Transcript for:
Emma Holiday- Surgery Exam Review Notes

but it's not officially sanctioned by the school. This is basically something I made for myself to study for step two this summer, kind of going back all over all my surgery notes and the books and test questions or QBank questions that I used to study for both my surgery shelf and for step two. So you know, will all of this absolutely be on your shelf? No. But I tried to cover what I remember being important and what the review books and the QBank questions seem to hit over and over again.

So you'll also notice that I'm not going to teach you a lot of surgery in the next two hours because there's not a lot of surgery on your shelf. So I tried to pick out the medicine concepts that are related to surgical patients, which is really the most common thing you're going to see in these clinical vignettes. So I tried to make this PowerPoint fairly interactive.

It's not like hardcore pimping. But it was my goal to make this a way to kind of see what you know and see what you still need to study before Friday. So there are questions.

Please participate if you would like to. Harlingen, you guys have little buttons and stuff you can push. So please participate also if you know the answer.

And keep me honest. If they're saying stuff and I'm not repeating it, let me know if you're getting lost or if I'm not remembering to repeat things like I should. Any questions before we get started?

Yes ma'am. Yes, so it is being audio and video-ly recorded right now, so the actual presentation is going to be posted. Dr. Hinze is going to send it out first thing tomorrow morning, and the slides also will be sent to you guys tomorrow if you want to review it.

So I'm gonna go kind of fast, so unless you are a compulsive note-taker, it might just be easier to listen and enjoy. So all of this material will be available for you guys tomorrow. All right. So we'll begin like most of our patients begin before surgery and their preoperative evaluation. So, you know, surgeons love to operate.

There are very few absolute contraindications to surgery. But there's one that seems to come up over and over in the in the QB questions for surgery. Anybody know it? When can you absolutely not do surgery?

Any ideas? Besides patient death, that one doesn't count. So diabetic coma, DKA is an absolute contraindication to surgery, or sky-high glucose, just because the risk of operative complications and infection is just too high.

So that's one of your number one absolute contraindications to surgery. Poor nutritional status is another thing that's going to make the surgeons wary to take someone to the OR. And there are three things we look at that are measures of nutritional status.

Anybody? When would we think someone's nutrition sucks? Albumin. So if the albumin's low, what else? We can weigh them.

That's easy. If they've lost more than 20% of their body weight, that's also a marker of poor nutritional status. And the other one, lipostatic surgeons check it a lot. Pre-albumin.

Prealbumin, I agree. That's not the one I put in here. It was transferrin. So, albumin less than 3, a transferrin less than 200, or overall weight loss greater than 20% of the body weight are all pretty strong indicators of poor nutrition.

So, if the surgery is not emergent, these are good reasons to delay surgery and maximize nutrition. So, if we're trying to maximize someone's nutrition, what's the best way to do that? Should we shove them full of TPN or what? Is that the best way? No.

What's the best way? Yes, enteral feedings are always preferred. If it's possible to feed somebody through their gut, that's always going to be a more optimal way to get nutrition into somebody. So severe liver failure is also a reason that surgeons will delay surgery if possible or not take a patient to the OR right away.

And there are some things we can check to measure liver function. what are those? Billy Rubin, so we look at Billy Rubin. If we're cutting somebody open, what are we particularly interested in?

COAG, yeah, so we for sure want to take a look at the PT. So Billy Rubin, PT, we're also interested in the ammonia level or signs and symptoms of encephalopathy. Those are some things that are really important to look at in the preoperative evaluation.

So good, and if they're a smoker? What is our best advice? Okay, quit. Yes, good.

And if possible, two months before surgery, just because smoking affects... Wound healing because of the way it negatively affects the remodeling of tissues. So we'd really like our smoker friends to stop smoking two months before surgery, particularly in plastic surgery cases.

I know my attending was a real big stickler. If he was going to do a flap reconstruction on somebody, he was not going to do it if they were still smoking. So that's important. And also with our smoker patients, what is important as they're coming out of anesthesia?

We've always got a pulse ox monitor on our patients as they're coming to, as the anesthesiologist is waking them up. Do we want to keep their SATs right at 100%? Why not? Absolutely.

So smokers, people with COPD, they tend to be chronic CO2 retainers. So the only drive they have, or the strongest drive they have for respiration is hypoxia. So if we keep their SATs too high, that's going to suppress their respiratory drive and actually might cause more problems in the...

waking up phase after surgery than would be worth. All right, so Goldman's Index, you can actually calculate a number from Goldman's Index to calculate preoperative or operative risk. So really what you need to know about it, not necessarily how to calculate it, but what it does. So it tells you about a patient's risk during surgery, and it allows you to kind of weigh the risks and benefits of taking somebody to the OR.

So. What you do need to know for your test, not necessarily calculating the score, but what's the most important factor? What's the, what, what?

CHF. So congestive heart failure, the ejection fraction, these are all things we're paying very close attention to in the preoperative evaluation because CHF gives us the biggest amount of points in Goldman's index, and it's the biggest predictor of perioperative mortality. So.

If we have a patient with known CHF, I think I spilled the beans on this one already. What are we checking? Ejection fraction. Yeah, so we're going to order an echo if the patient has known CHF. And if their ejection fraction is in the toilet, if it's less than 35%, no surgery for them unless it's absolutely necessary.

So the second most important factor for predicting mortality associated with surgery. Yes, so angina-ish, but more importantly, a recent MI. So six months is the cutoff, and it's kind of a surrogate for their cardiovascular status. So angina would factor in there, but really we're going to be super concerned if there's been a heart attack within six months. So what are we checking on all our pre-op patients here?

Everybody gets one of these if they're over 50, EKG, before surgery. So if the EKG is abnormal, then we'd send them for a stress test. If the stress test is abnormal, we've got to send them to the cath lab and do revascularization, or reperfusion either with stenting or revascularization with a cabbage. So unless the surgery is urgent, we really want to make sure that they're cardiovascularly optimized before we take them to the OR and put them under anesthesia. So some other things we can check, also that would show up on the EKG.

Arrhythmias are a strong predictor of whether or not someone's going to do well with surgery. If they're old, they're less likely to do well with surgery. They're less likely to do well with surgery if the surgery is emergent. And aortic stenosis is also a predictor of complications associated with surgery.

So what else should we check, particularly with number six? So we already got our EKG. PFTs, sure, but we're not especially concerned about that if someone's got a history of valvular disease.

Well, first we're just going to listen. So, and this is the way they try to sneak some medicine in with your surgery questions. They might describe a patient who comes in for his preoperative evaluation, and they might describe the AS murmur. So you're going to have to reach back into your memory banks from step one land and remember what the murmur of aortic stenosis sounds like. And it is late systolic.

It's a systolic ejection murmur, and it's got that characteristic crescendo-de-crescendo. So even though it seems very medicine-y, it could show up in a vignette concerning the preoperative evaluation. So...

Before surgery, what medications do we tell our patients to stop? Aspirin. How long before surgery do we need to stop aspirin? Yeah, seven to ten days.

Two weeks, I think, is even better, if they can. What else would we want them to stop? NSAIDs?

Sure. Metformin. Why? Yeah, so...

Remember, that was the big adverse reaction you had to memorize for step one with metformin, lactic acidosis. So those are the main ones. Aspirin, NSAIDs, also vitamin E because that can affect bleeding and clotting.

Optimally two weeks before, but seven to ten days is usually what we tell our patients. Warfarin also because of bleeding complications, and we monitor the INR for that. We want it to drop below 1.5 if possible. And metformin, which I don't have here, but it's absolutely true. due to its risk of lactic acidosis.

And then if the patient is diabetic requiring insulin, we always instruct the patient to take half the morning dose since they are NPO after midnight before surgery. So if they are chronic kidney disease and they're on dialysis, when do they need to have dialysis before surgery? Yeah, 24 hours before, absolutely.

And why do we check BUN and creatinine? in a patient with a history of kidney disease? How does that affect surgery?

