table 1). As a rough guideline, the percentage of lesions that are malignant averages approximately 50 percent.

Primary lung cancer — Although all cell types of primary lung cancer can present as a solitary pulmonary nodule, this particular type of presentation is seen most commonly with adenocarcinoma (including the subtype bronchioloalveolar cell carcinoma) and, to a lesser extent, large cell carcinoma. These histologic subtypes commonly originate as peripheral lesions. However, even small cell carcinoma and squamous cell cancer, which typically present as central endobronchial or mucosal lesions, respectively, can occur in a peripheral location.

Carcinoid tumors — Although carcinoid tumors tend to be centrally located endobronchial lesions, approximately 20 percent arise peripherally and present as a solitary pulmonary nodule. These tumors are generally well circumscribed in their radiographic appearance.

Metastatic cancer to the lung — Primary sites of extrapulmonary malignancy that are most likely to produce a solitary pulmonary nodule from metastatic disease include malignant melanoma, sarcomas, and carcinomas of the colon, breast, kidney, and testicle. However, the vast majority of metastases to the lungs occur as multiple lesions. Rarely, malignant lymphomas may present with either a solitary nodule or numerous lesions.

Infectious granulomas — Tuberculosis and the endemic fungi (especially histoplasmosis and coccidioidomycosis) are the most frequently recognized causes of infectious granulomas presenting as a solitary pulmonary nodule. Atypical (ie, nontuberculous) mycobacterial disease can also present in this fashion, with the cause of the nodule generally not being recognized until the lesion is resected as a presumed primary lung cancer. Pneumocystis carinii infection may produce a solitary pulmonary nodule, which sometimes may cavitate, in the patient with acquired immunodeficiency syndrome

Pulmonary dirofilariasis — Pulmonary infestation with the dog heartworm, Dirofilaria immitis, is a rare but well-recognized cause of a solitary pulmonary nodule. Dogs are the usual animal host, but cats, wolves, coyotes, and foxes can also harbor the organism. The greatest concentration of human cases in the United States is found in eastern, southeastern, and southern coastal states.

Hamartomas — Hamartomas are generally considered to be benign tumors of the lung. They typically present in middle age and often have a pattern of slow growth over years. Hamartomas can have a variety of components observed histologically, including cartilage The characteristic appearance of a hamartoma on chest radiography is a solitary nodule with a "popcorn" pattern of calcification.

FACTORS AFFECTING THE LIKELIHOOD OF MALIGNANCY — Although no clinical or epidemiologic characteristics can separate unequivocally those patients who have benign versus malignant nodules, several features do affect the likelihood of malignancy.

Patient age — The probability of a solitary nodule being malignant rises with increasing patient age. Malignancy in 65 percent of lesions in patients 50 years of age or older.

Presence of underlying risk factors — Due to the strong association of cigarette smoking with primary lung cancer, the possibility of lung cancer is a concern when a solitary nodule is found in a patient with a history of smoking. Similarly, other risk factors for lung cancer, including exposure to asbestos or other occupational carcinogens, should be considered when evaluating the patient with a solitary pulmonary nodule. A previously diagnosed malignancy increases the likelihood that a solitary nodule may represent metastatic disease.

Size of lesion — Lesions larger than 3 cm are particularly likely to be malignant. Since primary lung cancer arises from a single cell that becomes malignant, and a 1 cm tumor nodule represents 10(9) or 1 billion cancer cells, a lesion of any size detectable on imaging studies must be considered as malignant in the appropriate setting.

Border characteristics of lesion — Benign lesions tend to have a relatively smooth and discrete border, whereas malignant lesions often have more irregular and spiculated borders.

Calcification of lesion — Certain patterns of calcification of a solitary nodule, sometimes observed on plain radiographs, but best established by computed tomography, are strongly suggestive that a lesion is benign. These include diffuse, homogeneous calcification dentral calcification,laminated (concentric) calcification. In contrast, "eccentric" calcification (ie, an area of asymmetric calcification within a lesion) is not characteristic of a benign lesion and should raise concern about carcinoma arising in an old granulomatous lesion (ie, a "scar" carcinoma).

