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

1. If someone comes in with acute cholecystitis, don't operate on them immediately-- IVF, watch them; percutaneous cholecystostomy if a fluid collection collects and you need to drain. Go through liver to have something between the gallbladder and abdomen wall so you dont leak bile into your peritoneal cavity.
2. Distal pancreatectomy-- options for spleen management:
-Take spleen and pancreas together. Will need pneumovax/meningococcal every 5 years, annual flu shot.
-Take pancreas tail, take splenic aa/vv, leave spleen supplied by short gastrics: if the tumor is integrated with splenic aa/vv, it's hard to save those vessels. to save the short gastrics though you have to be very careful of cutting on the greater curve of the stomach or manipulating that area (i.e. flipping up the spleen), since if you damage those vessels the spleen wont have any blood supply. There is a low chance of splenic infarction, esp in the inferior part of the spleen. If it goes necrotic, they will have bad LUQ pain and you will have to go back in 8-10 days out from surgery.
-Take pancreas tail, leave splenic aa/vv. This is hard, technically, and adds ~1 hour; you have to dissect the pancreas off the splenic vessels. You may get unacceptable bleeding
3. If you're doing a re-anastomosis after a hartmann, if the anastamosis is <6 cm from the anal verge, you may have to do a diverting ileostomy to take pressure off the new anastamosis.
4. For DVT prophylaxis, some people like to do subQ heparin in the first 24 hours after surgery and lovenox after that-- lovenox can't be reversed, and in the first 24 hrs postop the risk of bleeding is higher. People without a CI (bleeding) should be anticoagulated while they're in the hospital. Some people may need prolonged DVT prophylaxis-- up to 28 days, notably people with cancer, with big incisions (big laparotomy), obese, history of DVT. Lovenox is renally cleared so is dose-adjusted to 30mg/day (rather than 40 mg/day) in people with GFR <30, although small studies have shown that it does not increase major bleeding events, though it may increase minor bleeding events. {Chest} Lovenox has been shown to be slightly more effective than heparin, although with proportionally increased bleeding risk. The main benefit is lovenox is once daily subQ injections, while heparin is usually administered as TID subQ injections. The main disadvantage of lovenox is that it's more $$$$, so if your patients can't afford it, they'll have to inject themselves TID.
5. Things to do to speed up recovery of bowel motility:
-exercise, mobility
-chewing gum stimulates bowel "Sham feedings and the action of chewing stimulate bowel motility by a cephalic-vagal mechanism and have been shown to increase levels of neural and humoral factors that subsequently increase function in several different segments of the gastrointestinal tract." - {JAMA surgery} From the same article, speculation on the origins/cause of postoperative ileus: "The etiology of postoperative ileus remains controversial. Bowel motility is suppressed postoperatively owing to sympathetic hyperactivity and increased concentrations of circulating catecholamines.6 Pacemaker dysfunction owing to bowel manipulation is another postulated mechanism of postoperative ileus.7 In addition, electrolyte abnormalities, peritoneal and/or retroperitoneal irritation, and narcotic analgesia effects may contribute to postoperative ileus.8 The focus of more recent studies has been on neural and humoral factors. Vasoactive intestinal peptide directly inhibits smooth muscle contraction in the intestine, and levels of it are increased after operation.9 In addition, pain increases the release of substance P, which is also known to inhibit bowel motility.10,11 Operations also inhibit the promotility hormones gastrin, neurotensin, and pancreatic polypeptide.8"
6. Pneumonia definitions: 
-community-acquired: clinical or radiographic findings within first 48 hours of admission.
-healthcare-associated: CAP patients with recent contact with healthcare system.
-hospital-acquired: findings 48-72 hours after admission.
-ventilator-acquired: 48-72 hours after getting ET tube.