Like sure their kidney function isn't that great but the surgeon shouldn't care about that just cutting on them for an hour. Absolutely. So what he said was if you guys didn't hear him, people with chronic kidney disease who have uremia, uremic toxins actually interfere with platelet function. So even though if you check a CBC the platelet counts will be fine, There's still an increased risk of bleeding because the uremic toxins prevent them from interacting in a normal way.

So particularly if the BUN is super high, above 100, we would definitely worry about that. So that's one of the reasons we want to make sure they get their dialysis before surgery, and we monitor their BUN and creatinine closely. So what would you expect on the COAG panel? Kind of told you already.

The platelets are normal. They'll try to throw you off with that one. but the bleeding time is still prolonged because bleeding time doesn't necessarily measure platelet number, but definitely platelet functionality. Okay, so if you are a whiz with the ventilator, you're a better med student than I.

I kind of boiled it down to the four things you really need to know to answer questions about these surgical ICU patients. So assist control, what do we use this for? Or how much is the machine actually doing for patients when they're on a cyst control setting? Yeah, so we set on the machine, we set the tidal volume that we want the patient to receive and the rate, the minimum rate that's acceptable for us, for the patient to be breathing. But if the patient, you know, is exercising their respiratory muscles and takes a breath, the ventilator will go ahead and give that predetermined volume.

That's different for pressure support, where the patient is going to breathe however often they're going to breathe, but the machine provides pressure support so that if they're not able to take in the whole tidal volume on their own, the ventilator will give a little bit of oomph, a little bit of help with that. And as I noted on the slide, this is an important weaning setting. That's probably where you'll see it if you see it in a clinical vignette. You've got someone that's been vent-dependent after a bad accident or whatever.

and you're trying to wean them off the ventilator so they can be downgraded, pressure support setting is an important stepping stone in that process. And then CPAP, my daddy's got one of these. So again, the patient has to have sufficient respiratory drive to breathe on their own, but a CPAP gives continuous positive pressure in order to make sure those alveoli stay open in order for gas exchange to occur.

And then PEEP. Yeah, so again, this is more important, keeping those alveoli open. As I've noted on the slide, where you'll see this is as the setting that's used in patients with ARDS. So the alveoli are collapsing, and that's what's causing the problems in patients with ARDS, not being able to facilitate gas exchange. The PEEP setting is going to keep those open in order to facilitate that.

So if you have a patient on a ventilator, What tests do you want to order with some regularity to check how well the ventilator is working? ABG, absolutely. So you're going to check your oxygenation status and then how well your CO2 is being taken care of as well.

So if the PaO2 is low, what does that tell you? Is your patient getting enough oxygen? No.

So how do we want to remedy that? Absolutely. So we'll increase the FiO2 if our PaO2 is unacceptably low on the ABG. If the PaO2 is too high, yeah, we'll decrease it. Why?

Is there such a thing as too much oxygen? And what does too much oxygen do? Yeah, free radical damage.

So it can actually paradoxically end up worsening ARDS or lung injury if you have too high concentrations of oxygen. So if... we're taking a look at our PaCO2, if it's too low and our patient is alkalotic, what should we adjust on our ventilator settings?

Oh, I can't hear you. So we could. What would we want to do to frequency? We want to make them breathe faster or slower?

We would want to make them breathe slower because if their PaCO2 is low, that means they're blowing it out, right? They're breathing too much. They're, like, hyperventilating. Is that the only way we could adjust this PaCO2? Height of volume.

Frequency and tidal volume are the two parameters you could change. And I think I might have taught you this way back in first year in physiology. Which one is better to adjust? Do we want to adjust rate or do we want to adjust tidal volume to get the most bang for our buck in terms of efficiently getting rid of CO2?

Tidal volume. Why? Multiplicative effect. What do you mean?

Um, oh, so you didn't press your button. That's okay. So what he said is it was a multiplicative effect, and it's because you multiply rate and tidal volume together to get your minute ventilation. I agree with that.

The only thing I would add in that you might want to look for in the answer choices is when you're increasing your respiratory rate, you're also increasing ventilation to the dead space. So. when you increase rate, you're getting more air to your alveoli, sure, but you're also getting more air to the dead space in your trachea and your bronchi and stuff like that, whereas when you increase your tidal volume, that gives more benefit to the amount of air that's going into the functional spaces where gas exchange can occur. So that's a pretty classic question and a good thing to remember, how physiology does apply to real life. So then conversely, if the PaCO2 is high and the patient's acidotic, we could increase either rate or tidal volume.

But again, tidal volume is going to be preferred because we're not wasting any of that additional oxygen on dead space. So, okay, very good. So for acid-base disorders, you'll see these acid-base disorders on pretty much every shelf exam you take this year. So it's good to get it down early.

And then you can get the questions right on the rest of the exams also. So... Remember, when you're worried about acid-base status, obviously the first step is going to be to check the pH. You can get that on your ABG. And if it's less than 7.4, you've got an acidotic situation.

The next step is going to be to check the bicarb and the PCO2, because then you can see where the problem is. Do we have a problem with the kidneys or a metabolic issue, or do we have a problem with CO2 retention or blowing off of CO2? So if the bicarb and the PCO2 are both high, What type of acidosis do we have? Respiratory. Very good.

So if our PCO2 is high, right, we're retaining our PCO2, and because of the carbonic anhydrase equilibrium equation, more PCO2 means more protons, and that gives us acidosis. So if bicarb and PCO2 are both low, then what type of acidosis do we have? The other one? Metabolic, right.

So if we have too little bicarb, then the problem is with metabolism. So once you have determined you've got a metabolic acidosis, the next best step on your test should be to see if they gave you electrolytes so that you can calculate the anion gap. So remember the equation for anion gap.

You're likely going to need to use that on one of your questions on Friday. And it's just sodium minus the negatively charged components, chloride and bicarb. And what's normal? 8 to 12, 8 to 12, somewhere in there.

There's a more sophisticated equation where you can calculate the normal anion gap based on the patient's age, but that's an internal medicine thing. We don't care about that now. So 8 to 12 is a good enough ballpark for normal. And what are some things that can cause an anion gap acidosis? Or just give me the cute acronym that was in first aid.

Mud piles. All right, so what are these? Let's see if I can remember. M is methanol, I think.

Is U uremia? D, DKA? P?

Yeah, okay, paraldehyde? I? Isoniazid? L?

The most common one, lactic acidosis? E? Ethylene glycol? Or ethanol, sure.

Then S? Salicylates, good. Okay.

So the non-GAF acidoses are easier to remember for me because there are fewer of them. What are they? The main one?

The main one is diarrhea, right? Because your colonic and intestinal secretions are high in bicarbonate. So if you're pooping a whole bunch, you're going to poop out a lot of your bicarb.

And low bicarb indirectly gives us a metabolic acidosis. So some other random ones that are more internal medicine things are the renal tubular acidosis and then abusive diuretics or overuse of diuretics. So if our pH, instead of being low, is too high, is greater than 7.4, we've got an alkalosis on our hands. And, again, the next best step is to check the bicarb and CO2.

And if they're both low, what type of alkalosis do we have? Bicarb and CO2 are both low. What type of alkalosis is that? Respiratory, right. Because low bicarb, we just talked about that.

That should give us an acidosis. So low bicarb isn't going to give us an alkalotic situation. It's got to be the CO2. And if they're both high, then conversely, that's a metabolic alkalosis. So to determine between the main classes of metabolic alkalosis, you can check the urine chloride.

And vomiting, because you're puking up HCL, which is rich in chloride, you're going to have low chloride when you check it because you're ejecting it into the outside world. If the chloride is high, then it's something a little bit more mysterious. It might be some kind of hyperaldosterone state or one of these random genetic nephron.

electrolyte transporter problems like barters or Gittleman's. So that's kind of down and dirty, the stuff that you need to recall, pull out of the memory banks for the acid-base questions you might be asked. So as far as electrolytes, low sodium, what causes hyponatremia?

Yes, too much water, fluid overload. So if you remember from second year, hyponatremia is not a sodium problem. Right. It's not that you have too little sodium.

