1. Injuries that warrant further exploration solely by mechanism of injury: 
-unprotected (i.e. pedestrian vs vehicle, bike/motorcycle accidents, assault/battery with object)
-high-impact: unrestrained driver, death at scene, fall > 15 feet, ejection from vehicle, etc.
-vulnerable populations: immunocompromised, elderly, chronically ill, many other medical conditions.
2. Evaluating the abdomen s/p blunt trauma (i.e. car accident): 
-Abdomen looks benign, flat, no evidence of injury: can observe unless one of #1 is true.
-Severe abdominal pain: indicates presence of blood or GI contents (both peritoneal irritants), emergency ex-lap
-Significant superficial markers of damage (lots of bruising, a tire mark): need imaging; DPL/FAST if unstable, CT if stable.
-Coma: need imaging, DPL/FAST unstable, CT stable
-CXR showing diaphragmatic hernia or free air: emergency ex-lap
-Unstable vital signs with flat, unchanged abdomen: DPL/FAST, then OR.
-Unstable vital signs with distending abdomen: emergency ex-lap
-Unstable vital signs with obvious pelvis injury: DPL/FAST to r/o abdominal injury (if you see one, emergency ex-lap). Otherwise go to the angiography suite to try to embolize the bleed, also external fixation would be good.
3. Spleen/Liver injury: 
-Spleen/liver injury with perisplenic fluid and unstable vitals: go to OR.
-Grade III or less injury, stable- manage medically.
-Grade IV or higher injury, stable- manage operatively or with angiogram/embolization.
4. Injuries to root of the mesentery often require large forces, such that they are often accompanied by bowel injury. If you see suspicion of such injuries on CT, go to the OR.
5. Neuro trauma:
-LOC < 5 mins buys you observation in the ED for several hours (+/- CT scan, depending on attending)
-LOC >5 mins buys you CT scan, 24 hours obs
6. Coagulopathy in trauma can be due to: 
-Hypothermia-- leads to platelet and coag factor dysfunction. (Hypothermia can also lead to poor tissue perfusion and acidosis)
-Thrombocytopenia from DIC, sepsis, transfusion reaction. Transfuse to > 60

1. Melanoma margins based on Breslow's depth: 

-Melanoma in situ: 0.5-cm margins

-Melanoma with Breslow's thickness <2 mm: 1.0-cm margins

-Melanoma with Breslow's thickness ≥2.0 mm: 2.0-cm margins

2. Sentinel node biopsy based on Breslow's depth: If the Breslow depth is <0.75 mm (or 1mm by some more liberal guidelines), sentinel node biopsy is not necessary as the risk of spread is very low. 

3. The sun should never set on a complete bowel obstruction. If they are partially obstructed, you can NPO/NG/IVF wait it out, but if it's entirely obstructed (obstipation) with a mechanical cause, you should go to the OR. 

4. Very high (>104) fever within 24 hours postop-- must rule out gas-forming would infection. Within first 12 hours, most likely to be C. perfrigens or group A strep. Atelectasis unlikely to cause this high of a fever unless its very extensive. 

5. Postoperative hemoptysis: likely due to PE, other causes: bronchitis, pneumonia, TB, cancer. If the hemoptysis is long-standing, it's most likely to be due to malignancy (or some sort of vasculitis), if the first episode is postop, likely PE. 

6. Postoperative acute hypotension and hypoxia: big PE, MI, tension pneumothorax. ABCs, auscultation should r/o the pneumothorax. Enzymes, EKG, D-dimer.
7. Elective surgery in someone with pulmonary disease:
-If they smoke, they should quit; 6-8 weeks of abstinence is necessary before statistically significant differences in postop pulmonary outcomes.
-Green sputum: rule out pneumonia by getting CXR, listening to lungs. If those are OK, then its' likely just a bronchiits. Give antibiotics, do surgery after the abx are done and the disease resolves. If it seems more like pneumonia (decreased breath sounds on exam, consolidation on CXR, vital sign changes-- tachypnea, tachycardia, decreased sats) then work up and treat the pneumonia before proceeding with surgery.
-Open > Lap surgery in CO2 retainers, as lap surgery adds more CO2 to blood.
-Hemoptysis: rule out cancer. CT +/- bronchoscopy.
-ABGs are good to determine the extent of pulmonary disease; pCO2 > 45 associated with increased perioperative mortality
8. Emergency surgery in someone with pulmonary disease: 
-If someone looks pretty sick and could have pneumonia, get a CXR
-preoperative bronchodilators, limited time on anesthesia, aggressive early postoperative ambulation, IS use, postop pulmonary preventative care.
9. Predictors of cardiac complications after vascular surgery: 
-Q waves on EKG (indicates transmural MI-- non-q-wave MIs are more likely subendothelial, and may progress to transmural during surgery. Workup with thallium stress test to see areas of ischemia, may need revascularization before surgery)
-Ventricular ectopy bad enough to need treatment (>5 PVCs/minute associated with increased perioperative mortality)
-Angina
-Diabetes needing medications
-Age > 70
10. Prophylactic antiobiotics: not necessary in clean wounds, necessary in clean-contaminated and contaminated wounds.

1. Cardiac workup in someone who has suspected ischemic heart disease (i.e. has peripheral arterial disease and other risk factors) in high-risk surgery
-EKG
-Persantine Thallium stress test or dobutamine stress echo (in someone who can't walk on a treadmill for the persantine thallium)
-If reversible ischemia is found, do preoperative revascularization
2. Elective surgery in a patient with liver failure
-Child's A is ok, Child's C is a no-go, Child's B could go either way
-Optimize medically before surgery: k sparing diuretics for ascites, monitor electrolyte status, treat coagulopathy with vitamin K, optimize nutritional status, make them stop drinking.
-Be wary of hemorrhoid surgery in these patients, as portal hypertension can lead to uncontrollable bleeding
2. Elective surgery in a patient with kidney failure:
-If they have a transplant and are in the midst of rejection, surgery will accelerate the process. If the organ is salvageable, salvage it first; if not, go on dialysis and wait until everything (electrolytes, creatinine, hydration/fluids, etc) are stable before proceeding.
-Bleeding intraop: may be due to uremia-induced platelet dysfunction. Desmopressin may help, as will FFP. Platelet transfusion will not help.
-Hypotension intraop without sign of beeding: May be due to adrenal dysfunction from a long history of steroid use. Give stress dose steroids: 25mg intraop, 100 mg in the next 24 hrs.
3. Surgery in someone with mitral valve stenosis:
-If compensated, 5% perioperative mortality. Avoid anything to increase pulmonary hypertension (hypoxia, hypercapnia, acidosis), avoid tachycardia as it decreases diastolic filling, and you'll want endocarditis prophylaxis (ie. abx). Intraop, a-line to monitor pressures, TEE to monitor LV filling. Keep their fluids up enough to get cardiac output, not so high for pulmonary edema.
-Workup: look for a-fib, R heart failure with echo. If they have a-fib, b-blockers for rate control and warfarin for anticoagulation.
4. Surgery in someone with bad heart disease such as MVS + CHF (risk of death is 20%). Critical AS, cardiomyopathy, etc. Do a more extensive cardiology workup, do extensive intraop monitoring.
5. Types of gastric ulcers: 

6. Management of type 1 ulcers: due to mucosal erosion, not to overproduction of acid. During EGD, biopsy to rule out cancer. If its benign, try medical management first: stop all NSAIDs, take PPIs, test for H.Pylori (if positive, treat with PPIs and flagyl+clarithromycin or amox). If medical treatment succeeds, follow up clinical symptoms. If medical treatment fails after 12-18 weeks, consider surgery: distal gastrectomy with some re-anastomosis: billroth I/II or roux en y. NO vagotomy, because theres is no acid overproduction

7. Management of type IV ulcers: also not due to acid overproduction, but erosion. Same medical management, with biopsies. If surgery is needed, you'll need to do close to a total gastrectomy: can connect remaining stomach to jejunum, or just do roux-en-y with esophagus-jejunum anastomosis. 

8. Management of type II ulcers; Usually due to acid overproduction. In addition to the abovementioned medical treatment modalities, consider testing blood gastrin levels to r/o zollinger ellison. Surgery would be highly selective vagotomy plus antrectomy. 

9. Management of type III ulcers; same as type II, also due to acid overproduction. Surgery would be vagotomy & pyloroplasty.

10. Gastric cancer:

-You need a 6cm margin, so if its at the G-E junction you may need to resect the entire esophagus (intrathoracic anastamoses spare more esophagus, but are a disaster if they leak, whereas neck anastomotic leaks are more easily managed) with an interposition graft.

-Comes in 2 types: intestinal and diffuse; Intestinal is glandular and presents like an ulcer, diffuse is signet ring cells that at their worst cause linitis plastica, which is a poor prognostic indicator, and cure is rare even with a total gastrectomy/japanese D2 nodal dissection (incl spleen) 