{source}
7. Most common pathogens of pneumonia... 
-CAP: s.pneumo, h.flu, atypicals, viruses
-Hospital-acquired: s.pneumo, h.flu, atypicals, legionella, aspiration, viruses
-ICU: s.pneumo, staph aureus/MRSA, gram negatives, legionella, h.flu
8. Criteria to admit someone with CAP: CURB-65
-Confusion
-BUN>20
-Resp rate>30
-BP systolic <90, diastolic <60
-Age>65
If they have 0-1 criteria, they are low risk and should be treated as an outpatient, 2 criteria they should be admitted, 3+ criteria should go to ICU (esp if 4 or 5 criteria)
9. Treatment for CAP in 
-outpatient setting: z-pack, 500 mg qd for 3 days. or clarithro, 500mg BID for 5 days. Or doxy 100mg BID for 7-10 days.
-inpatient setting: respiratory quinolone (moxi/levo) or b-lactam (ceftri, ceftax, unasyn) PLUS macrolide, since macrolides have limited gram-neg coverage.
-ICU setting: b-lactam (see above) PLUS either azithro or a resp quinolone. If you're worried about pseudomonas, double cover with an anti-pseudomonal b-lactam (zosyn, cefepime, mero, imipenem) and an anti-pseudomonal quinolone (cipro-- make sure not resistant in your hospital). If you're worried about MRSA, add vanc or linezolid to your cocktail.
10. Surgical patients do not all need H2-blocker/PPI prophylaxis for stress ulcer/chemical aspiration. Risk factors for chemical aspiration: post-op ileus (esp not NPO), opiate narcotics that worsen ileus, plus sedation in the form of an anxiolytic or sleep aid = bad cocktail for chemical aspiration. Keep the head of the bed elevated 30-45 degrees. If someone doesn't have GERD/didn't come in on a PPI/H2 blocker, it's not necessarily good policy to reflexively put everyone on one. Changing the acidity of the stomach may encourage increased and/or worse type bacterial overgrowth; increasing likelihood of GI infections or lung infections from microaspiration.

1. A patient that comes in with tachycardia, hypotension, and diminished breath sounds in one lung has a tension pneumothorax until proven otherwise. Stick a needle in them (mid clavicular line, 2nd intercostal space) immediately, ask questions later; use a large-bore needle (14+, push until you hear a hiss). You do not need any other clinical signs (tracheal deviation, JVD, etc), you don't need confirmation via CXR. If you see tension pneumo on a CXR, you waited too long.
2. Places your patients can hide blood/hemorrhage:
-thighs
-pelvis
-abdomen
-chest
-the floor... check the floor.
3. When you do your FAST ultrasound to detect intra-abdominal bleeding, look in the following four places where blood tends to pool: {source}
-Rectovesical pouch/Pouch of douglas in the pelvis
-Hepatorenal recess (pouch of morison): look at pleural space, sub-diphragmatic space, morison's pouch, R paracolic gutter/inferior kidney pole
-Splenorenal recess: same 4 places as above; fluid in LUQ tends to accrue in subphrenic before splenorenal. additionally, fluid on LUQ is blocked from going down L paracolic gutter by the phrenicocolic ligament (sustenaculum lienis-- slings under and supports spleen) so it tends to move across the midline to the R
-Pericardial space to r/o tamponade. Don't panic if you see a small amount of fluid-- its only bad if its circumferential.
4. Things to remember about FAST exam: {source}
-While some people say you can detect as little as 100cc of fluid, you normally need around 500-600, so recheck if the first one was negative
-Fat can sometimes be mistaken for free abdominal fluid, as can fluid contained within GI lumen. Free abdominal fluid will tend to have "pointy" edges,.
5. ABCDEs again, because anyone can't get enough of this: 
-Airway. Assess by trying to speak to someone, attempting to rouse them with pain.  Check patency by figuring out if you can ventilate them-- can you bag-mask them? meaning when you mask, do their sats improve, can you hear breath sounds? Try to DL them, can you see anything?
-Breathing: are they breathing? Does their chest move, can you feel air moving out of their mouth, can you hear lung sounds?
-Circulation: what are their vital signs? Make sure to use big IVs above the diaphragm, because you don't want to worse any potential abdominal hemorrhage. Initial bolus 20-30 mL/kg or just give them 2L. You also want to continually assess perfusion-- pulses, mental status, urine output.
-Disability: check long bones for fractures, check mental status/GCS
-Environment: remove all clothing, check everywhere for injury.