It's that you have too much water. So the first the next best step, if you see on your chemistry that you've got a patient with hyponatremia, you want to check the plasma osmolarity because there are some mimickers of hyponatremia where you've either got high glucose and that makes it look like your sodium is too dilute. So you want to check the plasma osms to to rule that out.

And then the next step is to take a look at the patient and assess the volume status. So. If your patient is hypervolemic, they're puffy, their lungs are crackly and wet, and they've got hyponatremia on chemistry, what might cause that?

Yeah, so the big three, CHF, nephrotic syndrome, or cirrhosis, can all cause fluid retention and lead to hypervolemic hyponatremia. Well, that's the same thing twice, isn't it? So, Pretend that second arrow is pointed down, and you have got a patient with dry mucous membranes, skin tenting. They look like they're volume depleted, but they're still hyponatremic on chemistry.

So what could cause that? Yeah, diuretics or vomiting, or this isn't the psychiatry shelf, but if someone's just vomiting free water. Never mind.

So diuretics or vomiting are going to be your main ones. And then if their volume status is stone-cold normal, but they're hyponatremic, the big cause there is SIADH. So the next best step, once you've established that, especially if the patient is a smoker, would be what? Chest X-ray.

SIADH is a perineoplastic syndrome associated with lung cancer. Okay, so how do we treat hyponatremia? Kind of depends, right? It depends on the volume status.

In general, the garden variety answer is fluid restriction and diuretics. But if they're hypovolemic, what do we want to do? Hypotensive, tachycardic, dry mucous membranes, skin is tinting. Got to volume resuscitate them, right? So even though they're hyponatremic, we're going to want to give them fluid to correct for hypovolemia.

Something I always found confusing when I was taking practice questions and when I was taking the real test is what is the role of hypertonic saline? When do we use this as opposed to just fluid restrictions and diuretics? And there are some pretty clear-cut criteria.

Does anyone know them? So if you've got severely symptomatic hyponatremia, so if you're like seizures, altered mental status, like severe, severe symptoms, or if the sodium is super, super low. I've seen cutoffs either 110 or 120. I don't think the test is going to be dirty in, say, 115, but, I mean, you'll see it's very, very low, or the patient is symptomatic from their hyponatremia. So why don't we go willy-nilly with this hypertonic saline and correct all our sodium up to normal in, like, five minutes?

Central pontine myelinolysis is the big fear from Lawsuit City, right? So we want to make sure we replete the sodium or correct the volume problem rather very slowly so we don't induce this life-threatening complication. And what's an appropriate rate of correction of the sodium?

It's between 0.5 and 1 milliequivalent per hour. or between 12 and 24 mEq a day. Any faster than that, and you're asking for central pontine myelin alysis. So for hypernatremia, again, the problem is not with sodium, it's with water. It's when we've lost too much water with respect to our sodium content.

So the treatment for this is we want to replace the water. So we're going to replace fluid with a hypotonic solution. And if we go faster than 12 to 24 milliequivalents per day, what do we worry about?

What's the complication? Cerebral edema. Good.

So cerebral edema is the feared concentration here. Got a lot of fist bumps going on over there. Okay.

So some other electrolyte abnormalities and how they might present in a clinical vignette. If you've got a patient with numbness, those two dead people sign. or prolonged QT interval, what electrolyte is out of whack? Calcium. Too high or too low?

Too low. So that's hypocalcemia. And what about the classic bone stones, groans, psychiatric overtones? That's hypercalcemia.

And what we worry about with hypercalcemia is this shortened QT interval. With hypocalcemia, as you can see on the slide, you've got a prolonged QT interval. So...

Anytime you see that the calcium is either too low or too high, an EKG would be an appropriate next best step to make sure your patient isn't at risk for developing torsades. Okay, so what about a patient with paralysis, ileus, or ST depression and U waves on the EKG? Hypokalemia. And how do we treat hypokalemia?

Yeah, we'll give them potassium. Good. So we'll put potassium into the IV fluids. We just want to make sure that we monitor their renal function.

If their creatinine is too high, if they're in renal failure, we can bump them into hyperkalemia pretty quick. So which brings us to this last situation, peak T waves and other EKG changes, like a prolonged PR or QRS, that's hyperkalemia. And the treatment of this is super, super importante.

So what do we want to do to a patient with hyperkalemia? Calcium gluconate first. This is going to stabilize the cardiac membranes.

What else? So we can give insulin and glucose to shift the potassium into the cells. Albuterol or a beta agonist can also shift potassium intracellularly.

And then if it's really bad, we really have to do dialysis to get the potassium out of the body. So very good. Okay, exolate.

We don't really use that very much at University Hospital, but they still use it at the VA from time to time. That makes you poop out potassium. So it's another way to kind of get it out of the body. Okay, so for fluid and nutrition, the maintenance IVF of choice is D5, half normal saline. And we can add 20 milliequivalents of KCL if the patient is peeing.

And for maintenance fluids, how do we calculate it? Up to 10 kilograms. How much fluid do they get? This is also muy importante. What?

Yeah, so there's different formulas, whether you're calculating daily requirement or hourly requirement. I've got the daily requirements here. So 100 milliliters per kg per day for the first 10, then 50 milliliters per kg today per day in the next 10, and 20 milliliters per kg per day, all kilograms in excess of 20. As we discussed before, enteral nutrition is always preferable over parenteral nutrition.

And really, we only use TPN when we have to. When there's a problem with gut absorption, that would prevent us from getting the patient nutrition internally. Okay, so our burn patients. For circumferential burns, well, first of all, what degree burn do we have going on here? It's erythematous.

It's fairly painful, but not peeling. So that's first degree. And what layer of skin is involved? Epidermis.

And so in this second example, we've got loss, you know, loss of integrity of the epidermis. It's very painful. Oh, there you go.

JK. Second-degree burn. And then lastly, this example of a third-degree burn shows you that it can either become dark or pale. And really, we have no sensation here because the damage to the skin goes all the way through the dermis and starts to affect the nerves. So even though this doesn't hurt, this red stuff all the way around the area of the third-degree burn hurts like hell.

So. Just because the patient has a third-degree burn doesn't mean something doesn't hurt. Okay, so particularly what are we worried about in circumferential burns?

Compartment syndrome. Very good. So we'll look out for those signs, and if we see them, we'll definitely want to consider a bedside surgical procedure to relieve that pressure. If a patient comes in with kind of burned hairs in their nose, they're wheezing, they've got black stuff all the way around their mouth. What's the complication we would fear there?

So we're worried about their airway. They could develop laryngoedema, so we're going to have a low threshold for intubation there. And then if a patient who was kind of in a house fire or something comes in with confusion, they've got a headache, and their skin is really, really red, carbon monoxide, we'll want to check the carboxyhemoglobin.

Remember that a pulse ox doesn't do you any good here. Why is that? Yeah, absolutely.

So carbon monoxide actually causes a leftward shift of that hemoglobin oxygen dissociation curve, and the hemoglobin molecules are more saturated. Good. So the treatment here, we want to give them 100 percent O2. And if we have a lot of carbon monoxide on board, we might consider hyperbaric treatment.

OK, so clotting. What is the cause of clotting that we worry about in old people, particularly me? I worry a lot about this.

Not for me, but for my future patients. Giving you a hint and it's not being helpful. Cancer, yes.

Cancer is a hypercoagulable state. So in old people that have a sudden, you know, increase in clots, hypercoagulability, we're going to worry about cancer. What about a patient who's got some new clots and they're edematous, they've got high blood pressure and foamy pee? What might be a cause of a hypercoagulable state that would cause edema, hypertension, and foamy pee?

Not cirrhosis, but it's an osis. Nephrosis. So nephrotic syndrome is a hypercoagulable state because, remember, in nephrotic syndrome, we're losing protein in the urine.

And some of the first proteins to go are things like antithrombin 3 and a lot of other clotting factors. nephrotic syndrome in and of itself is a hypercoagulable state. So that's important to remember.

This is kind of one of those instances where medicine sneaks into your surgery shelf. If a young person has a positive family history of clotting, the most common inherited hypercoagulability is factor V Leiden. And why do we care about antithrombin 3 deficiency as surgeons, or at least as surgery students?