1. Surgical management of perforated ulcer: primary closure with graham patch
-If there is a history of ulcers through medical treatment (PPIs etc), or a medical need for daily NSAID use, consider doing a highly selective vagotomy procedure at the same time.
-If the patient starts to look septic, or the ulcer looks like its been perforated for a while (>12 hours), then just do the primary repair and get out ASAP.
2. ICU patient that starts to get coffee ground emesis or coffee ground drainage from NG: think ulcer. Treat empirically. If the blood turns bright red, resuscitate with IVF, type & cross, then endoscopy.
3. Endoscopic findings:
-duodenal ulcer with white base: hasn't bled recently, unlikely to bleed. Treat with PPIs/H2 blockers to keep pH>5
-duodenal ulcer with adherent clot: has bled, 10-15% chance of rebleed soon. Mange with endoscopic methods-- injecting epi or sclerosing agents, argon or laser coagulation, suturing.
-duodenal ulcer on top of giant artery: local control endoscopically, go to the OR for definitive repair (i.e. oversewing vessel) within next 24-48 hours.
-duodenal ulcer in ESRD: coagulopathy 2/2 uremia treat with DDAVP or FFP, ESLD: coagulopathy 2/2 platelet sequestration (transfuse, or DDAVP), defect in coagulation factors (FFP/cryo), portal hypertension.
-Gastric ulcer: biopsy to r/o cancer once the bleeding is under control (i.e. within 2 weeks)
4. Gastritis: erosions without ulcers, common in ICU, burns, sepsis, increased ICP, vent patients, trauma, renal failure, etc. Keep pH>5. If that doesn't work, and it still bleeds, you will need to cut out whatever stomach is bleeding-- endoscopic or partial surgery doesn't work.
5. Acute management of bleeding from esophageal varix:
-First: IVF/blood resuscitation, FFP/cryo, platelets (if they are thrombocytopenic), B-blocker, IV octreotide (or vasopressin but that causes coronary vasoconstriction and is CI in people that are old or have a cardiac history), GI banding/ligation
-If that doesn't work: re-scope, band/ligate/sclerose again.
-If that doesn't work: tamponade balloon such as Minnesota (can cause esoph/stomach necrosis, can increase aspiration risk so only can do in people who are intubated, only works while inflated), TIPS, go to OR for portosystemic shunt (50% mortality in emergent cases of people who have bad ESLD)
6. Prevention of future bleeding after successful control of acute variceal bleed:
-In people who have good synthetic liver function and good overall health, TIPS or portosystemic shunt can offset the need for transplant for 5-10 years
-In people who don't have good synthetic liver function, a shunt procedure can be devastating, list them for transplant.
7. Gastric lymphoma:
-Staging: CT C/A/P with IV and PO contrast to look for other tumor, biopsy enlarged nodes, check waldeyer's ring.
-If it's MALToma, eradicate H.Pylori usually cures it.
-If it's stage I or II, surgery, III or IV, chemoradiation.
8. GB: 
-Asymptomatic gallstones: <10% of patients will develop symptoms requiring surgery over 5 years, no surgery unless they are high risk (immunocompromised and can't tolerate sepsis, people with porcelain GB or stones > 3cm since they are assoc with GB cancer development)
-RUQ pain, no fever, doesn't look toxic, mild leukocytosis (<15), mild jaundice: likely biliary colic, schedule surgery. NO antibiotics.
-RUQ pain, fever, thickened GB wall and stones: acute cholecystitis. Usually GNR and anaerobes (e.coli, enterobacter, kelb, enterococcus), treat with 2nd gen cephalosporins with anaerobic coverage (cefotetan, cefoxime). IVF, NPO, NG tube if they are vomiting or nauseous. Lap chole within 2-3 days.
-RUQ pain, fever, stones + elevated LFTs and very elevated bili: probably CBD stone. See other post for determining risk of CBD stone (in brief: Tbili>4 or seeing a stone in CBD on u/s: ERCP for stone removal; if the CBD > 6mm and Tbili 2-3, MRCP then ERCP if its positive). If there's a stone, ERCP then lap chole, or lap chole with intraop cholangiogram.
-GB cancer: open chole + wide resection of liver, with 2-3 cm margins around GB.
-Polyp: excise if >2cm in size because of 7-10% risk of developing adenocarcinoma.
-Porcelain GB: 50% risk of developing adenocarcinoma.
9. Hepatic masses:
-cyst with no internal echoes: simple cyst, leave it alone or if there are symptoms, drain and inject w sclerosing agent
-cyst with internal echoes: likely echinococcal cyst, inject w sclerosing agent
-cyst + signs of systemic infection: bacterial/amebic abscess. Serologies to r/o amebic abscess. Drain bact abscess + abx, flagyl for amebic abscess.
-hepatic adenoma: assoc with OCP use, resect if it's big because there's a greater chance of rupture (esp during pregnancy)
-solid mass: r/o hemangioma (w tagged RBC scan), then biopsy. Check afp, cea.
10. Resectable HCC:
-1 cm  margins attainable
-not invading vessels
-<5cm in size
-solitary
-noncirrhotic liver
-NO METS (look at hepatic hilar nodes, celiac nodes, diaphragm, local structures). CT C/A/P to look for mets.

1. The two most effective chemotherapy regimens for advanced pancreatic cancer are gemcitabine-abraxane and FOLFIRINOX (folate, 5-FU, irinotecan, oxaliplatin). Gem-abraxane is less toxic, but less effective; if the person is relatively young and healthy, go for folfirinox; gem-abraxane if they can't take it.
2. Most common presenting symptom of cholecysto-duodenal fistula: gallstone ileus (the enlarged stone pressing upon the small bowel is thought to lead to erosion and fistula formation). Most common presenting symptom of cholecysto-colonic fistula: bile in the stool (bypasses absorption in terminal small bowel)
3. Subcostal vs vertical incision: subcostals offer better lateral access (distal panc, splenectomy, liver) but cutting the rectus muscles leads to more pain, and later on there can be problems with muscle pooching during engagement of the abdominal muscles. Studies focusing on the effect of subcostal incisions (theorized effects on wound healing, incidence of respiratory complications post-op) have not found conclusive evidence.
4. Fecal elastase < 200 indicates pancreatic insufficiency, <50 will lead to steatorrhea.
5. Neuroendocrine tumors: definitive classification requires positive staining with chromogranin and synaptophysin. These tumors are clinically sub-categorized-- i.e. gastrinoma is defined by elevated levels of blood gastrin, not histological staining for gastrin. These tumors are often hypervascular on CT, rendering them easily confused for vessels. They are often slow growing.
6. PNET tumors: Ki67 expression is associated with worse outcomes: >20% is associated with significantly increased mortality (i.e. poor 5-year survival) relative to <5% (excellent 5-year survival). The liver is a common site of metastasis/recurrence after resection; visible lesions can be resected, however dissemination is often widespread. These tumors grow slowly, but invariably. Tumors <2cm with no radiographic evidence of spread and no symptoms can be watched at 6-mo screening intervals. Larger ones should be resected-- enucleation to manage symptoms in benign masses, oncologic resection with margins for more malignant tumors. For patients with small tumors who request surgery out of nervousness; consider the fact that the point of surgery is to either manage symptoms or prevent recurrence. If they do not have symptoms (i.e. non secreting tumor), they will gain no benefit if you do not attempt a full oncologic resection with an attempt to get negative margins (i.e. whipple); a compromise in the form of an enucleation still subjects them to surgical risk with no proven benefit.
7. You can treat unresectable liver metastases with isolated hepatic perfusion: cannulate GDA to IVC above liver, clamp common hepatic artery to prevent back-flow, run high-dose chemotherapy through circuit. Percutaneous veno-veno bypass IVC below liver to subclavian to maintain preload, clamp portal vein. This has morbidity, including possibility of liver failure-- screen patients well before for pre-existing liver pathology. Liver transplant is a possible treatment for pancreatic neuroendocrine tumors with liver mets.
8. Clavicle fractures: do angiogram and neuro exam on extremity to r/o neurovascular damage (brachial plexus, subclavian). Middle clavicle fractures- closed reduction, figure of 8 brace. Distal clavicle may need ORIF.
9. Ankle-brachial index (compare dorsalis pedis or posterior tibial to brachial aa, leg/arm systolic pressure): normal is 1-1.3, <0.9 is sensitive and specific for >50% occlusion of artery, <0.4 is c/w limb ischemia. Measure with a sphingomanometer and doppler distal: instead of listening, you use the doppler. Inflate cuff, when you see the signal first return that is the systolic pressure.
10. Post-cholecystectomy jaundice ddx: 
-Retained stone in CBD
-Stricture
-Bile leak
-Cholestasis 2/2 other disease process (i.e. sepsis)
-Cut the CBD instead of cystic.

1. Generally, in a surgical abdomen, pain precedes nausea/vomiting, while the reverse is true of a medical abdomen.
2. In clinically obvious appendicitis (pain started in umbilicus, moved to RLQ, severe pain, anorexia, rebound, guarding, rigid abdomen, +psoas sign, +Rovsing's sign, elevated WBC, fever) no CT scan is necessary, just go to the OR. Sensitivity of H&P is >95%. Groups where there's a higher false-negative (ie. negative ex-lap) rate: women of childbearing age, elderly people. For them, CT is indicated.
3. In a patient with trauma to both abdomen and pelvis, with an inconclusive FAST exam, do a DPL before you go to the OR.
4. Risk factors for gastric cancer: 
-H.Pylori infection
-History of atrophic gastritis
-Diet: high-salt (damages mucosa), nitrosamines (smoked foods)
-Lifestyle: Obesity, Smoking (NOT alcohol)
-History of gastric cancer (billroth II > billroth I, 2/2 alkaline reflux)
-Genetic: type A blood, hereditary diffuse gastric cancer (e-cadherin truncation mutation, also predisposes to lobar breast cancer)
5. Workup/staging for gastric cancer: 
-CT C/A/P with IV and PO contrast-- to look for mets
-EGD to find the exact location, EUS for depth of invasion and nodes.
-Laparoscopy
The first of these will inform you about the role of preoperative chemotherapy, and whether you should operate at all.
6. PET scans have no role in the workup of gastric cancer-- only 2/3 of these cancers are PET sensitive, false negative and positive reactions are common. Cancers for which PET scans are shown to be beneficial in diagnosis: melanoma, RCC, lymphoma. Cancers for which PET is not shown to be beneficial: gastric, pancreatic.
7. Treatment regimens for gastric cancer: 
-Mcdonald's protocol, SW oncology group trial 0116: surgery followed by chemotherapy and radiation
-Cunningham trial: chemotherapy first, then surgery, then more chemotherapy
-If you do a total gastrectomy, reconstruct with roux-en-y: more physiologic than billroth II.
8. Surgical management of ulcerative colitis: 
-proctocolectomy with end-ileostomy: pros- one surgery; cons- permanent ostomy
-ileal pouch anal anastomosis: pros- no ostomy; cons- risk of pouchitis (up to 50% incidence), frequent BM ranging from 4-12 times a day, anastomotic leak, may take up to 3 surgeries (end ileostomy, pouch creation and anastomosis with diverting ileostomy, ileostomy takedown)
9. Risk of PSC with UC decreases with colonic resection-- thought to be due to less formation of memory neutrophils. Risk of re-developing PSC in a transplanted liver thought to be up to 50%
10. Diagnosis of UC does not require imaging, it is a clinical diagnosis. However there are imaging modalities that can be used:
-CXR to see toxic megacolon
-CT to see nonspecific wall thickening and fluid
-Barium enema: can see psuedopolyps, lead pipe sign, ulcers
-Colonscopy: full circumferential involvement (no skip lesions)