6. If you think you put an air embolus in someone, have them lie trendelenburg so that the air bubble becomes stuck in their heart and doesn't go to their lungs.
7. If you take someone to the OR for abdominal hemorrhage, open them up with a big incision and see if there is blood there; attempt to suction; if you are unable to keep up, then proceed to pack the crap out of it, like this: put your hand on the liver, press down, and shove lots of sponges behind the liver (like 4, 5 entire packs), then put your hand on the spleen, shove a lot behind that, then put your hand on the bladder and pack around that, and then pull up the mesentery and pack behind that. Then proceed to remove the least blood-soaked laps first and find and stop the bleeding, proceeding to bloodier areas.
8. In trauma, blood may be a better primary resuscitation fluid than crystalloids, avoiding dilutional coagulopathy; and it may be best to administer blood, ffp, and platelets in a 1:1:1 ratio. {review article}
9. If you go to the CT scan for someone who's been in a MVC with a star-sign (i.e. shattered windshield), do a non-contrast head CT first to r/o brain bleed, then do with-contrast chest abdomen pelvis to find an internal bleed.
10. LR may be a better resuscitation crystalloid than NS, possibly because of less acidosis and more coagulation-- i.e. less bleeding, as the calcium in LR soaks up the citrate chelator in pRBCs.

1. HIT can cause paradoxical arterial thrombi; antibody binding to platelets may activate them, and if platelets are fragmented, they are even more thrombogenic than whole platelets
2. DDx of acute-onset dyspnea:
-cardiac: failure to pump blood forward, leading to back-flow of fluid into the lungs. This failure can be due to arrhythmia, valve failure, ischemia, acute CHF decompensation, etc.
-pulmonary: failure to ventilate or perfuse. This can be due to alveolar collapse (atelectasis, pneumothorax), alveoli filling with non-oxygen (pneumonia/aspiration), upper respiratory tract obstruction (OSA, anaphylaxis, asthma, bronchitis, larygneal/tracheal edema, foreign body), failure to perfuse (PE, pulmonary HTN)
-blood: anemia, CO poisoning, metabolic acidosis
-brain: stroke
-psych: panic attack, hyperventilation
-neuromuscular: guillain-barre, myasthenia gravis, ALS, deconditioning
3. Dumping syndrome: hyperosmolar contents moving from stomach to small bowel. Often associated with gastric bypass, but can also be caused by things like pyloroplasty or antrectomy for medically refractory GERD. Leads to osmotic diarrhea, small bowel volume overloading (cramping, bloating, vomiting), and hypovolemia (weakness, dizziness). Can also lead to hypoglycemia, as the rapid-loading of small bowel with glucose triggers excessive insulin release.
-Early-onset: 15-30 mins after meals
-Late-onset: 1-3 hours after meals,
4. Both analogues of vasopressin and somatostatin both cause splanchnic vasoconstriction, but somatostatin analogues cause less coronary vasoconstriction.
5. For management of DVT or PE, put them on a heparin drip: 70-100 U/kg as a bolus, and then 15-25 u/kg as maintenance. Heparin is anti-coagulative and also anti-inflammatory, reduces pain associated with DVT. Check PTT 6 hours after you initiate treatment (should be 1.5-2x normal). Monitor PTT TID the next day, and then qd every day after that. Also follow platelets to monitor for development of HIT. Bridge to coumadin (4-5 day overlap). Anti-coagulate for 3-6 months. If DVTs continue to recur, they may need to be on lifelong a/c.
6. Fever and increased WBC after lap chole: either infection or anastomosis leak. Do a HIDA scan +/- ERCP to look for possible leak, CT if you suspect abscess. If there's an abscess, drain it. If there is a leak, put in a temporary stent to drain bile with ERCP. If they don't get better quickly, go back to the OR.
7. Biliary/Foregut cancers:
-5-year survival with pancreatic adenoCA, even with complete resection 10-15%, although some new data suggests survival may be up to 40% with early enough detection and no local spread. Median survival for those getting palliative care for unresectable tumors: 8 mos
-5-year survival for cholangioCA, 5-10%, <5% with spread. These tumors are often detected late and quickly invade local vascular structures and the liver because of their location.