What can't we give to someone with AT3 deficiency? Heparin, because it won't work. Very good. So a young woman who has multiple spontaneous abortions, lupus anticoagulant, we might be concerned about that.

And in a patient post-op who has thrombocytopenia, but increased clotting. They've got some arterial clots or some venous clots, and maybe they received heparin. Yes, good, hit. So sometimes they'll be real obvious and tell you that they gave the patient heparin, and sometimes they'll just say it's a post-op patient, and most post-op patients receive heparin. So either way, any time you see low platelets plus clotting, think hit.

Those are kind of the two factors that should trigger that alarm in your mind. So if it is hit, what do we treat it with? Protamine.

Oh, so protamine is the antidote for heparin, but um, yeah, so it's what, what? Is that Harlingen? Synthetic heparin. Synthetic heparin, like leperudin or agotriban, yes. So leperudin or agotriban are going to be our drugs of choice.

We obviously want to get heparin out of the picture as soon as possible, but we don't necessarily need to reverse it, because remember with heparin, the problem is we get an antibody that's formed. to heparin bound to PF4. So just reversing the heparin isn't necessarily going to correct the problem. So with bleeding, if we see an isolated decrease in platelets, what are we thinking?

Maybe in a young woman, ITP, so idiopathic, well, ITP. And if we have a patient with normal platelets but increased bleeding time and PTT, This might be another young woman who's got heavy periods, nosebleeds, bruises really easily. but the platelets are normal, but the bleeding time is high, von Willebrand's. So von Willebrand's. So again, this is a problem with platelet function, not necessarily platelet number.

And why do we care about this medicine stuff? Because if our surgery patients have it, it's going to make a difference to how we treat them in the OR. So lastly, if the platelets are low, the coags are high, fibrinogen is low, D-dimer is high, and you see schistocytes on the smear.

Are we worried? Yes. What are we worried about?

DIC. That is badness. So some important causes to remember. Gram-negative sepsis because of the LPS can cause DIC.

Disseminated carcinomatosis can cause it. And then some random OB stuff that we care a little bit less about at this stage. Okay, so for a patient with a burn, remember the rule of nines and how it's a little bit different between adults and kids. And remember the Parkland formula for determining fluid resuscitation of a burn victim. So you'll see some discrepancy in the sources as to whether to use three or four.

And for kids, whether to use two to four. I've even seen six to eight. I think it was in the Pistania packet. These are the numbers that I found in the most sources. So these are the ones that I memorized for my test.

But, you know, again, it kind of depends on what source you're using. Things to remember about burn patients, they are more susceptible to infection, but we don't give them IV or PO antibiotics. Why is that? Yeah, it breeds resistance.

Very good. So we're going to give topical antibiotics instead. And there are three main topical preparations we give to burn patients, and you'll want to know the differentiating factors between them.

So one factor or one Topical medicine doesn't penetrate eschar, but can cause leukopenia. Which one is that? Oops.

Okay. Yes, silver sulfadiazine. Very good.

So the side effect of silver sulfadiazine that you need to remember is leukopenia, and it's not the best for third-degree burns because it won't penetrate that eschar. So what does penetrate the eschar but is very, very painful? Maffinide, maffinide.

And then the third one also doesn't penetrate the escher, and the side effects that you watch out for are hypokalemia and hyponatremia. Silver nitrate, very good. So I definitely had a question about one of these, determining between the three of these agents based on their side effects.

So go back and review this before your test if you have time. So some other random burn stuff. You've got a chemical burn, particularly in your eyeballs.

What do you want to do? Flush it even before you come to the ER. If you've got an electrical burn, the next best step, very good, because what's going to kill you? The arrhythmia after the electrical burn. So first best step for an electrical burn is an EKG.

If that's abnormal, we've got to monitor them on telemetry for two days. If we've got a burn patient, especially an electrical burn patient, who's got a urine dipstick positive for blood, but there's no RBCs, Seen on the microscopic exam. What does that tell us? Their pee is red, but there's no red blood cells in it. Rhabdo.

Very good. So rhabdomyolysis causing myoglobinuria causing renal failure. So that's another kind of medicine-y thing that they could sneak in there. So if we find myoglobinuria, what do we check?

What would kill you? Potassium, absolutely. Because if you've got rhabdo, your cells are bursting and dying.

That intracellular potassium gets out and can cause fatal arrhythmias. So we've got to check the potassium. So what if a burned extremity becomes really tender, numb, white, cold, and we can't get a Doppler-Bowl pulse?

What is that called? Some bad stuff. Compartment syndrome. So the swelling can cause compartment syndrome. The criteria are those five Ps.

Or an old school way would be to measure the compartment pressure greater than 30 millimeters of mercury. And how do we treat it? Yeah, fasciotomy.

And they even do it at the bedside, I've heard. I didn't do the burn rotation, but I hear you get to do these with some frequency. Did anyone do them?

Fasciotomy? Yeah? Was it scary?

Surgery scares the poop out of me. It really does. I'm not doing it. Anyway, glad someone will. Okay, so trauma, very, very high yield on this exam.

So you can get a lot of test questions, you know, bang for your buck points-wise if you review your trauma stuff. So what do we do with an airway if our patient comes in and is unconscious? Innovate! Good.

What if the GCS is under 8? Innovate! What if a dude gets stung by a bee and he's starting to get strider?

And he's doing some tripod posturing. Innovate! What if a dude gets stabbed in the neck, but his GCS is 15, he's talking to you like nothing's wrong, but he's got this expanding mass in his lateral neck?

Innovate! Yes. What if a guy gets stabbed in the neck and you hear some crackly sounds when you're palpating around his neck?

It feels like Rice Krispies under his skin. Be careful while intubating with a fiber optic bronchoscope. Yes, so that crackly Rice Krispie stuff, that subcutaneous emphysema, and you might have a laryngal injury or an airway injury, so you'll want to take a look at what you're doing with a fiber optic bronchoscope if at all possible.

So what about a dude with huge facial trauma, can't really see what's nose and what's face and what's mouth and all that stuff, and the GCS is 7. Crike. Good. So when you can't assess where you're putting your tube, your airway, this is a good indication to do a cricothyrotomy. All right.

So you intubated your patient. Next best step. What did you do in the pit? Listen for breath sounds. Good.

It's almost too easy, right? You've got to take your stethoscope out and listen. If they're decreased on the left after you've placed your airway, pull it back.

because you have intubated the right main bronchus. So what do we do? Pull it back.

And next step? Well, listen again. Let's say we know we got it now. You do usually get a chest X-ray, but we also want to check the oxygenation status. So, okay.

Speaking of chest X-rays, check these out. So what do you think about this one right here? Is anything there worrisome to you?

So this patient might come in hypotensive. Their chest really hurts because they were in a really high-velocity accident. They're dyspneic. There's some new murmurs. Yeah, so this is traumatic aortic injury.

So the treatment here, OR like yesterday. They've got to get there soon. because we need surgical reconstruction with a clip.

So this is traumatic aortic injury. What about this? Pay no attention to this word right here. So what is this chest X-ray? Oh, that's a pneumo.

That's a pneumothorax. And can you see the darker lung fields here? It's a little more hyperlucent because it's air. There's no lung tissue. So this little shrivelly dude here is the collapsed lung.

as they've so nicely told us, got a pneumothorax. So what might we see on physical exam with our pneumothorax friend? What might we hear?

So we hear absent or decreased breath sounds on this side, hyper-resonance to percussion. What, what? If it's attention, pneumo, sure.

Yeah, so we definitely want to pay careful attention to the neck veins because if they were distended. and the trachea were deviated away from the side, then we'd be worried about attention pneumo. So what about this one? Does this look like a normal chest X-ray or not?

That looks pretty crappy. So what does this patient have? Let's say we listened over here, and we hear decreased breath sounds. It's dole to percussion.

Yes, that's a hemothorax. Very good. So what are we going to do?

Chest tube. Very good. Chest tube. So what are the indications to take somebody with a hemothorax to the OR? That's another thing they like to ask about on the shelf.