1. Contraindications to whipple:
-Mets: this is an absolute CI. Mets to liver, pancreas, omentum, extra-abdominal sites, celiac LN and other LN not removed by surgery. If you see these on laparoscopy, close and go home.
-Involvement of SMA, IVC, aorta, celiac aa, hepatic aa
-Encasement (>50%) of portal vein-SMV confluence
2. Infections/inflammation can cause ileus: pneumonia, UTIs, nephrolithiasis, appendicits, pancreatitis, sepsis, etc. Someone with a spinal cord injury with distention and obstipation is a UTI until proven otherwise.
3. The incidence of UTI is much higher among people with spinal cord injuries-- the neurogenic bladder leads to urine stasis and frequent caths, which introduces bacteria into the urine. In fact, most of these patients' urine is always colonized with bacteria, rendering the diagnosis of acute UTI difficult. Current diagnosis are >100 cfu/mL; >50 wbc/hpf indicates severe pyuria.
4. Microbiology of UTIs in spinal cord injury: usually polymicrobial, often the bugs form dense biofilms that are difficult to treat: proteus, klebsiella, pseudomonas, serratia, providentia, plus staph and enterococci. There's some data that intentionally colonizing the bladder with less virulent organisms (e.coli) decreases morbidity. Empiric treatment is with fluroquinolones, watch out for the side effects. In-hospital management options; amp/gent, imipen/cilastatin, b-lact/b-lactamase inh, 3g cephalosporin, aminoglycosides. Treat for 7-14 days (as short as 4-5 in those with more clinically benign presentation). If it doesn't get better in that time-frame, evaluate further for stones or aberrant anatomy, re-culture to look for resistant bugs.
5. Prophylaxis and management of asymptomatic bacteriuria in SCI: Because so many are colonized, the threshold to treat is high to avoid overtreatment: some advocate treating >10,000 cfu/mL plus >8-10 wbc/hpf. Prophylactic bactrim reduces incidence of UTI, but may increase resistance. Some advocate alternating methenamine (turns into formic acid which is bacteriostatic) TID with nitrofurantonin BID, alternating q2 mos.
6. Lesions above T6 can result in autonomic dysreflexia to noxious stimuli (such as an over-distended bladder), whereby spinal levels below the injury have uninhibited sympathetic output, resulting in severe vasoconstriction and reflex bradycardia; treat with alpha-blockers.
7. Septic thrombophlebitis: palpable cord on skin, with overlying erythema or pus: incise and pop it out. Ice, elevation, NSAIDs.
8. The small bowel does not tolerate radiation: radiation enteritis occurs in nearly 50% of those irradiated. Radiation causes damage to mucosa (erosion/ulceration, ischemia, fibrosis) which can lead to lifelong symptoms of pain, diarrhea, malabsorption, hematochezia, even obstuction/perforation. A significant portion (20%?) of those who get radiation to the rectum end up incontinent.
9. Hypokalemia worsens ileus
10. In someone who has been vomiting, they lose H+Cl through vomiting, there is also a contraction alkalosis (via aldosterone? lose K and H in urine). Treat with fluids-- NS, to replenish Na-Cl and volume.

1. AAA: more pain = increased likelihood of rupture = more emergent
2. Subclavian steal can happen with vertebral aa; someone who experiences arm claudication and neurological symptoms at the same time needs a doppler of their subclavian artery.
3. In evaluating peripheral arterial disease, look for a gradient on doppler; the presence of one indicates stenosis, and thus ability to be resolved with bypass graft. No gradient means the problem is in the smaller vessels, which will not be fixed with surgery. Do an angiogram to find the stenosis and a good distal vessel; smaller blocks can be stented, bigger ones need grafts. Do not do prophylactic grafts, wait until the symptoms interfere significantly with normal life (until then, lifestyle changes and cilastazol). When evaluating perfusion with the doppler, if they don't have symptoms at rest, you may need to induce exercise in order to get good findings.
4. Skin cancers: diagnose with full-thickness punch biopsy at margin including normal skin.
-Basal cell, ulcer or raised waxy lesion, favor face above mid-lip line, do not metastasize, 1mm margins.
-Squamous cell, ulcerated lesion, favor below mid-lip line, can metastasize, need up to 2 mm margins, LN dissection if margins+
-Melanoma: <1mm invasion good prognosis, 1-4 do aggressive resection and LN dissection, >4 bad prognosis. Mets to weird places, unpredictable course
5. Optho: 
-Strabismus in a kid that develops later in infancy may be due to refraction error; glasses will correct immediately.
-Glaucoma: frequently presents as pain and seeing halos around lights after a long session of dilated pupils (movies/TV at night). Physical exam, eye is hard, cornea is greenish, pupil is mid-dilated and non-reactive. Next step: refer to optho, in the meantime treat with diamox (carbonic anhydrase inhibitor) or mannitol, topical b-blockers, a2-agonists, or pilocarpine.
-Orbital cellulitis: key is pupil is dilated and non-reactive, no extraocular movements. Next step: emergency CT and drainage
-Retinal detachment signs: flashes of light + floaters (more floaters= worse outcome). Bad signs: see snowstorm in eye, curtain coming down.
-Emboli to opthalmic artery: sudden loss of vision. Breathe into paper bag and have someone press and release on their eye: the idea is to vasodilate and propel clot further downstream so a smaller part of the retina is lost to ischemia.
-Every new DM diagnosis needs to have a retinal evaluation, since it may have been undiagnosed for years.
6. Peds ortho diagnosis & management: 
-DDH: dx with ortolani and barlow, tx abduction splinting with pavlik harness for 6 mos
-Legg-Calve-Perthes: dx with AP and lateral xrays, treat with casting and crutches
-SCFE: sole of affected foot points towards other foot; when you flex the hip, the thigh will not internally rotate; AP x-rays. Tx: surgery to pin the femoral head into place.
-Septic hip: toddlers who hold their hip flexed, abducted, and externally rotated, resistant to motion. Aspirate joint fluid to r/o transient synovitis (also: Kocher criteria, fever>101.5, ESR>40, WBC>12, non-weight-bearing, >2 criteria = >40% chance of septic hip), open drainage if the aspirate is pus. Antibiotics to cover gram-pos.
-Osteomyelitis: bone scan, antibiotics
-Genu varum: no treatment until age 3, at which point it's blount disease (medial growth plate overgrowth), surgery to shave it down.
-Genu valgus normal between age 4-8.
-Osgood Schlatter: TTP at tibial tuberosity or with quad flexion. Treat by putting knee in extension cast for 4-6 weeks
-Club foot (plantarflexion, inversion, adduction of forefoot). Serial casts to correct first adduction, then  inversion, then plantarflexion. 50% are corrected this way, the other half require surgery after 6-8 mos but before 1-2 years.
-Supracondylar fractures (along with growth plate fractures, are worrisome in kids): 2/2 hyperextension of elbow from fall on extended arm. Volkmann contracture can occur-- from damage to brachial artery either directly or via compartment syndrome, leading to ischemia, and later fibrosis of muscles of the arm. All muscles are affected, but the flexors are more numerous and stronger than extensors, so there are more flexor than extensor features; both are engaged, so it is painful to attempt to straighten the fingers. Treat these fractures with normal casting, but watch out for the development of these contractures
-Growth plate fractures: closed reduction if the growth plate is in one piece and it's laterally displaced from metaphysis, ORIF if its any more complex.
-Osteosarcoma: ages 10-25, around knee, sunburst. Ewing's 5-15, diaphysis of long bones, onion skinning.
7. Adult ortho
-Bone pain, suspect mets: bone scan first, then x-ray, because bone scan is more sensitive but less specific and x-ray is vice-versa.
-Old man with anemia, bone pain, protinuria, hypercalcemia: think multiple myeloma. Tx with chemo, or thalidomide if chemo fails.
-Sarcomas metastasize to lungs, not LN.
-Closed reduction: fractures that are not badly displaced/angulated that can be easily reduced.
-Clavicle fracture: figure of 8 device for 4-6 weeks
-Shoulder dislocation: anterior (arm is adducted and externally rotated, may have some deltoid numbness from axillary nerve stretch), posterior (adducted and internally rotated)- rare, occurs after massive muscle contraction (seizure, electrical burn), may go undetected for a long time; need axillary or scapular lateral x-rays.
8. Ortho specific fractures: 
-Colles fracture: fall on extended wrist, radius displaced dorsally, "dinner fork" wrist. Tx: closed reduction, cast.
-Monteggia fracture: blocking a nightstick. Fracture of proximal ulna, anterior displacement of radial head (part closer to elbow)
-Galeazzi fracture: fracture of distal radius, displacement of distal ulnar posterior.
-Scaphoid fracture: fall on extended wrist, fracture of scaphoid, TTP over anatomical snuffbox. Tx with thumb spica cast even if x-rays are negative (i.e based on history/physical); these are notorious for non-union.
-Metacarpal neck fractures: usually 4th/5th, from punching with a closed fist; closed reduction and unlar splint if its mild, ORIF for bad.
-Hip fractures: femoral neck (esp displaced) need total hip replacement since it's likely to damage vascular/nerve structures; intertrochanteric needs an ORIF with pins, diaphyseal can treat with intramedullary rod fixation.
-Complex bone fractures: if they are open need OR fixing within 6 hours, comminuted can lose a lot of blood, watch out for shock; if they are multiple watch out for fat emboli
-Collateral ligament: knee swelling, TTP on affected side; knee flexed 30 degrees, passive ab/adduction wil make pain. Tx with hinged cast, surgery if there are multiple injuries
-ACL: anterior drawer. Surgery if its someone whos going to be active, can immobilize and do rehab if its a relatively immobile person.
-Meniscal tears: hard to dx on physical, show up great on MRI. Protracted pain and swelling, knee catches and "clicks" upon extension.
-Tibial stress fractures (shin splints): TTP over specific point, x-rays will be normal at first. Treat with cast/crutches, re-x-ray in 2 weeks.
-Achilles injury: popping sound. Cast in equinus position.
9. Ortho emergencies: 
-Pain under a cast is never OK to be watched-- always take off the cast and look at the limb. Forearm and lower leg most likely to develop compartment syndrome.
-Posterior hip dislocation: patient holds leg adducted, flexed, internally rotated. emergency reduction to avoid fem head ischemia.
-Gangrene: looks toxic, treat with high dose IV Penicillin, debridement, hyperbaric oxygen.
-Radial nerve injury: from upper humerus oblique fractures. Weakness of hand extension. If it doesn't get better with closed reduction, the nerve is caught, go to surgery.
-Posterior knee injury: watch out for pop artery damage (get pulses). If you missed it for a while, do prophylactic fasciotomy.
10. Ortho, arm and hand and feet: 
-Anterior arm dislocation, worry about axillary nerve damage.
-Humerus fracture, worry about radial nerve damage.
-De Quervain's tendonsynovitis: hand flexion and thumb extension, pain in tendons of anatomical snuffbox, worsened by flexing thumb and ulnar-devation of wrist
-Trigger finger: finger acutely flexed,  tendon caught on tendon sheath, treat with steroid injections
-Depuytren's contracture: finger contracture, palmar nodule, treat with surgery
-Gamekeeper thumb: ulnar collateral ligament of thumb injury, caused by hyperextension, treat with casting
-Morton's neuroma: mass or tender point between 3rd and 4th metatarsals. Inflamm of common digital nerve.