8. Management of uncomplicated acute pancreatitis: NPO (TPN if you think their nutrition status requires), IV hydration, pain control, monitor electrolytes (esp Ca). Not everyone needs a CT. Perhaps do an u/s to rule out stones; if there are stones, do a lap chole when they are stable (follow amylase and lipase)
9. Ranson's prognostic signs: (developed originally for alcoholic pancreatitits)
At presentation
-Age>55
-WBC>16
-Glucose>200
-LDH>350
-AST>250
At 48 hours
-Hematocrit decrease >10%
-Fluid sequestration > 6 L
-BUN increase 5mg/dL
-Ca<8
-PaO2<60
-Base deficit>4
If someone meets 3 criteria, 28% mortality, 5-6 criteria mortality is 40%, 7-8 criteria, mortality is 100%
10. If someone comes in with acute-onset epigastric pain, elevated amylase/lipase, and signs of septic shock, think acute necrotizing pancreatitis, or bowel ischemia/perforation (PUD, volvulus, etc). With acute pancreatitis, there is a massive systemic inflammatory response that can cause significant third-spacing of fluids leading to distributed shock and poor perfusion of all organs, as well as ARDS that may be worsened with the large amount of fluids you're about to give. Treat with fluids, fluids, fluids; CT scan to make sure it's pancreatic pathology and not bowel or anything else, and to look for an abscess (drain it if you see one... try catheter first, but if its too loculated or complex you may need to go to the OR for drainage). IV antibiotics that have good coverage of gram negatives and anaerobes. ABG to determine adequacy of oxygenation (pO2) and ventilation (pCO2) if their breathing is starting to get compromised or their sats go down; you may need to intubate. If they get more septic-looking after a few days of care, suspect abscess, drain it. If they don't get better, suspect pancreatic pseudocyst; keep them NPO and give fluids and observe. Most psuedocysts will resolve on their own in 6 weeks; if not, then either drain percutaneously or surgically create a connection between pseudocyst and posterior stomach wall. You have to wait 7 weeks because it takes that long for the walls of psuedocyst to become amenable to suture.

1. PICC:
-Indication: med term infusing things (chemo, abx, TPN), or withdrawing things (HD, plasmapharesis)
-CI: coagulopathy, renal failure Cr>3 (need to save peripheral veins for dialysis access grafts/fistulas-- use IJ)
-Complications: infection, thrombus, hit an artery instead of vein and cause hematoma
2. Non-tunneled central lines: uldall, quinton-- temporary, used for urgent dialysis access. IJ/fem/subclavian, avoid subclavian to avoid central vein stenosis
3. Tunneled central lines: hickman, groshong, broviac- have cuff which stimulates tissue growth, keeps line in place. Good for putting things in long term: TPN, antibiotics. Not for dialysis
4. EVDs drain to gravity, set the cmH20 pressure by setting the height of the drain relative to the height of the patient. When placing the shunt, put it in Kocher's point: frontal horn, lateral ventricle
5. For internal shunts: VP shunt first line, VA or V-pleural if you can't get the VP (scarring/adhesions, infection).
6. Axillary lymph node dissection (ALND): 
-Benefits: full axilla dissection, staging, decrease local recurrence which eventually decreases mortality
-Cons: increased morbidity (lymphedema), postop complications (seroma, drain infections, cellulitis)
Sentinel node biopsy lower complications, same survival compared to ALND.
"Available evidence suggests that axillary node dissection is associated with more harm than benefit in women undergoing breast-conserving therapy who do not have palpable, suspicious lymph nodes, who have tumors 3.0 cm or smaller, and who have 3 or fewer positive nodes on sentinel node biopsy" {JAMA review}
7. Melena in an older man (>50) is colon cancer until proven otherwise, particularly with R colon/cecum if there is black, tarry stools. Workup: CBC, iron. Colonoscopy to find the lesion. CXR, LFTs, to rule out mets. CEA too.