Growth of lesion — Review of available old chest radiographs is a critical part of the diagnostic evaluation. Lesions that are malignant tend to have a doubling time (DT) between approximately 20 and 400 days.

USE OF CT DENSITY ANALYSIS — Despite the absence of grossly visible calcification, the density of a lesion may be a helpful feature for suggesting that the lesion is benign. One group of investigators, for example, proposed that a density cutoff of 164 Hounsfield units could be used to separate benign from malignant lesions [29].

USE OF BIOPSY TECHNIQUES — If clinical and radiographic features do not provide sufficient evidence that a lesion is either benign or malignant, a consultation with a pulmonologist is warranted to decide whether the lesion should be biopsied or excised. Biopsy can be performed by approaching the lesion through the airway (using a fiberoptic bronchoscope) or through the chest wall (by percutaneous needle aspiration). Excision can be performed via either thoracoscopy (video assisted thoracic surgery, VATS) or thoracotomy.

Fiberoptic bronchoscopy — Although fiberoptic bronchoscopy may provide a reasonable approach for diagnosis of larger pulmonary masses, it is much less useful for the diagnosis of the smaller solitary pulmonary nodule.

Percutaneous needle aspiration — Percutaneous aspiration of a solitary nodule, often called fine needle aspiration (FNA), can be performed through the chest wall, using either fluoroscopy or CT scanning to guide placement of the needle within the lesion. The yield from a percutaneous approach is generally higher than the yield from fiberoptic bronchoscopy, as placement of the needle within the lesion is much more reliable by a percutaneous approach than is placement of a brush or biopsy forceps by an endobronchial approach. Percutaneous needle aspiration may be complicated by development of a pneumothorax, particularly following sampling of lesions that have no associated adhesions to the chest wall. In patients with emphysema, this may be a significant complication. Bleeding is a less frequent complication.

RECOMMENDATIONS — if determined to be malignant

DIAGNOSTIC EVALUATION — Diagnostic evaluation is focused upon confirmation of the presence and histopathologic type of tumor, staging of the lesion, and in many cases, functional evaluation of the patient as a potential surgical candidate.

Staging of non-small cell lung cancer involves a traditional approach based upon the characteristics of the primary tumor (T), the presence or absence of hilar or mediastinal lymph node involvement (N), and the presence or absence of distant metastatic disease (M) . In contrast, staging of small cell carcinoma of the lung involves distinguishing between disease restricted to the ipsilateral (ie, same side) hemithorax (limited disease) and disease extending beyond the ipsilateral hemithorax (extensive disease). Functional evaluation is performed when patients are considered potential surgical candidates for lung resection, and is particularly important given the common coexistence of COPD and lung cancer based upon their shared risk factor of smoking.

GENERAL APPROACH TO TREATMENT — Treatment decisions are based primarily upon the histopathologic type of tumor (broadly categorized as either small cell or non-small cell carcinoma of the lung) and the stage of the tumor. The following general principles apply to management of non-small cell carcinoma: Surgical resection is the preferred management for patients with stage I non-small cell carcinoma of the lung. ((**this pt most likely Stage 1= Stage I disease represents local disease, 1-3cm, without regional lymph node or distant metastasis)). Surgical resection, with or without an additional therapeutic modality (radiation or chemotherapy), is the preferred treatment for patients with stage II non-small cell carcinoma of the lung. Small cell carcinoma of the lung is managed primarily with systemic chemotherapy, based upon its predilection for early metastatic disease, which may be subclinical. (See "Treatment of small cell carcinoma of the lung"). In the occasional cases where small cell carcinoma presents as a solitary pulmonary nodule, surgical resection may be considered, in addition to systemic chemotherapy. (See "Role of surgery in multimodality therapy for small cell carcinoma of the lung"). Regardless of histology or stage, unresectable tumors which compromise the trachea or large airways may be palliated by local techniques to maintain airway patency, including brachytherapy, laser therapy, airway stents, and/or photodynamic therapy.

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A 20-year-old, struck by a line-drive during a baseball game, passes out 40 minutes later ...