1.Differential Acute Abdomen: 
-Perforation: sudden onset, pain is constant, generalized, and very severe; classic peritonitis signs-- no movement, rebound, guarding. Examples: perforated gastric ulcer, perforated bowel.
-Obstruction: sudden onset, colicky pain, location and radiation indicates its source; patient is moving all over the table, can't get comfortable. If there is a bowel obstruction, there may also be distention, nausea, vomiting, anorexia. Examples: biliary colic, nephrolithiasis, small bowel obstruction
-Inflammation: gradual onset (gradual buildup over 6-12 hours), pain is constant, starts generalized and localizes. Peritoneal signs are found where the process is occurring, usually there are systemic signs of fever/leukocytosis except pancreatitis. Examples: appendicitis, pancreatitis
-Ischemia: gradual onset, severe pain out of proportion to exam, blood in the gut (the only process that combines acute abdomen with GI bleed). Get a lactate.
2. When facing an acute abdomen, first rule out everything that is not surgically managed, then go for an ex-lap to find and fix the problem.
-Lower-lobe pneumonia: CXR
-MI: EKG, enzymes
-PE: d-dimer
-Primary peritonitis (i.e. infection of extant ascites: treat with abx)
-Pancreatitis: amylase, lipase
-Nephrolithiasis: KUB or CT
-Diverticulitis: CT (manage with IVF, NPO, antibiotics, go the OR if things worsen)
3. Jaundice may be hemolytic, hepatic, or obstructive: 
-Hemolytic: bilirubin high but not very high (<10 not >30), indirect fraction elevated. Next step: labs to figure out the cause of the hemolysis (haptoglobin, autoimmune workup, pregnancy test, genetic workup for G6PD, LDH deficiency, thalassemia)
-Hepatic: both indirect and direct bilirubin elevated, AST/ALT often very high, alk phos not very high. Next step: labs to determine the cause of the hepatitis (viral serologies, labs for wilson's, tylenol levels)
-Obstructive: direct bilirubin elevated, alk phos through the roof. Next step: ultrasound to look for dilated bile ducts, examine gallbladder for stones and for thickness; stones in CBD are rarely seen. Thick gallbladder full of stones, think choledocolithiasis: do ERCP to remove stone, do sphincterotomy, schedule later cholecystectomy. Thin gallbladder: think cancer, do CT scan to look for cancer (head of pancreas, cholangio, duodenal ampulla). If the CT scan is positive for a mass, do a percutaneous biopsy; if it's negative, do an ERCP/EUS to get a closer look, as they can see smaller masses that would be missed on CT.
4. Cancers leading to obstructive jaundice:
-Head of Pancreas, poor prognosis even with whipple;
-Ampullary (obstructive jaundice + GI bleed), good cure rate with whipple
-Cholangiocarcinoma: very high alk phos, good prognosis if extra-hepatic or small
5. Range of cholestatic processes: 
-Acute Biliary Colic: stones that temporarily impact cystic duct, pain attacks that last 10-30 minutes. Triggered by fatty meals, accompanied by nausea and vomiting but no systemic signs. Treat with anticholinergics. Diagnosed by visualizing stones on u/s. Schedule elective cholescystectomy.
-Acute Cholecystitis: stones in the cystic duct that remain lodged until an inflammatory process develops in the gallbladder. Pain progresses to constant, modest systemic signs, modest peritoneal signs. No LFTs, u/s shows thickened gallbladder, pericholecystic fluid, stones in GB. Treat with bowel rest- NG, NPO, IV fluids, antibiotics. If things improve, schedule elective cholecystectomy. If they do not improve, do emergency cholecystectomy or percutaneous transhepatic cholecystostomy for those who cannot tolerate surgery.
-Acute ascending cholangitis: stones have reached CBD, are partially obstructing, and there is an ascending infection. Strong systemic signs of infection-- fevers to 105, chills, high leukocytosis, sepsis-like picture. Labs show elevated bilirubin and very elevated alk phos. Treat with IV antibiotics and emergent CBD decompression-- ERCP or percutaneous transhepatic cholangiogram (to put in a drain), schedule cholecystectomy soon.
6. Range of pancreatic processes:
-Acute edematous pancreatitis: occurs after heavy meal or bout of pancreatitis, constant pain radiating to back, with n/v, mild peritoneal signs over epigastric region, elevated serum amylase/lipase, elevated hematocrit. Treat with bowel rest, will resolve in ddays
-Acute hemorrhagic pancreatitis: begins with edematous form, but with a lower hematocrit, + other Ranson's criteria (elevated WBC, low Ca, elevated glucose, and then sepsis-like picture with pre-renal labs, metabolic acidosis, hypoxia). Finally multiple abscesses develop.
-Acute suppurative pancreatitis (pancreatic abscess): develop fever and leukocytosis ~10 days after the onset of symptoms, treat with percutaneous drainage.
-Pancreatic pseudocyst: occurs 5 weeks after acute pancreatic incident (pancreatitis, trauma). Collection of pancreatic fluid in cyst, compressive symptoms of stomach (early satiety, mass on deep palpation, vague discomfort), diagnose with CT. For cysts that are <6cm or <6 weeks old, can be observed. For larger or older cysts, manage with drainage (percutaneous, endoscopic) or surgical removal.
7. Causes of surgical hypertension: 
-Primary aldosteronism: either adrenal cortical adenoma or hyperplasia. Key to diagnosis: hypokalemia and hypertension in someone not on diuretics; mild hypernatremia, metabolic alkalosis. Hyperplasia will respond appropriately to position, adenoma will not. Renin is low in both.
-Pheochromocytoma: diagnose with 24 hour urine VMA or metanephrines, or octreotide/MBIG scan.
-Renal artery narrowing (fibromuscular dysplasia in the young, bad PAD in old): stent in young, may not be worth operative risk in old.
-Aortic coarctation: correct when there is a >50mmHg gradient, or signs of angina, syncope, CHF.
8. Post-op low urine output: in the face of good perfusion (ie. not shock) it's either inadequate volume or intrinsic renal failure. Test with 500mL or 1L fluid bolus-- if the UOP goes up, it was inadequate volume. If it doesn't change, it may be renal failure. Also can test with FeNa
9. Electrolytes:
-Hypernatremia: due to loss of free water. Replenish with D5 half NS if it was grandual onset, D5W if it was fast-onset.
-Hyponatremia: too much water. Either too much ADH in the context of normal volume, or loss of volume (diarrhea) without replenishing isotonically. In the former, fluid-restrict; in the latter, infuse isotonic fluid- LR, NS.
10. Lung lesions;
-Coin lesion on x-ray, in someone >50 has an 80% chance of being malignant. First step: compare with previous CXR. Next step: CT (chest + liver) & sputum cytology + maybe PET. After this you start getting into invasive tests, so you have to decide if the tumor is operable (mets to mediastinum/carina/liver/other lung) and if the person could survive treatment (FEV1, then determine % lung contribution with vent-perfusion scan, if FEV1 remaining <800, don't do surgery). Then, next step: percutaneous biopsy (peripheral) or bronchoscopic biopsy (central). Next step: thoracotomy/wedge resection.

1. Most missed injuries in abdominal survey during trauma:
-G-E junction
-Ureters
-Ligament of treitz
-Mesenteric borders of small bowel
-Posterior wall of transverse colon
-Extraperitoneal rectum
2. "Bail out injuries": i.e. injuries such that if you see these intra-op, do not attempt to completely fix everything in one go. Convert to damage control surgery. Depending on how stable they are, either fix the most life-threatening injuries, or just pack it and get out. Either way, leave the abdomen open and go the ICU. Resuscitate, wait until they are more stable, then go back to the OR to fix things.
-Significant vascular injury plus hollow viscus injury
-Penetrating injury to aorta or IVC
-High grade liver injury
-Pelvic fracture with expanding hematoma
-Injuries requiring simultaneous surgery elsewhere-- thorax, head, neck.
3. Trauma triad of death: hypothermia, coagulopathy, acidosis. These signs are an extremely poor prognosis. If you wait for these to come on before you decide to close and go to the ICU, it will be too late.
4. Intraoperative cues of impending hostile physiology (i.e. precursors to trauma triad of death): if you see these signs, stop operating as quickly as possible, get to the ICU.
-Diffuse oozing
-Bowel mucosa edema
-Midgut distention
-Dusky serosa
-Noncompliant, swollen abdominal wall
5. Options for bleeding vessel control:
-sutures
-packing
-packing + hemostasis agents (surgicel, floseal, thrombin)
-if is a big vessel, you can insert a foley catheter into it, blow up the cuff and pull up
6. If you're operating a long time on an extremity and doing vascular surgery, consider a presumptive fasciotomy to stave off compartment syndrome.
7. Postop fever etiology mnemonic 
-POD 1-2 wind (pneumonia)
-POD 3-4 water (UTI)
-POD 4-5 walking (DVT/PE)
-POD 5-7 wound
-POD 7+ wonder drugs (drug fever - esp anticonvulsants & bactrim)
8. On the pupillary light reflex: {source}
"Because of the different paths these two nerve supplies take, brain and brainstem
trauma interrupt the sympathetic and parasympathetic tracts in different patterns.
Consequently, the pupillary reflex can be a valuable assessment tool. For example,
damage to the hypothalamus destroys only the sympathetic branch allowing the
parasympathetic to predominate. Parasympathetic nerve supply causes constriction with
reaction to light. In the lower brainstem (pons and medulla), damage causes a similar
response, but more exaggerated. In this case, the pupils are tightly constricted
(“pinpoint”) and unreactive or “fixed.” Notice that midbrain, mesencephalon, damage
disrupts both the sympathetic and the parasympathetic pathways resulting in pupils being
midposition and “fixed.”

In usual situations, both pupils respond similarly (bilaterally). However, if the
parasympathetic occulomotor nerve is damaged outside the brain and at some point along
its course to the eye, parasympathetic supply is disrupted only to that one eye. In the affected eye sympathetic predominates and the pupil dilates while the other eye remains
normal. This condition is common with temporal lobe herniation as the protruding lobe
of the brain presses on the occulomotor nerve on the herniated side. Thus, the dilated
(“blown”) pupil indicates the side of herniation."