8. Biomarkers:
-CEA to detect recurrent colon CA, 30% recurrent cancers are CEA neg-- usually poorly differentiated or if the primary was CEA-
-Octreotide is taken up by neuroendocrine tumors (i.e. carcinoid)
9. Radiation has no role in colon cancer. Chemo may be helpful in bad T2 colon cancers (signet ring, mucous making, +perforation, +venous invasion) and is helpful in T3 cancers. 5FU + leucovorin (not used as rescue as for methotrexate, but rather synergizes with 5FU because it inhibits thymidylate synthase)

1. Breast cancer stats
-1 in 8 women who live to 85 will get it
-3.4% lifetime risk of death
2. NSABP B04 trial: role of radical mastectomy. Among patients with clinically node negative (i.e. no palpable nodes, because this was done in an era before scans) there was no difference in survival between those who got radical mastectomy (breast, pec major, entire axillary contents) and those who got simple mastectomy +/- node radiation.
3. Clinically node-negative: 30% will still have cancer in their nodes; clinically node-positive (i.e. palpable nodes) 70% will have cancer in their nodes, since frequently caused by things like inflammation, particularly after a biopsy
4. What actually kills you in breast cancer is mets (brain, bone, adrenals, lung, liver), and so by the time most of these breast cancers were detected in the early days, it was already too late for surgical resection to make a difference thus it is thought why no survival difference between radical and simple mastectomy.
5. NSABP B06 trial: role of breast conservation. Compared modified radical mastectomy to lumpectomy and ALND +/- radiation. No difference in survival between breast-losing and breast-conserving therapy, but the addition of radiation significantly decreased likelihood of local recurrence-- which many decades later was shown to be associated with increased survival, but the effect was subtle, visible only in the long-term and with high-power: {Lancet}
6. Options for tissue diagnosis of breast cancer:
-FNA: tells you limited information, essentially cancer vs non-cancer. Good to r/o the possibility of cancer/reassure someone when they are young, healthy, and 99% likely to have a fibroadenoma but are anxious and want a biopsy
-Core needle: standard for diagnosis. Gives you enough tissue for histology, grading, receptors-- HER, ER, etc.
-Incisional: biopsy of skin-- i.e. peau d'orange for inflammatory breast cancer, or a weird looking nipple looking for pagets
-Excisional: rarely done, because we rarely go to OR without tissue diagnosis. Often because you went to the OR to excise what you thought was a benign mass (ductal papilloma) but later happened to find DCIS in the sample.
7. Options for breast cancer surgery: mastectomy (+/- immediate reconstruction) or lumpectomy; if you get lumpectomy, you HAVE to get radiation.
8. Absolute contraindications for breast-conserving surgery:
-Inability to get radiation-- i.e. previous chest/mantle radiation for hodgkin's
-Multi-centric diagnosis-- 2+ cancers in different quadrants.
-Diffuse malignancy with microcalcifications-- will make future tracking of progression difficult to impossible.
-Persistent positive margins after multiple (1-2x) reasonable attempts at surgical resection.
9. Relative contraindications for breast-conserving surgery: 
-Large tumor size relative to breast size
-Pregnancy, particularly in the 1st and 3rd trimester. Radiation is CI in pregnancy, chemo is not.
-Collagen vascular diseases? Increased risk of late-complications? Maybe, maybe not.
10. Things that are NOT contraindications to breast-conserving therapy:
-Lymph node +/-: the breast surgery is independent of the axillary surgery. You can still do ALND
-Location in breast
-Family history, genetic mutations
-Aggressiveness of cancer, risk of systemic relapse

1. CDH: pulmonary HTN from thickening of pulmonary vessels due to increased intrathoracic pressures; additionally, ipsi and contralateral lung hypoplasia from pressure on the mediastinum on the opposite side.
-Bochdalek: failure of pleuropericardial folds to fold. this occurs on L more than R, posterior more than anterior.
-Morgani: failure of septum transversum to form properly.
2. Treatment for CDH: Breathless intubation. Get the tube in before the baby even cries, because crying could lead to increased gas in the GI tract which will worsen the compression on the lungs. Do not try to bag, for the same reason. Put in an NG tube to decompress, go on ECMO if you need to.
3. If you seen any midline anomaly (like TEF), work up/examine for signs of VACTERL anomalies--
-vertebral (CXR, u/s to look at spine-- kids have windows between vertebrae so you can look with u/s)
-anorectal (exam)
-cardiac (echo)
-TEF (NG + xray)
-renal (check that they are making urine, renal u/s to look at upper GU, VCUG to look at lower GU)
-limb (exam).
