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.