9. Fixed, dilated pupils are possibly due to brainstem ischemia, as well as to cranial nerve III compression by uncal hernation. {Neurosurgery, 162 patients GCS<8 underwent xenon CT scans to determine blood flow, found significantly higher brainstem  blood flow among those with fixed, dilated pupils vs reactive pupils; pupil reactivity/size did not correlate with ICP or the presence of a brainstem lesion} 

10. Uretopelvic junction obstruction: able to tolerate normal urine outflow without trouble, but fails when there is a large diuresis-- hence the adolescent presenting symptomatically (with colicky flank pain) after their first binge-drinking session 

1. Preparing for trauma surgery:
-2 large bore (18 g) peripheral IVs is better for resuscitation than a central line. In a trauma situation, if you got 2 big peripheral IVs, don't waste time getting in a central line for the purposes of getting in fluids. You don't need it.
-Get an A-line.
-Prep and drape before you induce anesthesia; induction can drop perfusion, and you want to be ready to go immediately if you start losing vital signs.
-For emergency ex-laps in an abdominal trauma situation, prep chin to knees: you may need to enter thorax, you may need to harvest vein grafts from the legs.
2. Emergency surgery on a traumatic abdomen: 
-Get in fast: 3 passes of the knife and in. Don't waste time getting in clean and slow with the bovie.
-Above the umbilicus, the pre-peritoneal fat is really thin, so you can just push your finger through it, and then lift up the peritoneum with your hand and bovie between your fingers.
-As soon as you get in, pull out all the bowels so you can see what's bleeding.
3. How to pack a bleeding liver: pack above, below, and anywhere inside (i.e. if there is an avulsion) where it's bleeding
4. Retroperitoneal bleeding: when to surgically explore vs medically manage
-Zone 1 (central abdomen): explore
-Zone 2 (lateral abdomen): explore if the patient is unstable, the hematoma is expanding, the injury mechanism is penetrating, or there is obvious injury to a vessel or the colon. Otherwise, in blunt trauma, leave it.
-Zone 3 (pelvis): explore if there was penetrating injury. For blunt injury, better go to IR.

5. Pringle Maneuver: clamp across hepaticoduodenal ligament/portal triad, controls liver hemorrhage. Maximum time debated, around 30-45 minutes. 

6. Kocher Maneuver: incise the bloodless plane to the R of the duodenal C-curve, that will allow you to flip the duodenum and head of pancreas to the L and expose the aorta and IVC, SMA/SMV, gonadal and renal vessels. 

7. Mattox Maneuver: incise the white line of toldt lateral to the descending colon, flip up the colon to the opposite side, rotate up the spleen, either leave kidney in place (if its damaged and/or surgical target) or flip kidney out of the surgical field if its intact, you gain access to IVC/aorta and L renal vessel. 

-Pitfalls during mattox maneuver: you can injure the kidney or spleen in your manipulations, or you can injure L lumbar vv (comes off L renal) 

8. Cattell-Braasch Maneuver: similar to Mattox, but on the R side, and slightly more involved. You have to do the Kocher maneuver, then incise the white line of toldt on the right side, then connect the two together. Then, importantly, you have to extend the incision from the bottom of the white line of toldt across the mesentery of the small bowel, diagonally towards the ligament of treitz. Do not cut any mesenteric vessels while you do this. Then you can lift the whole thing over to the L and have exposure to the great vessels. 

-Pitfalls: do not cut R gonadal vein or SMV. 

9. Maneuver to get to thoracic aorta for cross-clamping when all else fails and you can't control the hemorrhage: incise through hepatogastric ligament, along the lesser curve of the stomach to enter lesser sac. Retract the stomach down and lateral, you should now be able to get behind stomach and esophagus and see the aorta coming out of the aortic hiatus, with the diaphragmatic crus on either side. Cut through the crus (they will be soft) to get maximally high on the aorta, and cross-clamp. Note, this is only for massive hemorrhage that is leading to impending crash despite your best efforts at packing. 

10. Retroperitoneal bleeding can track between the fascial planes, around the kidney, down into the pelvis, up into the upper abdomen. 

1. Principles of damage control resuscitation: 
(applied to trauma patients in hemorrhagic shock)
-Permissive hypovolaemia (hypotension): sacrifice perfusion for hemorrhage control. Titrate pressures (with 250mL boluses) to mental status in awake patients, or to palpable radial pulses, or to systolic > 70-80 in penetrating and >90 in blunt trauma. Too much volume, esp with non-FFP, leads to worsening of hemorrhage, dilution of coag factors and loosening of platelet plugs, also increases ICP.
-Haemostatic transfusion (resuscitation): 1:1:1 of FFP, pRBC, platelets + tranexamic acid if you can give it within 3 hours (PROPPR trial currently underway to eval 1:1:1 vs 2:1:1 ffp/rbc/platelets). Avoidance of crystalloids (NS, Hartmann’s, LR) and colloids (gelofusion, haemaccel, or volulyte), they dilute out clotting factors and hemoglobin and worsen hypothermia.
-NO PRESSORS: early vasopressor use is independently associated with an increased risk of death with published HR's ranging from 2 to 17(!!); that means that they are associated with increased mortality after adjusting for severity of injury and volume status. Use only if cardiovascular collapse is imminent and all attempts to resuscitate with fluids have failed (i.e. patient not fluid responsive)
-Damage control surgery or angiography to treat the cause of bleeding
-Once hemostasis is achieved, restore organ perfusion and oxygen delivery with definitive resuscitation
source: {BMJ Review Paper}
2. Optimal volume status: 
-A&O x3
-UOP 0.5-2.0
-CVP<15
In adults, optimal fluid access is 2 peripheral 16 gauge IVs. If unavailable, go to femoral central line (fastest, easiest to insert line; only CI is if you suspect massive IVC injury, in which case you'll have to go for IJ or subclavian) or saphenous vein cut-down. In children <4, IO (prox tibia) is second choice.
3. Shock diagnosis: 
-Hypotensive, low CVP: either hemorrhagic/hypovolemic (pancreatitis, burns, peritonitis, diarrhea) or vasomotor (i.e. anaphylaxis). Fluids will help in both, but the former will be much more responsive to fluids. Pressors will worsen things in the former, ameliorate in the latter.
-Hypotensive, high CVP: tamponade (u/s to r/o) vs tension pneumo (listen to lungs) vs cardiogenic failure from massive MI. In these cases, don't push fluids.
4. Cranial trauma:
-Linear fractures: if closed, leave to heal. If open (have wound over it) go to OR to close wound; if comminuted or depressed, go to OR to fix fracture.
-Skull base fractures: observation, no antibiotics unless indicated for some other reason, CT c-spine to evaluate for damage.
-LOC in the context of a head injury-- always get a CT to r/o bleed.
-Neurological damage from trauma comes from 3 places: initial blow, bleeding that causes midline shifts (manage surgically) and increased ICP later (manage medically).
5. Acute brain bleeds:
-Epidural: ends with fixed dilated pupil on ipsilateral side, decerebrate on opposite side. Emergency craniotomy leads to impressive recovery.
-Subdural: usually really bad trauma, really sick patient; if there is a midline shift go for craniotomy, if not, put something in to follow ICP (i.e. IVC) and manage medically to prevent more ICP: hyperventilation, fluid underload, mannitol/lasix, head of bed > 30 deg, sedation/hypothermia to decrease O2 need. Try not to drop systemic pressures so low that you start losing other organs, but realize that the brain takes priority. Prognosis is poor.
-Diffuse axonal injury: surgery only if there is hemorrhage. Otherwise maintain ICP medically.
-Chronic subdural: surgical evacuation provides rapid cure.
6. Penetrating neck trauma:
-Go to surgery only if there are signs of expanding hematoma, deteriorating vital signs, or obvious signs of esophageal/tracheal injury (coughing up blood). For GSW to upper neck, do angiograms; for lower neck, angiograms, gastrografin then barium swallow if gastrografin shows no leak, scopes of trachea and esophagus. Knife wounds: watch.
-CT c-spine for everyone
7. Spine injury:
-Transection (nothing below), Brown Sequard (lose pain/temp contra, feeling/motor ipsi): clean cut
-Anterior cord (lose STT/CST, fine DCML = no pain or temp or movement, OK positional and vibratory senses): vertebral burst fractures
-Central cord (lose STT/CST = so burning pain and paralysis in limbs): forced neck hyperextension in old people, i.e. getting rear-ended.
-MRI to evaluate, steroids (don't help if it was transected)
8. Chest injury facts:
-Rib fracture can lead to pain, atelectasis and eventually pneumonia
-Pneumothorax: chest tube anterior, superior
-Hemothorax: chest tube posterior. Lung is low pressure, bleed usually stops on its own. If > 1.5 L evacuated at beginning or >100-200 cc/hour afterwards for 4-6 hours, then a systemic vessel was probably hit (intercostal, or internal mammary), thoracotomy will be indicated.
-Sucking chest wound: occlusive dressing (taped 3 sides), chest tube
-In bad trauma, screen for internal injuries, pulm or card contusion or aortic transection/rupture in bad trauma.
-Pulm contusion: can happen immediately or 48 hours out, monitor with ABG and CXR (white out lungs). Sensitive to fluids, can get pulm edema easily, so restrict fluids, give colloids, diuretics, fluid restriction, vent support if needed.
-Cardiac contusion: suspect if you see a sternal fracture; monitor with EKG, cardiac enzymes (troponins are sensitive, send for them anytime you see sternal fracture). Watch out for arrhythmias.
-Aortic rupture: no symptoms until the adventitia ruptures, killing the patient. Suspicion must be very high. Anytime there is a big deceleration injury, injuries of hard to break bones (scapula, first rib, sternum), get a CXR. If you don't see mediastinal widening, only non-invasive tests indicated (spiral CT is fastest, can also do transesophageal echo, MRI angio). If you see mediastinal widening, still try the noninvasive tests first but aortogram is indicated if the others are inconclusive.
-Rupture of trachea/bronchus: persistent air leak in chest tube, subQ emphysema (esp upper chest/neck), dx with CXR, find lesion with bronchoscopy, intubate and go to OR. Other causes of subQ emphysema- esophageal rupture, usually in setting of endoscopy.
-Fat embolism: long bone trauma, DIC-picture: respiratory distress, petechiae (axilla/neck), fever, tachycardia, platelet consumption. Tx with respiratory support
9. X-ray will not diagnose acute osteomyeltis: even early changes like swelling or periosteal elevation may not be obvious for several days, and bone destruction will not be visible for weeks. use bone scan: "Radionuclide scanning (ie, bone scan) sensitivity: (84 to 100 percent) specificity: (70 to 96 percent) for the diagnosis of osteomyelitis in children. In addition, scintigraphy is helpful early in the course, usually readily available, relatively inexpensive, and it may not require as much sedation as MRI in young children. However, it may not perform as well in neonates or in patients with community-associated methicillin-resistant S. aureus infections, and will not reveal foci of purulence within and near bone (eg, intramedullary abscesses or muscular phlegmon) Scintigraphy is useful when: MRI is not available and imaging other than plain radiography is needed to confirm a diagnosis of osteomyelitis, The area of suspected infection cannot be localized, or Multiple areas of involvement are suspected" (from uptodate)

10. Pathologic fracture in an adult means tumor, usually mets. Bone scan, whole body PET to look for mets and primary-- in women, breast; men, prostate; smokers, lung. 