4. Bilious vomiting requires an upper GI series STAT. This is a surgical emergency, because it indicates malro/volvulus until proven otherwise.
5. Omphalocele is associated with many other defects. There is a peritoneal covering over bowels, its usually midline, there are occasionally other organs that herniate, the defect is usually >4cm. Other defects tend to be above the omphalocele (cardiac, lung hypoplasia) or below (GU, kidneys). They are rarer than gastroischesis 1:5000. These cannot be pushed in like gastroischisis, you have to wait for skin to grow around it, and then push it in around a year of age, sometimes you can't.
6. Gastroischesis: R>L, <4cm, not associated with other defects, you push it in after they're born. Put the whole thing into a silo, slowly twist the top of the silo so it pushes the guts back in.
7. Metabolic defects assoc with pyloric stenosis: chronic vomiting, you get loss of K and H, so hypokalemia, metabolic alkalosis with paradoxical aciduria. You lose volume from vomiting, so you secrete aldo which increases resorption of Na, lose K and H. Treatment is with boluses of NS until they pee (which tells you the volume is adequate). Then you give maintenance D5 0.45NS +20mEq K @1.5x maintenance rate until the electrolyte abnormalities are corrected.
8. Malro: the cecum doesn't do its counter-clockwise rotation, and stays up by the duodenum. Additionally, the mesentery of the small bowel is tight and bunched up, making volvulus much more likely. Ladd's bands form between cecum and R abdominal wall, crushing the duodenum and causing bilious vomiting. Treat by cutting the ladd's bands, stuff the small bowel on the R side of the abdomen, the large bowel on the L side, remove appendix because if you don't, if they get appendicitis they will get LLQ pain and it will go undiagnosed. Diagnosis of malro: do an upper GI series, watch for the contrast to go into stomach and then make the C-curve to the R, down, left back across the midline indicating a continuous duodenum. If the dye fails to re-cross the midline, suspect malro.
9. Intussuception: ileo-ileo is common, happens frequently, nothing to worry about. Ileo-colic is the bad one.
10. Hydroceles usually go away by 1 year, no need to fix it surgically, unless it is a communicating hydrocele, or there is a hernia. Transillumination will not tell you the difference between a hydrocele and a hernia. The way to tell is that a hydrocele can only be palpated in the base of the scrotum near the testicle, while the hernia can be palpated up the spermatic cord. Inguinal hernias are at a higher risk for incarceration in kids vs adults, so you should repair them; preemies get hernias more than full term babies, so fix their hernias before they leave the hospital.

1. Borders of inguinal canal: 
-Superior: conjoint tendon (aponeuroses of internal oblique & transversus abdominis)
-Inferior: inguinal ligament
-Dorsal: tranversalis fascia
-Ventral: external oblique
2. Hasselbach's triangle: bordered by lateral rectus/semilunar line medially, inferior epigastric vv laterally, inguinal ligament inferiorly. Direct hernias occur into hasselbach's triangle, indirect hernias lateral to the epigastric vessels.
3. There is a space medial to the femoral vein, between the it and the lacunar ligament, at the most medial part of the space inferior to the inguinal ligament and superior to the ligament of cooper; this space is tight, and anything that gets stuck there is unlikely to be able to be manually reduced.
4. For hernia repairs, putting in a mesh has a lower recurrence rate (<1%) compared to Bassini repairs (sewing conjoint tendon to inguinal ligament)
5. Hernia tips:
-Hernias tend to occur on the R more than the L
-When you do abdominal surgery, make sure to repair the trnasversalis fascia well, because its the strength layer of the abdominal wall
6. Richter hernias-- the anterior/ventral wall of a segment of bowel is trapped -> venous edema -> necrosis. If you then reduce this hernia, it may perforate. If someone comes in with a relatively unimpressive looking hernia but with a lot of pain, after you reduce them, observe them for signs of rupture or peritonitis.