When do you go to the OR? Yes. So if there's high output greater than a liter and a half in the first immediate time when you put the chest tube in, then we take him to the OR. Or if there's greater than 200 cc's per hour over the first four hours. So high output is a reason to take someone with a hemothorax to the OR.

Otherwise, you just kind of let it drain. And this last one also looks bad. So this patient also may have had some rib fractures on this side. They had a really bad car accident where their chest hit the steering wheel. If this were described in the clinical vignette, it might be called a whiteout lung.

Yeah, it's a pulmonary contusion. Very good. And treatment for pulmonary contusion. Do we take him to the OR?

No. Basically just good pulmonary toilet. We want to make sure that they're expanding their lungs. If they've got some pain from their rib fractures, we need to control their pain.

But these people don't get surgical intervention. We just want to make sure that they're coughing, clearing their secretions, and taking deep breaths. Okay, so a little bit more about chest trauma. If a patient has inward movement of the right rib cage upon inspiration, what is that?

So that's paradoxical movement, right? If it moves in when you inspire. So that's flail chest from rib fractures that are three consecutively.

And how do we treat it? How do we treat flail chest? What? Nerve block. Good.

So we want to control pain and you are psychic and read my mind to the next question. What do we do for pain control? We give nerve block.

What if this patient is screaming and crying? Doctor, I hurt. I need some morphine.

I need some Demerol. Why not? Yes, because opiates can decrease the respiratory drive, which we don't want in our patient with a rib fracture. Okay, so patient has confusion, petechial rash in the chest, axilla, neck, acute shortness of breath, maybe after a really bad car accident, fat embolism. That was on House the other day.

Did you guys see it? Yeah, yeah. See, now you'll never forget it.

So when do we suspect a fat embolism? Long bone fracture usually. Femur is classic. So if we have a patient who dies suddenly after a third-year medical student removes the central line, that's not funny because that would be like the worst thing ever.

That's an air embolism. So you also suspect air embolism when there's lung trauma, using a ventilator that's overzealous with the tidal volume, or during vascular surgery. where the vessels are being violated. Okay, so more on cardiovascular. If the patient is hypotensive and tachycardic, what's that?

Shock, right? So we worry about shock any time we see on vital signs hypotension and tachycardia. If the neck veins are flat and the central venous pressure is normal, what type of shock is that probably? The most common type of shock, yes, hypovolemic, so maybe with hemorrhage if it's in the right clinical situation. So the next best step here, got to do fluid resuscitation.

So two large-bore peripheral IVs, got to give two liters of normal saline or lactated ringers over 20 minutes, and then followed by blood if we don't see an appropriate rise in the vital signs. If we hear muffled heart sounds, we see some JVD, and our EKG shows electrical alternans, and we see some pulses paradoxes on inspiration, tamponade. So now we're real worried. What are we going to do to confirm pericardial tamponade? We can do it fast.

We can do that quick ultrasound if it's readily available. But if you really have strong clinical suspicion, you go ahead and treat. Then what's the treatment?

Needle decompression. So we've got to get that blood out of the pericardial sac so the heart can contract properly. So if we have, kind of talked about this already, decreased breath sounds on one side, tracheal deviation away from the collapsed lung, tension pneumo, and next best step, do we want to get a chest x-ray?

Shove a needle in it. So we do not need to confirm tension pneumo if we have the strong clinical suspicion. like the physical exam findings I've outlined here.

So chest x-ray will be wrong. Needle decompression will be right. And after you decompress with the needle, add a chest tube. Okay, so this is a busy slide, and I'll let you guys review this on your own.

But the differences between the types of shock does come up in test questions, particularly the differences between, like, neurogenic shock after a spinal cord injury versus hypovolemic versus... cardiac. So pay special attention when you're studying to what you see on physical exam, whether they're tachycardic or bradycardic, for example, and pay special attention to what your pressures would be measured by your Swann-Gantz catheter.

Okay, so head trauma. Remember how to calculate a GCS, and I've just listed the maximum for the Glasgow Coma Scale on this slide. So the best you can get for eyes is a four, motor is six, and verbal is five. So expect a question where you're given a clinical vignette and you're asked to calculate the Glasgow Coma Scale. What if you get this?

Oh, actually, I should ask this first. If a patient comes in with head trauma or they've ever been unconscious, what's the next best test? CT, right?

Because we want to see if there's any kind of bleeding. We're looking for this badness right here. So what is this badness? That's an epidural hematoma.

It's that biconcave disc. What about this badness? Is it subdural? Is it acute or chronic? It is acute.

How do you know? Yeah, so acute blood is bright on a CT. Old blood, and it's kind of a small one, but you can see it here, this little crescent is dark. It's already been partially reabsorbed and remodeled. So that's a chronic subdural.

This would be like an old person whose mental status has been going down the crapper for the past two weeks, like they're getting more demented and they've never been demented before, and then they fell off a horse two weeks ago. That would be a chronic subdural. Acute subdural is like after a really bad high-velocity car accident.

So symptoms to look for that indicate increased intracranial pressure include hematoma on a CT or edema, papilledema on fundoscopic exam or tumor can all cause increased intracranial pressure. And what are some symptoms? How do we know our patient has increased ICP by what they're telling us? headache, projectile vomiting, that's always fun, and then any type of change in mental status.

And how do we treat increased ICP? Elevate the head of the bed. We can give mannitol to help relieve some of the pressure.

What else? And we hyperventilate. We hyperventilate so the PCO2 is lower than normal. It's between 28 and 32. Okay. So when do we do surgical intervention?

Or what would we do for surgical intervention? Have you seen the neurosurgeons do it? That's also pretty scary.

That makes me want to poop my pants also. So ventriculostomy or a burr hole. They can do a burr hole for some of these hematomas.

The ventriculostomy, that's a little bit more controlled in the OR sometimes. That's a little bit less scary. Okay, so for neck trauma, review your anatomy and make sure you've got the difference between zones three, two, and one, and the differences in treatment or workup when the injury is in one of these three places.

So for penetrating trauma, anytime we have a gunshot wound or a stab wound, we want to make sure we know where in the neck the issue is occurring. So zone three, what are the boundaries? Yeah, so above the angle of the mandible. And what do we do if there's a penetrating trauma there?

Yeah, so we want to check the aorta with an aortogram or aortograph, aortogram, and triple endoscopy. So you've got a lot of passages up in zone three, right? The trachea is up there. The esophagus is there.

We really want to make sure all those major passageways are still viable and uninjured. So zone two is between the angle of the mandible and the cricoid, and the workup there is a little bit different. We want to do 2D Doppler to check.

the patency of the vessels, and we may want to do exploratory surgery. I couldn't find a definitive answer in the books that I read about it. It kind of just said plus minus. For zone one, that's below the level of the cricoid, and the workup there, we want to check the aorta.

So, okay. So what about penetrating abdominal trauma? If we have a gunshot wound to the abdomen, where are we going?

If we see this on chest X-ray, where are we going? Yes, immediately, right? This is free air under the diaphragm. Even if you suck at interpreting x-rays, make sure you can pick this out, okay?

And as we said, gunshot wound to the abdomen, we need to go to the OR and get X-slap plus a tetanus shot if it's warranted. So what about a stab wound and the patient is unstable and they've got rebound tenderness on physical exam? OR, yes, do not pass go.

What if they've got a stab wound, but the patient is stable? Yeah, so we'll kind of want to shove a finger in it, right? See if we have violated the peritoneum, if there's evisceration. The other thing we'd want to check is whether there's intra-abdominal bleeding.

So the FAST exam is a pretty good way to do that in the ER quickly, or the DPL, the diagnostic peritoneal lavage, if the FAST doesn't give us the answer we're looking for. And then if either the DPL or the FAST are positive, OR. So what if we've got blunt abdominal trauma and the patient is hypotensive tachycardic?

OR. So anytime we've got an unstable patient, OR. OK, so more on blunt abdominal trauma.

If they're unstable, OR. If they're stable, what's the next best step? CT. Yeah. So we're going to do an abdominal CT if they're stable enough to go to the scanner.