1. Billroth I: 
-resection: distal stomach, pylorus, proximal duodenum (before ampulla of vader)
-anastomosis: end-to-end, duodenum to stomach edge.
-pros: somewhat physiologic-- maintains somewhat normal flow of fluids, no backleak of alkaline fluids into stomach/esophagus
-cons: may be more tension on the anastomosis, since you have to pull the duodenum all the way up to the mid-gastric region.
2. Billroth II: 
-resection: distal stomach, pylorus, proximal duodenum (before ampulla of vader)
-anastomosis: end-to-side, jejunum to stomach. The cut end of the duodenum is stapled shut into a blind loop, with the pancreatic and gallbladder drainage intact.
-pros: low-tension anastomosis
-cons: since pancreatic/biliary secretions are now upstream of gastric contents, there can be efflux of bicarb and/or bile into the stomach and up the esophagus. This can be prevented by making an Omega loop, aka Braun entero-enterostomy, where you make a connection between the jejunum proximal to and distal to the stomach anastomosis, providing an alternate path for the alkaline secretions to go directly through rather than into stomach. The omega loop must be at least 40cm in diameter for the fluids to effectively bypass. Additional disadvantages of the billroth II: afferent or efferent obstruction, causing swelling of duodenal loop, and finally mucous ulcer formation from stomach contents moving directly across to unprotected duodenum.

3. Roux-en-y
-resection: distal stomach, pylorus, proximal duodenum (before ampulla of vader)
-anastomosis:
(1) resect distal jejunum, bring up to end-to-side with stomach (limb must be > 40cm long to avoid alkaline reflux.
(2) anastomose original duodenal limb with gastro-jejunal limb with continuing jejunum in a "Y" shape
-pros: fewer problems with efferent/afferent limb obstruction
-cons: erosive ulcer formation still occurs.

4. Lymph node resection for gastric cancer:

-D1: perigastric lymph nodes. For distal gastric cancer, you have to take the omental nodes, and nodes along distal lesser gastric curve. For proximal gastric cancer, you take the peri-gastric nodes around the proximal part of stomach. 

-D2: you take all of the D1 nodes, plus the nodes around the celiac vessels-- common hepatic, proximal GDA, proximal proper hepatic, proximal L gastric, all the ones around the splenic vessels to the spleen. In a Japanese D2, you take the spleen and the pancreas as well. 

5. D1 vs D2 lymph node resections landmark trials: 

-Cuschieri, RCT n=400, randomized to D1 vs Japanese D2 resection, no difference in death from gastric cancer, OS, PFS. Removal of spleen and pancreas independently associated with survival. 

-Bonenkamp, RCT n=711 randomized to D1 vs Japanese D2, similar 5-year OS rates, but more complications (43 vs 25%), longer hospitalizations, and most postop deaths in D2 resection. 

6. FOLFIRINOX is associated with significantly longer OS/PFS compared to gemcitabine, but also higher complication rates, when treating metastatic pancreatic adenocarcinoma: 

From the abstract, {NEJM, RCT, n=342}

"The median overall survival was 11.1 months in the FOLFIRINOX group as compared with 6.8 months in the gemcitabine group (hazard ratio for death, 0.57; 95% confidence interval [CI], 0.45 to 0.73; P<0.001). Median progression-free survival was 6.4 months in the FOLFIRINOX group and 3.3 months in the gemcitabine group (hazard ratio for disease progression, 0.47; 95% CI, 0.37 to 0.59; P<0.001). The objective response rate was 31.6% in the FOLFIRINOX group versus 9.4% in the gemcitabine group (P<0.001). More adverse events were noted in the FOLFIRINOX group; 5.4% of patients in this group had febrile neutropenia. At 6 months, 31% of the patients in the FOLFIRINOX group had a definitive degradation of the quality of life versus 66% in the gemcitabine group (hazard ratio, 0.47; 95% CI, 0.30 to 0.70; P<0.001)." 

(5-FU, leucovorin, irinotecan, oxaliplatin) 

7. Post-op bleeding:

-Don't overinterpret post-op Hb drops: being NPO before surgery likely leads to some degree of hemoconcentration, so Hb's measured intraop or immediately before op may be much higher than a Hb measured post-op and s/p many liters of crystalloids. 

-Look for vital sign changes and changes in urine OP and mental status if you're worried about a bleed. 

-Toradol can make people bleed more, particularly in combination with heparin or lovenox-- if you're worried, hold the anticoagulants for 5-6 hours after you give toradol. 

-If someone has a hematoma and they're stable and it's stable, you can drain it with IR. If it's clotted off and won't drain, you may need to go to the OR to scoop it out. 

-If they are acutely unstable, go to the OR. 

8. Be careful of putting in CABG grafts in people with subclavian stenosis-- if the LIMA is distal to the stenosis, you will get subclavian steal where the distal subclavian is a lower pressure than the coronary system and blood will flow backwards from heart to arm. Consider using RIMA if the stenosis is not bilateral.
9. Be careful of doing sternotomies in people with previous sternotomy scars and incomplete surgical history-- if they had a previous CABG with the RIMA, you may cut the RIMA on entry and give them an MI intraop. Poor form.
10. When putting in a central line in someone with an IVC filter, do not push the guidewire in too far, or it may get tangled with the IVC filter and require a trip to IR to bail you out.

1. If you find thyroid tissue outside of the thyroid/thyroglossal duct path, its metastatic follicular carcinoma. Do a radiolabeled-iodine scan to find the primary.
2. Hyperaldosterone: if aldo is lower when lying down, and increases upon standing, it's physiologic and more likely to be due to adrenocortical hyperplasia which is treated medically with aldactone (spironolactone, inhibits aldo effect in kidney). If the measurements are the same, or lower when standing, it's more likely to be an adenoma which needs to be treated surgically.
3. Duodenal obstruction in a newborn (bilious vomiting, double bubble)
-Complete: duodenal atresia vs annular pancreas
-Partial: duodenal stenosis vs annular pancreas vs malro (c ladds bands). Malro is a super emergency, diagnose with contrast enema or gastrographin upper GI study.
4. Peds surg: 
-Exstophy of the bladder has better outcomes if its fixed within 48 hours of birth
-Nec enterocolitis: IV fluids/nutrition, NPO, antibiotics; indications to go to OR: pneumoperitoneum, air in biliary tract, abd wall erythema
5. Barium can induce an inflammatory response (granuloma formation) in the peritoneal or mediastina cavity if it leaks, leading to peritonitis, ileus, etc. If you're trying to rule out an esophageal tear or worried about a bowel leak (i.e. intussuception reduction <1% risk perforation in good hands), use gastrographin instead. However gastrographin can cause damage to the lungs if aspirated, so in someone with a high aspiration risk, barium is better. Barium also has much better bowel mucosa coating ability and is a better diagnostic agent, gastrographin has more false negatives.
6. Ann Arbor staging for lymphoma:
I: in one LN, +/- local surrounding tissues
II: In multiple LN, same side of diaphragm
III: both sides of diaphragm, + spleen
IV: extranodal mets (liver, BM)
Modifiers:
A: no B symptoms
B: B symptoms
E: extranodal
X: disease >10 cm
S: splenic involvement
7. Lymph node location, drainage differential diagnosis {source}
Submandibular-- Tongue, submaxillary gland, lips and mouth, conjunctivae -- Infections of head, neck, sinuses, ears, eyes, scalp, pharynx
Submental -- Lower lip, floor of mouth, tip of tongue, skin of cheek -- Mononucleosis syndromes, Epstein-Barr virus, cytomegalovirus, toxoplasmosiss
Jugular -- Tongue, tonsil, pinna, parotid -- Pharyngitis organisms, rubella
Posterior cervical -- Scalp and neck, skin of arms and pectorals, thorax, cervical and axillary nodes
-- Tuberculosis, lymphoma, head and neck malignancy
Suboccipital -- Scalp and head -- Local infection
Postauricular -- External auditory meatus, pinna, scalp -- Local infection
Preauricular -- Eyelids and conjunctivae, temporal region, pinna -- External auditory canal
Right supraclavicular node -- Mediastinum, lungs, esophagus -- Lung, retroperitoneal or gastrointestinal cancer
Left supraclavicular node -- Thorax, abdomen via thoracic duct -- Lymphoma, thoracic or retroperitoneal cancer, bacterial or fungal infection. (Thoracic duct drains directly into L supraclavicular node, at junction of L subclavian and L carotid veins. Thoracic duct drains abdomen, L mediastinum; R mediastinum goes to R side.)
Axillary -- Arm, thoracic wall, breast -- Infections, cat-scratch disease, lymphoma, breast cancer, silicone implants, brucellosis, melanoma
Epitrochlear -- Ulnar aspect of forearm and hand -- Infections, lymphoma, sarcoidosis, tularemia, secondary syphilis
Inguinal -- Penis, scrotum, vulva, vagina, perineum, gluteal region, lower abdominal wall, lower anal canal -- Infections or cancers of the leg or foot, STDs (e.g., herpes simplex virus, gonococcal infection, syphilis, chancroid, granuloma inguinale, lymphogranuloma venereum), lymphoma, pelvic malignancy, bubonic plague

8. Nosebleed in a young adult, not anterior: either septal perforation from cocaine abuse or nasopharyngeal angiofibroma

9. You need an FEV1 of at least 800 to have an acceptable pulmonary quality of life (i.e. not dependent on 10L NC oxygen to walk). When considering significant lung resection, like pneumonectomy for central tumor, do a V/Q scan to see how much lung function comes out of what you're about to resect, subtract from FEV1 score. If its much less than 800, it's a no-go for surgery. {chart on normal FEV1 values by age, gender, height} 

10. Common ENT problems that are usually bilateral that present unilaterally in a kid: foreign object; in an adult: cancer. 