My guess= Epidural Hematoma

Background: Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull and the stripped-off dural membrane. The inciting event often is a focused blow to the head, such as that produced by a hammer or baseball bat. In 85-95% of patients, this trauma results in an overlying fracture. Blood vessels in close proximity to the fracture are the sources of the hemorrhage. Because the underlying brain usually has been minimally injured, prognosis is excellent if treated aggressively. Outcome from surgical decompression and repair is related directly to patient’s preoperative neurologic condition.

Pathophysiology: Approximately 70-80% of EDHs are located in the temporoparietal region where skull fractures cross the path of the middle meningeal artery or its dural branches. Frontal and occipital EDHs each constitute about 10%, with the latter occasionally extending above and below the tentorium. Association of hematoma and skull fracture is less common in young children because of calvarial plasticity.

EDHs usually are arterial in origin but result from venous bleeding in one third of patients. Occasionally, torn venous sinuses cause EDH, particularly in the parietal-occipital region or posterior fossa. These injuries tend to be smaller and associated with a more benign course. Usually, venous EDHs only form with a depressed skull fracture, which strips the dura from the bone and, thus, creates a space for blood to accumulate. In certain patients, especially those with delayed presentations, venous EDHs are treated nonsurgically.

Expanding high-volume EDHs can produce a midline shift and subfalcine herniation. Compressed cerebral tissue can impinge on the third cranial nerve, resulting in ipsilateral pupillary dilation and contralateral hemiparesis or extensor motor response.

EDHs usually are stable, attaining maximum size within minutes of injury; however, Borovich demonstrated progression of EDH in 9% of patients during the first 24 hours. Rebleeding or continuous oozing presumably causes this progression. EDH occasionally runs a more chronic course and is detected only days after injury.

Frequency:

• In the US: EDH occurs in 1-2% of all head trauma cases and in about 10% of patients who present with traumatic coma.

Mortality/Morbidity:

• Reported mortality rates range from 5-43%.
• Higher rates are associated with the following:
• Advanced age
• Intradural lesions
• Temporal location
• Increased hematoma volume
• Rapid clinical progression
• Pupillary abnormalities
• Increased intracranial pressure (ICP)
• Lower Glasgow coma scale (GCS)
• Mortality rates are approximately 0% for patients not in coma preoperatively, 9% for obtunded patients, and 20% for patients in deep coma.
• Age:
  • Patients younger than 5 years and older than 55 years have an increased mortality rate.
  • Patients younger than 20 years account for 60% of EDH incidences.
  • EDH is uncommon in patients who are elderly because the dura is strongly adhered to the inner table of the skull. In case series of EDH, fewer than 10% of patients are older than 50 years.

History:

• Fewer than 20% of patients demonstrate the classic presentation of a lucid interval.
• Following injury, the patient may be continually comatose, briefly comatose and recovered, or continually conscious.
• Severe headache
• Vomiting
• Seizure
• Patients with posterior fossa EDH may have a dramatic delayed deterioration. The patient can be conscious and talking and a minute later apneic, comatose, and minutes from death.

Physical:

• Cushing response consisting of the following can indicate increased ICP:
• Hypertension
• Bradycardia
• Bradypnea
• Level of consciousness may be decreased, with decreased or fluctuating GCS.
• Contusion, laceration, or bony step-off may be observed in the area of injury.
• Dilated, sluggish, or fixed pupil(s), bilateral or ipsilateral to injury, suggest increased ICP or herniation.
• Classic triad indicating transtentorial herniation consists of the following:
• Coma
• Fixed and dilated pupil(s)
• Decerebration
• Hemiplegia contralateral to injury with herniation may be observed.

Causes:

• EDH results from traumatic head injury, usually with an associated skull fracture and arterial laceration.

Lab Studies:

• Perform appropriate lab work for associated trauma.
• No specific tests are required.
• Coagulation abnormalities are a marker of severe head injury. Breakdown of the blood-brain barrier with exposed brain tissue is a potent cause of disseminated intravascular coagulation (DIC).

Imaging Studies:

• Head CT scan
• Immediate unenhanced CT scan is the procedure of choice for diagnosis.
• Head CT scan shows location, volume, effect, and other potential intracranial injuries.
• EDH forms an extraaxial, smoothly marginated, lenticular, or biconvex homogenous density.
• EDH rarely crosses the suture line because the dura is attached more firmly to the skull at sutures.
• Focal isodense or hypodense zones within EDH indicate active bleeding.
• Irregular hypodense swirling indicates active bleeding in the majority of patients.
• Air in acute EDH suggests fracture of sinuses or mastoid air cells.
• At surgery or autopsy, 20% of patients have blood in both epidural and subdural spaces.