If we see a lower rib fracture plus... Bleeding into the abdomen, what are we going to worry about causing the bleeding? Yeah, spleen or a liver laceration, depending on the side, right? Spleen on the left, liver on the right.

If you've got a lower rib fracture plus their peeing blood, kidney. So a kidney laceration could cause those symptoms. If they've got cursine positive and viscera in the thorax. When we look at their chest x-ray?

Yeah, I've got a diaphragm problem, right? Curve sign is where you have pain in your left shoulder. So it's referred pain because of the phrenic nerve. I was never the best anatomy student, but that I remember. Okay, so handlebar sign, that's where you've got pain and bruising, kind of like if you're riding a bike and you flip over the bike.

where the handlebars would hit you right here. What's right here? Pancreas. So handlebar sign, big bruising in the mid-epigastric with some abdominal pain after trauma.

Worry about pancreatic rupture. The CT will show you that as well. If they're stable with epigastric pain, this is a little bit vague.

I got a couple of USMLE World questions on this. I don't know if you guys have seen them. So we'll want to get... an abdominal CT to assess what's going on. And if you see retroperitoneal fluid on your abdominal CT, what might have been injured?

Duodenum, the duodenum. So duodenal rupture, they're stable. It's not a really acute abdomen picture.

But when you do the CT to work up their epigastric pain, if you see retroperitoneal fluid, the duodenum might have been ruptured in a way that's going to cause retroperitoneal leak. leakage. Okay, so for pelvic trauma, if the patient is hypotensive tachycardic, you want to make sure they're not bleeding into their abdomen.

You can bleed out into your pelvis, and the best way to stop that is by stabilizing the fracture, if it's present. If we've got blood at the urethral meatus, and if it's a man, obviously, the prostate is riding high, what are you worried about? Blood at the urethra, high-riding prostate.

So you might have a urethral or bladder injury associated with your pelvic fracture. What's the next best test? You want to evaluate the urethra with a retrograde urethrogram. Do not put a Foley if there's blood coming out of the pee-pee. Don't do that.

So if the retrograde urethrogram is normal, what might you want to check? So it's not the urethra. What might be bleeding?

The bladder. So we'll do a cystoscopy or a retrograde cystogram. And here we're looking for dye extravasating from the bladder.

And you have to do two views in this study to see whether or not the dye extravasates into the peritoneum. So if it's extraperitoneal, not that big of a deal. We just tell them to rest, place a Foley for comfort. If it's intraperitoneal extravasation of dye, that's a big deal. surgery needs to perform semi-urgently to repair the bladder injury.

Okay, so as far as ortho trauma, some fractures that go to the OR I've got listed on this slide. Anytime a depressed skull fracture is present, go to the OR. Anytime you've got a really severely displaced or angulated fracture, go to the OR.

Any fracture where bone is sticking out into the air, that's bad, go to the OR. Or ephemeral neck or intertrochiric fracture. goes to the OR as well. Some common fractures, if they give you a clinical vignette that describes shoulder pain after a patient had a seizure or had a really severe electrical shock, that's a posterior shoulder dislocation. What about an arm that's outwardly rotated and you've got numbness on the deltoid?

Anterior shoulder dislocation. And why numb over the deltoid? Axillary nerve injury.

Good. An old lady fell on her outstretched hand and her distal radius is displaced. That's Colley's fracture. That's the dinner fork deformity that you might have read about, Colley's fracture. It's usually when an old person falls on their outstretched hand.

If a young person falls on their outstretched hand and you palpate their anatomic snuff box and elicit tenderness, what's broken? Skateboard. Very good.

So you all saw this guy in the ER, right? I just punched a wall. It wasn't in a bar fight, I promise. So what?

And their hand hurts. What did they probably break? Yeah, it's Boxer's fracture.

It's a metacarpal neck fracture, usually of the fourth or fifth metacarpal. And the clavicle, where do we usually break it? Between the middle and the distal thirds. Good.

Back to scaphoid fracture, often when you get the x-ray, what will you see first off? Nothing, right? The x-ray can often be negative, and not having a high index suspicion for this fracture can lead to problems for your patient and maybe lawsuits for you.

So even if the x-ray is clear, it's important to have a high index of suspicion for this fracture because you can't often see it early. Okay, so here's kind of the things I was talking about. The depressed skull fracture that they might show you. See, right, this would be normal.

This is abnormal. This is Collie's fracture with the dinner fork deformity of the radius. Scaphoid fracture, it's kind of hard to see. This is where it's already been pinned surgically.

This shows a clavicle fracture. You can see it is not a continuous clavicle. And then femoral neck fracture versus intertrochanteric fracture.

So x-rays that they might put on your exam. Okay, so after surgery, fever on post-op day one, what is the most common cause? Very good, atelectasis. And how do we diagnose it? We can listen, we can take a chest x-ray, and usually the findings are pretty unimpressive, just some kind of bilateral fluffy stuff in the lower lobes for atelectasis.

How do we treat it? Pulmonary therapy. If you're my surgery attending, you scare the crap out of the patient, like, you better get up and breathe deeper, use your incentive spirometer, or you're going to get pneumonia and die. So scaring your patient can prevent atelectasis. I don't know if I'd use that technique, but whatever.

So on post-op day one, what if they have a really high fever to 104? They appear very, very ill. So neck fash is one thing that can cause a super high fever in the early post-op period. The pattern of spread is long scarpus fascia in the subcutaneous tissue and common bugs that can cause necrotizing fasciitis, strep, yep, and clostridium.

I already put it up there. Okay. So how do we treat it?

OR, OR, and debride, debride, debride. So heavy-handed debridement in the OR with IV penicillin is how we treat necrotizing fasciitis. So the other cause of a super, super high fever and muscle rigidity, like right after surgery in the PACU, what?

Malignant hypothermia. And what's it caused by? It's a genetic problem. Oh, well, so what causes it?

The anesthetic that's used during surgery, either succinylcholine or halothane. And the genetic defect is a problem with the ryanidine receptor. So that nugget of information might have been in your brains from physiology, but it actually could end up on your test on Friday for surgery. So how do we treat malignant hyperthermia? Dantrolene sodium.

Very good. And dantrolene sodium. Works because it blocks that ryanodine receptor and decreases the amount of intracellular calcium.

Okay, so fever on post-op day three through five. Got a chest x-ray that looks like that. Fever, cough, and diaphoresis.

So here's the heart. What's this? That's consolidation.

So that's pneumonia. This is pneumonia. And how do we treat it?

Antibiotics, right? So we'll want to check a sputum sample to culture, but we'll cover them with usually a fluoroquinolone in the meantime to cover for strep pneumo while we're waiting for the cultures to come back. So another common cause of fever on post-op day three, four, or five is fever, dysuria, frequency urgency, particularly if the patient has a Foley UTI. The next best test, UA and culture. Good.

And how do we treat them? Antibiotics, right? Take out the Foley or change it and then treat them with antibiotics until the culture comes back.

So post-op day seven or beyond, if there's tenderness at the IV site, worried about a line infection, and we treat it by taking a blood culture first to diagnose and then pulling the line and giving antibiotics. If there's pain at the incision site, edema and induration. And around that area, but there's nothing draining.

What is that? It's red, it's swollen, it's painful, but there's no drainage from the incision. Cellulitis. Good. So the no drainage with that clinical picture tells us it's cellulitis.

And what do we do to treat cellulitis? Leave it alone. Cut it open.

Give antibiotics. So we'll do blood cultures to make sure it's not bacteremia, and then we'll start antibiotics. If there's a similar clinical picture with pain at the incision site, but there is drainage, that tells us we have a wound infection. And how do we treat these?

No antibiotics. We'll open the wound, repack it. If you're the medical student, you have to change the nasty packing every day. You know what I'm saying.

You guys had to do that too, right? It wasn't just me? Okay.

So what if we've got... Pain at the incision site with salmon colored fluid that weeps from the incision. Dehiscence, that's also bad news. And how do we treat that? So depending on the degree of dehiscence, it requires a trip back to the OR.