1. Three worst kinds of abdominal pain- obstruction of a hollow viscous leading to spasm and intermittent increase in interluminal pressure (as it attempts to push through obstruction): nephrolithiasis, cholelithiasis, labor.
2. Don't forget that abdominal pain can be referred pelvic pain: esp in children, as they can be shy about talking about it, you need to examine GU/pelvic structures to rule out things like testicular torsion. Testicular pain after a sporting event-- likely just local trauma, manage with pain medication and observation, don't miss a torsion, which needs to go emergently to OR. Torsion can happen after sporting events as well, rule it out with a doppler
3. Pain with any movement ("I felt every bump on the ride here") = peritoneal irritation. The logic is that it's caused by passage of some non-sterile, pro-inflammatory contents into the peritoneal cavity; adhesions form quickly to contain the effluent; these adhesions are initially made of fibrin, which needs time to form. The peritoneal process stops GI motility (ileus) and stops the person from moving (severe pain with movement) to buy time for the fibrin to form.
4. DDx of peritoneal irritation, "rebound, guarding":
-Foregut: perforated gastric ulcer (very classic rebound/guarding exam), pancreatitis, cholecystitis
-Midgut/hindgut: appendicitis +/- rupture, bowel perforation, necrotic bowel,  diverticulitis +/- perforation,
-Pelvic: PID, ectopic, ruptured functional (or other) ovarian cyst (can be irritating to peritoneum)
-Systemic: spontaneous bacterial peritonitis, DKA (can cause abdominal pain), familial mediterranean fever (AD, polyserositis-- pleura, peritoneum; diagnosis with peritoneal bx, treat with colchicine)
5. Diagnosing appendicitis, relative constants: 
-Anorexia: present in almost all patients. If your patient is hungry, or has eaten recently, they are unlikely to have appendicitis
-Slow onset
-Vomiting/diarrhea not a significant component. If they describe these symptoms as starting first, and the abdominal pain as later, think of other etiologies.
-No history of similar symptoms.
6. Diagnosing appendicitis, what labs/imaging to order: 
-CBC, UA (r/o pyelo), pregnancy test (r/o ectopic), amylase/lipase/LFTs (r/o pancreatitis, cholecystitis)
-Gradient ultrasound if they can tolerate it-- many people can't. The u/s can't see through air, and there's often a lot of air in the cecum-- so you have to push pretty hard on the abdomen with the u/s probe to get a good imaging appendix and this is highly uncomfortable.
-CT: you will see the appendix coming off cecum, see if it is enlarged, edematous; look for fat stranding around it (normal CT fat, sort of a greyish ground glass background; fat stranding is when it sort of clumps into grey strands interspersed with grey background.
7. Surgical management of acute abdomen
-You have to weigh the risk of a sitting on an acute abdomen vs the morbidity of a negative ex-lap. Some people wait for signs of systemic infection (elevated white count, fever) in addition to an abdominal exam suggestive of acute abdomen.
-In people who may not be able to tolerate sepsis (sickle cell patients, immunocompromised), it may be worth it to go the OR earlier. People with sickle cell also unfortunately have more complications from big abdominal surgeries-- more susceptible to post-operative hypoxia, for example.
-You can find the appendix because its where the colonic tinea come together, forming a ring of longitudinal muscles around it.
-When you take the appendix, ligate the appendiceal aa in the mesoappendix.
8. Appendicitis in an older person- you have to rule out cancer. Appendicitis has a bimodal distribution: it's high in children (from before preteen years to 20s) with lymphoid follicle proliferation (appendix has prominent lymphoid follicles). It's also high in older adults, but the cause there is usually cancer-- it can be hard to detect intraop because inflammation around the appendix and cecum can lead to induration that hides a tumor to palpation. So remove the appendix, and then make sure to follow up with a colonoscopy weeks later when the inflammation has died down.
9. Hypotension in a young woman is a ruptured ectopic pregnancy until proven otherwise. 
10. Group A strep skin infections tend to cause local and systemic symptoms; strep agalactiae (aka GBS) can cause local infection without systemic signs.

1. Pearls about diagnosis of acute cholecystitis/cholangitis: 
-Acute-onset RUQ plus obstructed LFTs (increased alk-phos, GGT, bili): suspected choledocholithiasis.
-Workup: CBC to find leukocytosis (indicates cholangitis has set in), pancreatic enzyme levels. U/s won't reveal stones in bile ducts, but will reveal bile duct dilation (useless in someone who's had a cholecystectomy, because their CBDs can dilate to 1cm)
-If someone has symptoms/labs consistent with acute pancreatitis AND acute cholangitis/choledococystitis, ERCP is indicated.  If they only have symptoms/labs of acute pancreatitis, do not do an ERCP-- it won't help the diagnosis and will (possibly) worsen the pancreatitis. If they have pancreatitis and equivocal symptoms/labs of cholangitis, do MRCP.
-If you do an MRCP or EUS and it reveals stones, go to ERCP and remove the stone; if there are no stones, put in a CBD stent; the symptoms may be caused by abnormal sphincter of oddi spasm.
-Rectal NSAIDs (i.e. indomethacin) can reduce ERCP-induced pancreatitis; but not NSAIDs delivered by other routes.
2. Estimating risk of choledococystitis: 
Very strong predictors: you saw a bile duct stone on u/s, they have clinical cholangitis, Tbili>4
Strong predictors: common bile duct dilated to >6mm, Tbili 1.8-4
Moderate predictors: any abnormal LFTs other than bili, age>55, clinical gallstone pancreatitis
-High Risk: One very strong predictor, or both strong predictors. Estimated risk >50%, go to ERCP
-Medium risk: one strong predictor, or one moderate predictor: estimated risk 10-15%, do an EUS or MRCP first. If the MRCP is positive for stone, go to ERCP. If the MRCP is negative, but if you saw sludge or stones in the GB, schedule elective cholecystectomy later. If the MRCP is negative but the patient fails to get better, do EUS to get a better look (can do ERCP at the same time if EUS is pos)
-Low risk: no predictors. <10% risk. If you saw sludge and GB stones, schedule for surgery if they're stable for surgery. Otherwise medical stone dissolvers.
3. Acute SAH management: 
-watch Na (will often drop, incl because of ADH secretion)
-reverse all anticoagulation until the aneurysm can be clipped
-watch for increased ICP due to edema, obstruction: treat with mannitol, steroids, emergent craniotomy
4. Blood pressure & SAH: if the blood pressure goes too high, you will blow out the aneurysm and/or push more blood through an already ruptured aneurysm, worsening the bleed. If it is too low, you may not be able to have enough MAP to provide adequate cerebral perfusion pressure, esp if there is increased ICP and the brain will go ischemic.
General guidelines:
-Keep systolic <160. If you can measure CPP (i.e with EVD) and can monitor perfusion status because the patient is A&O, and thus utilize these two measures to assure adequate perfusion, then you can keep the systolic even lower, <140. If you don't have this clinical information, you don't want to risk underperfusion so go higher (esp if you suspect the reason for the loss of mental status was because of increasing ICP leading to less CPP)
-Do not use vasodilators (nitrates) to lower BP if it is high; it will worsen ICP by dilating intracerebral vessels. Use beta-blockers, ACE-I, Ca channel blockers
5. Incidence of angiographic vasospasm after SAH: 30-70%; incidence of clinically obvious vasospasm (i.e. loss of mental status) after SAH 20-30%
6. Most (90%) people with bad CF don't get pancreatitis: CFTR d508/d508 -> ductal bile inspissation in utero -> fibrotic pancreas before birth, complete fibrofatty replacement. Endocrine function is spared. The other 10% have some remaining functional exocrine pancreas and can still get pancreatitis.
7. Heterozygous d508 or other mutations (more common) don't necessarily lead to full-blown CF with lung involvement: they may present later in life as isolated pancreatitis, or isolated male infertility
8. SPINK1 is a protease inhibitor packaged with pro-pancreatic enzymes in zymogens. Mutations in it predispose to chronic pancreatitis, and may be triggered in someone who adds on risk factors (i.e. drinks heavily). N43S is the most common mutation. Caffeine triggers pancreatitis.
9. Bad chronic pancreatitis can lead to many consequences:
-Portal hypertension. Inflammation around portal vein can cause portal vein thromboses, or splenic vein thromboses.
-AV fistula. Inflammation and enzymes can erode through walls of arteries, weakening them and leading to pseduoaneurysms that eventually fistula-ize with neighbouring veins
-Duodenal compression secondary to progressive fibrosis of the region around the pancreatic head, leading to constriction of ducts, vessels, duodenum.
10. Aortic dissections: 
-A-type: aortic arch dissection, tend to dissect retrograde, can cause acute aortic regurg and heart failure, need to go to surgery immediately. Getting BP control buys you some time, you still need to go fast.
-B-type: Below the L subclavian. Only troublesome if it restricts blood flow through the renal arteries or celiac/SMA/IMA or iliacs, in which case you need to go to the OR. Otherwise just manage medically with BP control.