Other Tests:

• Cervical spine evaluation usually is necessary because of the risk of neck injury associated with EDH.

Procedures:

• Perform burr hole(s) if the following occur:
• Patient is herniating
• All other treatments prove insufficient
• Neurosurgery is unavailable
• Air or ground medical transport is prolonged
• Burr hole procedure includes the following:
• Drill hole adjacent to, but not over, skull fracture or in the area located by CT scan.
• In the absence of CT scan, place a burr hole on the side of the dilated pupil, 2 finger widths
• anterior to tragus of ear and 3 finger widths above. See Roberts and Hedges Clinical Procedures in Emergency Medicine for further details.

Prehospital Care:

• Stabilize acute life-threatening conditions and initiate supportive therapy. Airway control and blood pressure support are the most important issues.
• Establish IV access, administer oxygen, and monitor.
• Administer IV crystalloids to maintain systolic blood pressure (SBP) greater than 90 mm Hg.
• Intubation, sedation, and neuromuscular blockade per protocol

Emergency Department Care:

• Establish IV access, administer oxygen, monitor, and administer IV crystalloids as necessary to keep SBP greater than 90 mm Hg.
• Intubate using rapid sequence induction (RSI), which generally includes premedication with lidocaine, a cerebroprotective sedating agent (eg, etomidate), and neuromuscular blockade.
• Lidocaine may have limited effect in this situation, yet it carries virtually no risk. Intubate after a basic neurologic examination to facilitate oxygenation, protect airway, and allow for hyperventilation as needed.
• Elevate head 30º after the spine is cleared, or use reverse Trendelenburg position to reduce ICP and increase venous drainage.
• Administer mannitol 0.25-1 g/kg IV after consulting a neurosurgeon if SBP is greater than 90 mm Hg with continued clinical signs of increased ICP. This reduces both ICP (by osmotically reducing brain edema) and blood viscosity, which increases cerebral blood flow and oxygen delivery.
• Hyperventilation to partial pressure of carbon dioxide (PCO2) of about 30 mm Hg treats incipient herniation or signs of increasing ICP; however, this is controversial. Be careful not to lower PCO2 too far (<25 mm Hg). Perform hyperventilation if clinical signs of increased ICP progress; this procedure reduces ICP by hypocarbic vasoconstriction and reduces risks of hypoperfusion and death of injured cells.
• Phenytoin reduces the incidence of early posttraumatic seizures, although it does not affect late-onset seizures or the development of a persistent seizure disorder.

Consultations:

• Consult neurosurgery immediately for EDH evacuation and repair.
• Consult trauma surgery for other life-threatening injuries.

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A 40-year-old has epigastric pain radiating to the back ...

Because this is the classic description of pancreatitis I am going down that road

Differential DX

• Acute pancreatitis
• Pancreatic pseuocyst
• perforated viscus, especially from peptic ulcer
• acute cholecystitis
• biliary colic
• choledocholiathis
• cholangitis
• acute intestinal obstruction
• mesenteric vascular occlusion
• renal colic, myocardial infarction
• dissecting aortic aneurysm
• connective tissue disorders with vasculitis.
• Salpingitis

History

The cardinal symptom of acute pancreatitis is abdominal pain, which characteristically is dull, boring, and steady in quality. Most often, it is located in the upper abdomen, usually epigastric, but may be perceived more on the left or right side, depending on which portion of the pancreas is involved. The pain radiates to the back in approximately one half of the cases.

The duration of pain is variable but typically longer than a day.

The pain may be aggravated by meals or by lying supine, and it may be alleviated by fasting or lying on the left side with the knees and hips flexed.

Associated symptoms such as anorexia, nausea, and vomiting are common, and some patients experience diarrhea.