So we'll have to give them antibiotics and then close the fascia. Because in dehiscence, the problem is violation of the fascia, and we can't just let that go. So typically they need to go back to the OR to get that primarily closed.

Unexplained fever could be an abscess, especially if there was intra-abdominal surgery in the recent past. And we diagnose that mainly with a CT. And in the last resort, we may need to do a diagnostic laparoscopy or laparotomy to see what's going on. And treatment of an abdominal abscess, and most abscesses for that matter, drain it, drain it.

So almost all abscesses, with the exception of two that I know of. need drainage. So abdominal abscesses are no exception. Some other random causes of fever, thyroid storm, thrombophlebitis, particularly, now this tripped me up on my shelf.

There are a couple of OBGYN questions on the surgery shelf, usually after gynecologic surgeries. It's like after a C-section or after like a hysterectomy, a patient could have unexplained fever. You looked for all these sources and ruled them out.

They can have pelvic thrombosis. phlebitis and the treatment there is antibiotics, yes, but also heparin, because until you break up the clot that's got the little bacteria friends hanging out in there, the antibiotics won't do any good. So if they do give you a gynecologic surgery patient, unexplained fever late in the post-op course, think about thrombophlebitis. OK, so pressure ulcers. These are gross.

They're caused by ischemia in a word. And there are four stages. So stage one.

blanchable, so that's always a good sign. Anytime you see a pressure ulcer, you want to touch it, make sure it blanches. If it's stage two, it starts to look a little bit crustier and grosser. There's a blister, an actual break in the dermis. Stage three, it starts to erode into muscle, and stage four, that's super bad news, it goes all the way to the bone.

So one thing I will point out, because it was either on the midterm or the real shelf, I can't remember, and that's Marjolin's ulcer. Was that on the midterm? So what's Marjolin's ulcer and why do we want to do a biopsy to rule it out? Squamous cell carcinoma.

Very good. So in a chronic ulcer, all that remodeling and cell turnover for repair can predispose to carcinoma arising in that area. Okay, so treatment for stage one and two, get a mattress, put some cream on it, no big deal. Stage three or four really needs surgery with a flap reconstruction in most cases.

Okay, so for thoracic surgery, remember your pleural effusions. Be able to see them on a chest x-ray. And any time you have more than one centimeter of fluid in this little costaphragmic angle or more than one centimeter on a lateral decubitus x-ray, you've got to tap it.

You've got to do a thoracentesis to see what type of effusion you're dealing with. If it's transnative, it's more likely to be a systemic cause, like a congestive heart failure, nephrotic syndrome, or cirrhosis. Some random things they might throw in there.

If it's transidative with a low pleural glucose, rheumatoid arthritis can actually cause that. Not surgical, but whatever. If there are high lymphocytes in a transidative effusion, it might be TB. And if it's bloody, think cancer or a PE.

So if it's an exudative effusion, it's more likely to either be due to a pneumonia or a cancer. And a complicated effusion means there's bugs in there. We can see them on gram stain.

There's pH that's low. acidotic effusion or what you can't see there the glucose is low and the glucose is usually low because either cancer cells or bugs are eating it. So that makes sense.

And if it's complicated, we need a chest tube. And were you guys pimped a lot on Leitz criteria? No?

Okay. Well, Leitz criteria are how we determine whether it's transidative. And we check the LDH and compare it to the LDH between the effusion fluid and the serum.

If that ratio is less than 0.6, we're transidative. And if the protein ratio between effusion and serum is less than 0.5, we're transidative. Okay, so a spontaneous pneumothorax. Remember, these can happen in our emphysema patients when a subcloral bleb ruptures and the lung collapses. Or it could also happen spontaneously in a young, healthy man.

Usually they're tall and skinny and suddenly have some shortness of breath. So we do a chest x-ray to diagnose it, treat it with a chest tube. And important for you guys are the indications for surgery. When do we intervene in these folks who have the spontaneous pneumothoraces? if it recurs on the same side or the opposite side, if they're bilateral, or if the lung can't completely expand after the pneumothorax.

Also, if they've got some kind of occupation that would be really bad if they suddenly passed out, like if they're flying a plane or underwater or something, then we might want to do surgery. And the surgery we do is the video-assisted thoracic surgery. or pleuridesis, where we shove some stuff in there to make the pleura stick and prevent lung collapse from happening again. So lung abscesses, remember I kind of hinted that there were a couple abscesses that we don't drain as a first treatment. Lung abscess is one of those.

So if we have a patient with a lung abscess, we can see it on chest X-ray with an air fluid level. That's what you would see or that's what they would describe. And the initial treatment is not drainage.

but antibiotics. And since staph or anaerobic bacteria are most likely to cause a lung abscess, we're going to treat it with either penicillin or Clinda. So why would we drain it surgically?

If the antibiotics don't work or if it's super bad or if there's empyema. Okay, so if you have a patient with a solitary lung nodule, what's your first step? Find an old chest X-ray and compare it. Very good. So.

Some things on a chest x-ray that would reassure us, if we see a really small nodule like this one, if popcorn calcification is described, that usually means hammertoma, which is common and benign. Concentrant calcifications means it's an old granuloma, like a healed TB. Or if the patient's young, it's tiny, well-circumscribed, not as big a deal. So the treatment is just close follow-up. We don't necessarily have to go in there and get out the nodule itself.

However, if... If it's big, if it's speculated, if the patient is old and has been smoking for a million years, we're going to be a little bit more suspicious of that nodule and we'll want to get the nodule out for tissue. So depending on where it is, if it's central and we can get to it from bronchoscopy, we'll biopsy it that way. Or if it's in the periphery, we may have to do an open lung biopsy.

Okay, so about cancer. These are the symptoms in your clinical vignette that tell you your patient has lung cancer. They have weight loss.

They're coughing, they can't breathe, they're coughing up blood, or they keep having recurrent pneumonia in the same side. Kind of a post-obstructive pneumonia is what they call it. The cancer kind of gets in the way of mucus clearance, so you keep having pneumonia on the same side.

So once you've diagnosed lung cancer, there's four main flavors you need to know. So what's the most common type in non-smokers? Adno.

Adenocarcinoma is most common in non-smoking patients and it can occur in the site of old pneumonia like in the scar tissue there and adenocarcinoma is it peripheral or central? 50-50. Peripheral. So it's a peripheral cancer and it likes to go to the liver, bone and brain and the weird place that adenocarcinoma likes to go that they might ask you about are the adrenals.

That's kind of weird. And other weird thing about adenocarcinoma is that it is likely to cause an exudative effusion with high hyaluronidase, a little known fact. So what about we have a patient with these lung cancer symptoms that also has kidney stones, constipation, feels bad, low parathyroid hormone, and a mass in the central part of their lung?

What type of cancer is that? Squamous cell. Very good. So squamous cell is central, and its paraneoplastic syndrome is that it makes a parathyroid-related peptide, which causes hypercalcemia.

Okay, so a patient has shoulder pain, ptosis. A constricted pupil on one side and a puffy face, facial edema. A dead guy got his name on this type of tumor. Pancose, good, or superior sulcus syndrome. And small cell is the cancer that likes to go there.

So that is superior sulcus syndrome or a pancose tumor, but it's typically caused by squamous cell. What about a patient with ptosis that gets better after they look up for a minute? That's also a paraneoplastic syndrome. There are antibodies against the presynaptic calcium channels. Also some dead guys.

Lambert-Eaton, good. And Lambert-Eaton is also associated with small cell carcinoma. So, okay. So an old smoker who's got hyponatremia but no JVD. We talked about this a little bit earlier when we talked about electrolytes.

That's SIADH, and that also comes from small cell. So almost all the perineoplastic syndromes come from small cell, except for parathyroid-related peptide, parathyroid hormone-related peptide. Okay, so last one, a chest X-ray shows a peripheral mass.

It's cavitating, and there are mets all over the place, really advanced at presentation. The only lung cancer we haven't talked about yet. Not small cell, but large cell. So large cell carcinoma is the other peripheral cancer. So out of the four you need to know, adeno and large cell are peripheral lesions.