7. Spigelian hernias: at junction of arcuate and semilunar lines. The hernia only goes through the transversalis fascia, so it is unable to be appreciated on palpation, as it is still covered by the external and internal oblique muscles. Diagnose with CT, treat with laparoscopic repair.
8. Hepatic mass: before you biopsy, rule out hemangioma because they bleed a lot. Use radiolabeled RBCs, watch for filling from outside-in. Hepatic adenomas can also be bloody, and tend to respond to hormones-- i.e. OCPs or pregnancy. They are likely to rupture with pregnancy, so make sure to treat them before your patients get pregnant.
9. Hepatic cysts: simple hepatic cysts can be watched, complex cysts are suggestive of echinococcus; blood tests for echinococcus antigens to r/o. Drain carefully to prevent spillage of contents into the peritoneum, inject sclerosing agent (hypertonic saline).
10. Hepatic abscesses: Amebic abscesses can be treated with flagyl without drainage-- if you drain it, you might get a bacterial superinfection. Bacterial abscesses need to be drained, (if they are large and few) pts will usually have systemic signs of infection. IF there are many small abscesses, 4-6 weeks of IV abx. Bacterial abscesses can form from migration from GI tract into biliary system, or from bacteremia (from injection drug use or peritonitis working into the portal vein) seeding.

1. Anterior vs posterior decompression/fusion for cervical stenosis: ACDF procedures address the real cause of the problem in cases of disk herniation, by removing the faulty disk, but to do it you have to be able to remove the PLL without damaging the dura. So if there is excessive ossification of the PLL so bad that it actually impinges on or involves the dura, you have to do a posterior procedure. Posterior approaches temporarily relieve symptoms, but because they don't address the real problem, the disk will continue to herniate and the symptoms will eventually recur. Depending on how well you select your patients, ACDF procedures may alleviate pain for years, but the pain will also eventually return as well as for all spine surgery for pain.
2.ACDF complications
-Retracting on the longus coli, sometimes your retractor will slip upwards and catch the sympathetic chain, leading to ipsilateral horner's that may be irreversible.
-Retracting on the esophagus will cause brief (~1 day) postoperative difficulty swallowing, especially for thin liquids like water. For the time after surgery, it is good to stick to thickened liquidy things like mashed potatoes or yogurt and avoid thin liquids to prevent aspiration
-Retracting on recurrent larygneal can cause hoarseness.
3. CT w/o contrast to look at bony structures, CT w/contrast to look at things that take up contrast-- tumors, infection, bleed.
4. For spine and brain procedures, it is a good idea to have an a-line because these structures are very intolerant of ischemia, even brief ischemia, so you want to know immediately if there is hypotension.
5. Before bariatric surgery, you want people to attempt non-surgical weight loss regime, specifically a supervised exercise and diet program; the success of these programs at sustained, significant weight loss is relatively low (2-3%) but if it works the person will avoid surgery. More importantly, these programs will teach people the skills and knowledge necessary to maintain a healthy diet and exercise program after surgery.
6. Jejunoileal bypass surgery was one of the first bariatric surgeries developed, and has since fallen out of favor because it causes blind-loop syndrome, where bacterial overgrowth of the remnant jejunum leads to obstruction and nutrient malabsorption, esp B12 and fat-soluble vitamins. Additionally, there is an estimated 21% risk of cirrhosis at 15 years, so make sure to screen liver function in patients known to have had this procedure done.
7. Roux en Y procedures are associated with a 60-70% success rate (defined as >50% loss of excess body weight). Rough order of effectiveness: duodenal switch > roux en y > gastric sleeve > vertical banding > gastric banding. Increasing effectiveness also means more complications, including malnutrition complications.
8. Vasospasm after SAH: middle aged women tend to have the worst vasospasm, possibly hormonal role? However studies publish conflicting data about whether estrogen/progesterone promote or prevent vascular spasm/elasticity. Current recommendations: HRT has no cardiovascular benefit
9. Bypass grafts do not experience vasospasm, only native intracerebral vessels.
10. MRI
-T1: CSF is dark, fat is bright;
-T2: CSF is bright
-FLAIR: T2 where the CSF is factored out mathematically, so other things like bleeds and anomalous structures are easier to see.