1. Breast cancer screening recommendations:
-USPSTF: mammograms every 2 years from age 50 to 74, no self exams
-ACS: mammograms every year from age 40 on, no set age to stop (stop when other chronic diseases get bad), self exams should be done starting at age 20. If someone is high-risk, they should get annual to biennal mammograms starting age 30,
2. Mammography has 3 findings: mass, asymmetric density (can result from prev surg, rad, infection, or normal variant), microcalcifications.
For stratifying the risk of a mammographic finding, there is the BI-RADS system:
0: needs additional evaluation (i.e. u/s for masses or densities and spot magnification mammograms for microcalcifications)
1: normal
2: benign findings, normal screening
3: probably benign, short-follow up (6 mos). Risk of malignancy <2%. Biopsy only if the patients have other suspicious lesions, or are wanting to get pregnant or receive a transplant soon (because the immunosuppresive drugs may worsen the cancer prognosis or quicken its spread, also because the presence of cancer may be a contraindication to receiving a transplant)
4: suspicious, core biopsy warranted. Risk of malignancy 15-35%.
5: highly suspicious of malignancy.
3. A solid breast mass in any woman over the age of 35 is cancer until proven otherwise, and requires a mammogram (u/s if it feels cystic) and core biopsy. In a woman less than 30, it is 98% likely to be fibroadenoma; you can do FNA, core needle, or observation, depending on what the patient wants. Mammogram is indicated if there is a clinical or historical reason to suspect cancer.
4. Bloody nipple discharge is never normal and must be surgically investigated-- its likely an intraductal papilloma. Mammography is required to find an underlying mass (4-13% risk in older women of cancer), and then you must cannulate the duct, do a ductogram (inject dye) and excise the duct.
5. Other signs:
-Edema/peau d'orange, overlying ulceration: suggests inflammatory process
-Retraction of skin: suggests mass invading support structures
-Supraclavicular node: suggests stage IV disease, unresectable and uncurable. (the tumor usually drains to Level I nodes which are lateral to pec minor, then Level II which are deep to pec minor, then level III which are medial to pec minor, then it goes to systemic lymphatics and spupraclavicular simultaneously.
-Overlying skin nodules: may be satellite lesions, require biopsy
6. Treatment
-Stage 0 or small stage I (<1 cm): lumpectomy, radiation, hormone therapy is if its ER+, nothing if ER-
-Stage I with 1-2 cm: lumpectomy, radiation, hormone therapy if ER+, adjuvant chemo (esp in premenopasual women)
-Stage II (primary >2cm or +LN): lumpectomy OR modified radical mastectomy if relative or absolute CI to lumpectomy. radiation. hormone therapy if ER+, adjuvant chemo for everyone under 70.
-Stage III (primary >5cm, fixed nodes, or inflammatory lesions): neoadjuvant chemo (i.e before surgery), modified radical mastectomy, postop rad and chemo. 5 year survival 41%
-Stage IV (distant mets): palliative radiation and chemo. No surgery. 5 year survival 18%.
7. Altered mental status, lethargy, or coma in a patient with a history of breast cancer: rule out hypercalcemia due to bony mets or PTHrp secreting mass.
8. Breast masses in pregnancy: should be managed the same way as those in women who are not pregnant. If biopsy reveals cancer stage I or II, treatment is still excision: either lumpectomy + radiation or mastectomy. If its the third trimester, she can get excision and wait until postpartum to get the radiation. But if its the first or second trimester, she must get a mastectomy because she won't be able to get radiation. If it's stage III or IV, she'll have to get the full gamut of chemo, radiation, and mastectomy, which may require an abortion.
9. Breast lump in a...
-adolescent boy: gynecomastia, will self-resolve
-6 y/o girl: breast buds. Do not biopsy or excise, as it will alter future breast development
-50 y/o man: if its just enlargement, its likely hypertrophy due to medications (anti-fungals, anti-testosterones, marijuana or alcohol, digoxin, K-sparing diuretics). Watch, and biopsy only if it doesn't regress. If it's a firm, well-circumscribed mass, mammogram and biopsy are warranted.
10. Paget's disease of the breast is frequently (>95%) associated with underlying carcinoma. It's important to do a mammogram to look for an underlying mass; if its present, biopsy it. If no mass is present, biopsy the skin lesions.

1. External branch of superior laryngeal supplies cricothryroid, the muscle that pulls down the thyroid cartilage and stretches the vocal cords, increasing the pitch of the voice. Damage to this will result in an inability to make high pitched sounds, speech or song.
2. Papillary thyroid cancer: assoc with radiation; if there is a hx of radiation and a nodule, resection of entire thyroid is warranted. If its small <1cm, lobectomy may be appropriate, if not, thyroidectomy. Suppress thyroid function with exogenous thryoxine, consider I-131 ablation.
Follicular thyroid cancer: same management as papillary.
3. Medullary thyroid: measure calcitonin, test for MEN neoplasms (pheo, pituitary, pancreatic, neuromas, parathyroid) and mutations. These tumors are more aggressive and tend to spread-- total thyroidectomy +/- LN dissection. These tumors cannot be treated with thyroxine suppression or I-131 ablation because they do not take up iodine.
4. Anaplastic: survival is poor. Radical excision + chemotherapy and radiation are indicated.
5. Pheochromocytoma: incidence of 1 in 3 million. In addition to blood and urine VMA/HVA metanephrines, do octreotide scan (neuroendocrine tumors/chromaffin cells have increased expression of receptors that take up octreotide/somatostatin) or MBIG scan, which couples a marker to a precursor of epinephrine. Treat with phenoxybenzamine for a week before surgery, add a b-blocker in people with tachycardia or a history of heart disease who may not be able to tolerate the increased catecholamines acting on b-receptors. When operating, be very careful not to manipulate the tumor to avoid catecholamine release. Be wary of extra-adrenal tumors, which will present along the sympathetic chain.
6. Most common cause of primary hyperparathyroidism is adenoma. Can do a sestamibi scan to assess locations of parathyroid adeoma. Dissect out the adenoma, and 2 of the other glands. If you can't find 4, look in the thymus, and between the esophagus and trachea. Symptoms: hypercalcemia causes kidney stones and myalgias and arthralgias from deposition of Ca in tissues. Treating the hypercalcemia: increased Ca leads to osmotic diuresis, which worsens the hyperCa. First IV rehydrate, then give a lot of lasix to diurese off the Ca.
7. Secondary hyperparathyroid: often due to ESRD, inability to excrete phos => increased phos binds all Ca => Ca-sensing cells in parathyroid sense low Ca and secrete excessive amounts of PTH. Also renal failure may lead to decreased 25 hydroxylase activity and less uptake of Ca from gut. This leads to bone lesions (osteitis fibrosis cystica, fractures) as well as possibly Ca deposition in tissues. Treat by removing 3.5 parathyroid glands, +/- implanting last one in arm for easier future access.
8. Carcinomas that metastasize hematogenously: HCC, RCC, chorio, follicular thyroid
9. Sarcomas that are likely to spread to lymph nodes: embryonal rhabdoscarcoma, epithelioid, lymphangiosarcoma, malignant fibrous histiocytoma, synovial cell sarcoma)
10. High grade sarcomas: radical excision + radiation (63 gy); local recurrence is frequent. Lower grade: complete compartmental resection, limb-sparing surgery.

1. Most people have 500-600 cm of small bowel, you need at least 150 to prevent short-gut syndrome. If you have to resect beyond that (for strictures in IBD or perforated small bowel diverticulitis, say) then people will have to be on TPN. When you resect a portion of small bowel, be careful not to cut at the root of the mesentery-- if you take out the SMA by accident, the entire small bowel will go necrotic.
2. Principles of diverticulitis management: 
-Bowel rest, antibiotics, fluids. If someone is relatively healthy, you can have them stick to a liquid diet and take PO antibiotics at home (broad spectrum, 7-10 days), and then switch to a high-fiber diet later on. If they're old or sickly, you'll want to admit them, make them NPO, put in an NG, give IV fluids and antibiotics. If they get another event (30% chance), then elective resection is recommended 4-6 weeks after the inflammation dies down. Usually it affects a small segment of sigmoid colon, sparing the rectum and the proximal bowel.
3. Massive lower GI bleed-- likely vascular ectasia (AVMs) or diverticulosis. Other rarer explanations are aortoenteric fistula (suspect if they've had any major vascular surgery or stents in aorta or iliacs that could have eroded into bowel), varices, meckel's, polyps, IBD, hemorrhoids. Cancer is unlikely to cause massive bleeding. Stabilize first. Try to quickly find the source of bleeding with an NG lavage to r/o upper GI, and an anoscope to r/o hemorroids and varices. If the bleed stops (and 90% of AVMs and most diverticulosis cases will stop bleeding spontaneously, although there's a 20-25% risk of rebleed), then colonoscopy at a later date. If they will not stop bleeding and are crashing, do not attempt colonoscopy-- you won't be able to see, and you risk perforating. Instead, do tagged RBC scan (better for more stable patients) or angiogram (better for sicker patients), find the source, and then go to the OR for hemicolectomy. If you dont know where it's coming from, you may need to do a total colectomy. Most surgeons will wait to go to the OR until the person has gone through 4-6 units of transfusions of pRBCs; exceptions-- people who you don't want to transfuse, like Jehovas' witnesses or people with lots of antibodies or an odd blood type, people who are acutely highly unstable.
4. Sigmoid volvulus can be decompressed with a rigid sigmoidoscopy. Cecal volvulus is a surgical emergency, attempts to decompress with barium enema or scoping do more harm than good.
5. Ogilvie's-- dilation happens preferentially in the cecum and R colon because of the law of laplace. Try neostigmine first. Manage with surgery (R hemicolectomy) if the diameter exceeds 11-12 cm in an immunocompetent person, less in immunosuppressed.
6. For squamous cell anal cancer: very small, superficial lesions with no nodes can be superfically excised. Anything larger should not get resection first; it should get the Nigro protocol, and then surgery only if there is residual cancer afterwards. 

Nigro protocol:

-30 gy to the tumor, 2 gy/day for 5 days a week for 3 weeks (days 1-21) 

-5-FU, 1000mg/m2/day, continuous for 4 starting on day 1 of radiation, then another 4 days from days 28-30. 

-mitomycin-C 15mg/m2 IV bolus on day 1. 

This protocol has proven very effective, even in big cancers with +nodes, frequently able to lead to complete control without surgery, allowing people to avoid the major morbidities associated with abdominoperitoneal resections. {review 1} {review 2}
7. EC fistulas revisited: 
-High output (>500mL in 24 hrs) must be managed with total bowel rest: NPO, TPN.
-Low output, people can be allowed to eat.
-The further away the fistula is down the small bowel, the less likely it is to compromise nutrition and the more likely it is that things will be absorbed by the bowel proximal to the lesion and it'll be low output.
-EC fistula of the colon are much higher risk for infection
-Prophylactic antibiotics only if there is an indication-- increased risk of infection ie metastatic cancer that is obstructing distally and putting back-pressure on fistula, decreasing healing
-Wait at least 6-8 weeks to operate. 75% of EC fistulas will heal on their own. If you go in right away, and there is inflammation and infection, you risk making things worse as the bowel will just fall apart rather than healing strong.
-Principles of care while waiting for it to heal: sepsis control (drain any abscesses), nutrition, octreotide/NG/bowel rest.
8. Things that make EC fistulas less likely to seal on their own:
-Foreign body
-Radiation history
-Infection, inflammation (crohn's for example)
-Epithelialization
-Neoplasm,
-Distal obstruction
9. Pancreatic cancer: 
-Overall mortality, all-comers, for a whipple procedure: around 8%, <3% at high-volume centers. Risk tacks up if people are sick. Needing to do a portal vein reconstruction doubles your risk.
-Solid components and wall nodules in a cyst are a bad prognosis
-Vascular invasion is a bad prognosis-- watch out for portal vein, SMA/SMV, celiac a
-Neuro invasion is a bad prognosis-- presents as a constant, gnawing, non-radiating pain that feels like a hot poker in your back. Versus radiculopathy or mechanical back pain which radiates and changes with position. Back pain from pancreatic cancer represents invasion into sympathetic plexus
-CA-19-9 is normally 37, higher numbers represent increased likelihood of metastatic disease.
-Erlotinib plus gemcitabine are more effective than gemcitabine alone, increases mean OS 14 days....
10. Most insurance companies will not pay for epo if your hb is over 11; they will titrate you to 11 but then not beyond that, even if you are facing a surgery which could entail a significant blood loss