Obviously, ask other questions too that relate to other things in the differential, but these are the pancreatic questions

PE

1. Fever (76%) and tachycardia (65%) are common abnormal vital signs.
2. Abdominal tenderness, muscular guarding (68%), and distension (65%) are observed in most patients. Bowel sounds often are hypoactive.
3. A minority of patients exhibits jaundice (28%).
4. Few patients experience dyspnea (10%), which may be caused by irritation of the diaphragm, resulting from inflammation, or a more serious condition, such as respiratory distress syndrome.
5. In severe cases, hemodynamic instability is evident (10%), and, sometimes, hematemesis or melena develops (5%).

PE

1. The Cullen sign is a bluish discoloration around the umbilicus, resulting from hemoperitoneum.
2. The Grey-Turner sign is a reddish-brown discoloration along the flanks, resulting from retroperitoneal blood dissecting along tissue planes.
3. Erythematous skin nodules may result from focal subcutaneous fat necrosis.
4. Abnormalities on funduscopic examination may rarely be seen in severe pancreatitis. Termed Purtscher retinopathy, this ischemic injury to the retina appears to be caused by the activation of complement and agglutination of blood cells within retinal vessels. It may cause temporary or permanent blindness.

Etiology

Labs

• Amylase and lipase
  1. Serum amylase and lipase typically are elevated in patients with acute pancreatitis. However, these elevations may only indicate pancreastasis.
  2. Determination of serum amylase is routinely available but not specific for pancreatitis. Elevations can occur in patients with a small intestinal obstruction, mesenteric ischemia, tuboovarian disease, renal insufficiency, and macroamylasemia. Rarely, elevations also may reflect parotitis.
  3. The serum half-life of amylase is short, and elevations generally return to normal within a few days.
  4. Lipase has a slightly longer half-life and may support the diagnosis if a delay occurs between the episode of pain and the time the patient seeks medical attention.
  5. The level of serum amylase or lipase does not predict whether the disease is mild, moderate, or severe.
• Liver associated enzymes - Obtain alkaline phosphatase, total bilirubin, aspartate aminotransferase, and alanine aminotransferase (ALT) to search for evidence of gallstone pancreatitis.
• Calcium, cholesterol, and triglycerides: Obtain these to search for an etiology of pancreatitis (hypercalcemia or hyperlipidemia) or complications of pancreatitis (hypocalcemia resulting from saponification of fats in the retroperitoneum).
• Serum electrolytes, BUN, creatinine, and glucose: Measure these to look for electrolyte imbalances, renal insufficiency, and pancreatic endocrine dysfunction.
• CBC count
• C-reactive protein
  1. This can be obtained 24-48 hours after presentation to provide some indication of prognosis.
  2. A C-reactive protein (CRP) in double figures (>10 mg/dL) is very suggestive of severe pancreatitis. It is an acute-phase reactant that is not specific for pancreatitis.
• Arterial blood gases
• Measure these if the patient is dyspneic. Whether the tachypnea is due to ARDS or diaphragmatic irritation needs to be discerned

Imaging

1. U/S to assess presence of gallstones as etiology
2. CT scan – not necessary for mild pancreatitis
3. ERCP – diagnostic/therapeutic can retrieve gallstones, perform sphincterotomy

Treatment

• Fluids, possibly antibiotics in severe cases, ERCP, nutritional support
• Surgical treatment –
  1. Duct is not patent because of pancreatitis – stent placement
  2. Pseudocyst formation – percutatneous aspiration, transmural enterocystostomy, surgical cystenterostomy
  3. Acute Necrotizing Pancreatitis – Excision and Debridement
  4. Acute Pancreatitis without complication – No treatment

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A 55-year-old has difficulty swallowing after 10 years of heartburn ...

Differential Diagnosis of Dysphagia

1. Peptic Stricture
2. Esophageal Carcinoma
3. Strictures caused by chemicals, radiation
4. Zencker Diverticulum
5. Scleroderma
6. Achalasia
7. Vascular Rings
8. Mediastinal Mass
9. Neuromuscular problems.

History

Want to differentiate true dysphagia (difficulty swallowing) from odynophagia (painful swallowing) and globus (lump in throat, not a true defect)

HPI

• Onset- progressive or sudden – benign disease often has longer time of onset than malignancy
• Timing – intermittent or constant. Intermittent dysphagia is associated with Zencker Diverticulum
• Location – where is the food getting stuck. This is not always reliable
• Difficulty in initiating swallow vs. getting food down – oropharyngeal dysphagia vs. esophageal dysphagia. Difficulty getting the food down would lead more towards an esophageal pathology
• Any weight loss
• Pain with solids and liquids or just solids – trouble with both suggestive of neuromuscular vs. obstructive disorder except at the very end stages of esophageal obstruction
• Has there been a progression towards softer foods? This suggests expanding obstruction
• Any ingestion of chemicals? - if yes then duh, chemical stricture

PMH

Meds

PE

• General – signs of cachexia
• Skin – look for connective tissue disease
• Neuro – patient’s mental status. Motor and sensory, cr. Nerves, reflexes, cerebellar. If there are any abnormalities in the neuro exam than the problem may be neuromuscular
• Mouth – is there enough saliva production. If not this will lead to oropharyngeal dysphagia
• Neck – watch them swallow food and liquid. Nl pt. will not have any trouble. Extrinsic compressive masses (thyroid, lymphadenopathy) may be palpated

Tests

1. Barium swallow – can see filling defects, strictures, reflux
2. Endoscopy – Mass or lesion found on Barium swallow then proceed to Endoscopy. Should take biopsy of any lesion seen
3. Manometry – detects motor dysfunction of LGE sphincter. Should be done if both barium swallow and endoscopy are negative
4. pH probe – can diagnose reflux, we already know this to be true so whats the point

Treatment

• Peptic stricture – treat with dilators, PPI, H2 antagonists. The role of surgical treatment in peptic stricture remains in dispute. Indications include failed aggressive medical therapy or an unsuitable candidate for aggressive medical therapy. This usually is a rare occurrence in the era of PPI therapy. Various procedures advocated include the following:
  1. Esophageal-sparing procedures - Standard antireflux surgery (Nissen total or Belsey partial fundoplication), esophageal lengthening with antireflux surgery (Collis-Nissen or Belsey gastroplasty)
  2. Esophageal resection and reconstruction - Gastric or colon interposition or jejunal segment
• Esophageal carcinoma – depending on what stage tumor is found in either resection or palliation. If found early then resection with possible radiation and chemotherapy. Surgery – transhiatal esophagectomy (simultaneous abdominal and cervical incisions, stomach pulled to neck and joined with pharynx) or Formal Esophagectomy (upper abdominal and right thoracotomy incisions, excision ofesophagus, anastamosis in chest) 80% of patients with E Ca are dead within 1 year

Comments

Peptic strictures are sequelae of gastroesophageal reflux–induced esophagitis, and they usually originate from the squamocolumnar junction and average 1-4 cm in length.

• Two major factors involved in the development of a peptic stricture are as follows:
  • Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients with peptic strictures compared with healthy controls or patients with milder degrees of reflux disease. A study by Ahtaridis et al (1979) showed that patients with peptic strictures had a mean LES pressure of 4.9 mm Hg versus 20 mm Hg in control patients. LES pressure of less than 8 mm Hg appeared to correlate significantly with the presence of peptic esophageal stricture without any overlap in controls.
  • Disordered motility resulting in poor esophageal clearance: In the same study, Ahtaridis et al(1979) demonstrated that 64% of patients with strictures had motility disorders compared with 32% of patients without strictures.
• Other possible associated factors include the following:
  • Presence of a hiatal hernia: Hiatal hernias are found in 10-15% of the general population, 42% of patients with reflux symptoms and no esophagitis, 63% of patients with esophagitis, and 85% of patients with peptic strictures. This suggests that hiatal hernias may play a significant role.
  • Acid and pepsin secretion: This does not appear to be a major factor. Patients with peptic strictures have been demonstrated to have the same acid and pepsin secretion rates as gender-matched and age-matched controls with esophagitis but no stricture formation. In fact, some authors believe that alkaline reflux may play an important role.
  • Gastric emptying: No good evidence suggests that delayed emptying plays a role.

Frequency:

• In the US: Gastroesophageal reflux affects approximately 40% of adults. Strictures are estimated to occur in 7-23% of untreated patients with reflux disease. Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures account for less than 5%.

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