Squamous and small cell are central lesions. So that's one way to distinguish them. The other way they like to divide up lung cancers is between small cell and non-small cell. And why is the divide there? between small and non-small, different treatments.

And that's what we care about on the surgery shelf, right? Who gets surgery? Non-small cell.

Small cell carcinoma, come see people like my attendings right now. Small cell carcinoma is very chemo and radio sensitive. So we don't do surgery typically for small cell carcinoma, but we can do surgery for squamous cell and other non-small cells.

Okay, so ARDS, important in our SICU patients. The causes that you'll want to remember are gram-negative sepsis, gastric aspiration, pancreatitis can also cause ARDS. How do we diagnose it?

Three criteria. So radiographic, sure, that's what I'm trying to show you here. So radiographic criteria are bilateral fluffy infiltrates.

That's one. Yeah, so the PaO2 over FiO2 ratio over 200. And then the third one is, so we've established here we see pulmonary edema. The patient can't breathe very well. The last criteria is to make sure this pulmonary edema isn't cardiac.

So the last one is, yeah, the wedge pressure less than 18. Good. So the first one shows us that. our ratio is low, so we've got hypoxia. The chest radiograph shows our infiltrates and our pulmonary edema. And this last criteria tells us that it's not the heart that's screwed up, it's the lungs.

Okay, so how do we treat it? What's our event setting? Peep.

Very good. Okay, so some murmur buzzwords. You can pick out these murmurs in your patients. What's the systolic ejection murmur? That's, um...

Has parvus at tardis, gets louder when you squat. Say, aortic stenosis. What about another systolic ejection murmur that gets louder when you Valsalva? This might be a little kid or a teenager on his pre-sports physical, hypertrophic obstructive cardiomyopathy. The difference here is what happens with Valsalva.

Because Valsalva decreases preload, right? Back to physiology. So Valsalva decreases preload.

And if the problem is aortic stenosis, it's going to get softer when we decrease preload because there's less flow going through the stenotic valve. With HOCUM, the obstruction actually gets worse when there's less preload because the ventricular wall can get closer to the valve. So what happens with Valsalva is how you tell the difference between those two. Our other systolic murmur has got a click. Late systolic murmur with a click.

Might be a young woman. MVP. The last one is holosystolic.

That's what makes it different from the previous three. It's all throughout systolic. radiiates to the axilla, mitral regurg.

Okay, so some more murmurs. These are in your babies that you might be fixing in PD surge. Holosystolic murmur with a late rumble.

It's the most common congenital heart defect. VSD, continuous machine-like murmur. That's PDA.

Wide fixed and split S2. Usually these don't need surgical correction. ASD, very good.

Rumbling diastolic murmur with an opening snap. Maybe they had rheumatic fever back in the day. Mitral stenosis. A blowing diastolic murmur with a widened pulse pressure.

And the eponym parade. You know all those dead guys like the, I don't even remember them. It's been so long since I took step one.

You guys know though, all those dead guy names like the water hammer pulse and all those things. What's that one? Aortic regurg.

Very good. Pulmonary stenosis. I think that does give you a wide fixed and split S2. The rest of the clinical picture will be different. Mainly what's going to help you with a right sided heart murmur is they'll tell you it gets louder with inspiration.

So all right sided heart murmurs, if they're trying to lead you down that path, they'll say in the vignette that it gets louder when the patient inspires. Whereas this one is probably going to be a little kiddo. someone under the age of 15. Okay, so for GI, what if your patient's, well your patient's wife actually, tells you that their breath is really bad and when they wake up they've got some snacks left over in their mouth. Really gross.

Zinkers, good. We treat that with surgery. Is it a true or false diverticulum?

Good. It only contains mucosa. And they've got dysphagia to liquids and solids.

And this is the characteristic, oh, wait, okay, so good. So who has dysphagia to liquids and solids and might have a barium swallow that looks like that? A chalasia.

So that's the bird beak where we've got the spasm at the lower esophageal sphincter. And we can treat that medically with calcium channel blockers. The hellermyotomy is the surgery we would do if medical management fails.

So what about epigastric pain? that's worse after you eat or lie down. Might be wheezy.

They might be hoarse. Those are some atypical symptoms. Oh, I skipped that.

Okay, so over here, dysphagia that's worse with hot and cold liquids, that's diffuse esophageal spasm. And this is the barium swallow that's characteristic with that. So it's not just like achalasia, where the problem is at the lower esophageal sphincter, but you've got spasm at different areas in the esophagus.

But the treatment's the same. calcium channel blockers or nitrates. So what I was talking about down here is your garden variety GERD. The wheezing, the hoarseness, and the kind of chronic dry cough, those are atypical symptoms of silent aspiration, where you're regurgitating some gastric secretions and then they go down into the airway.

So indications for surgery, this is important for you guys. When do we operate on patients with GERD? So if they have like scary, scary complications like bleeding, a stricture from all of the acid regurg, ferrets, like you said, or they're at the maximum medical treatment and they're still symptomatic. Very good. Okay.

So hematemesis after vomiting, subcutaneous emphysema, pleural effusion. What's on your differential for hematemesis? After vomiting. Might be a drunk guy.

So Mallory-Weiss wouldn't have the subcutaneous emphysema. So subcutaneous emphysema means there was a total transmural tear. So I was going with Borjaves here, but Mallory-Weiss would be on your differential for hematemesis, for sure.

So next best test here, chest x-ray first, see what we can see. We don't want to give barium here if we can help it, because it's going to be more irritating if there's a rupture. And the treatment, we've got to repair it, especially if it's a full thickness rupture.

So also on your differential for hematemesis, especially if they're a big drinker, they've got a history of cirrhosis, think about gastric varices or esophageal varices. And if they're in hypovolemic shock, we do what we do for anybody with hypovolemic shock. We resuscitate them, check the ABCs. give them lavage with a nasogastric tube, and then resuscitate them if they're hypovolemic.

So some other treatments for... For varices, we can treat it medically with octreotide or somatostatin, and then balloon tamponade if it's very grave, and we need to control the bleeding as soon as possible. So the treatment of choice for varices, we can band them or sclerotherapy. The thing I want you to remember, I got tripped up on this on some of my QBank questions, if we see varices incidentally, when we're doing an endoscopy or something, we don't treat them.

We only treat them if they're symptomatic. So remember that. And then progressive dysphagia or weight loss, what are you worried about here? If they've got dysphagia that's getting worse, they're starting to lose weight, cancer, right? Esophageal carcinoma.

The different types being squamous cell versus adeno, and they are present in different locations of the esophagus. Our best first test, if we're considering esophageal cancer, Barium swallow first, but really we need endoscopy, because with endoscopy we've got the capability to biopsy and prove the cancer cells are there. Okay, so for the stomach, if we see acid reflux pain after they eat or when they're lying down, and this isn't your garden variety GERD, there's a kind of hernia involving the stomach, hiatal hernia. Good. And there's two main types.

Type 1, sliding, where the GE junction goes straight up into the thorax. And the second type is paraesophageal, where the area next to the GE junction slides up. So the difference is with type 1, really it kind of depends on the symptoms. You treat them symptomatically. But type 2, those are more likely to end up in your OR.

So in a patient with mid-epigastric pain, that gets worse when they eat. The risk factors would be... H. pylori, NSAIDs, or steroids.

That might be a ulcer, gastric ulcer, especially if it's worse after they eat. And for workup, what would we want to do? We'll definitely want to get some kind of biopsy.

We can do a barium swallow first, but really we'll want to do an EGD, so that way we can get a biopsy and make sure it's not something scary. We can do our testing for H. pylori.

but we can also make sure we're not dealing with a gastric cancer. We'll want to do surgery if the lesion persists after maximum medical treatment. That's kind of the running theme for most of these conditions. So for gastric cancer, adenocarcinoma is the most common, and it's more common in the Japanese population.

Some random eponyms that you might need to know, Kuchenberg associated with mets to the ovaries, Bloomer's shelf is something you can feel on rectal exam. in the shelf down there near the peritoneum. Verkhaus node, anyone remember where those are? Superclav, very good. Sister Mary Joseph node, belly button.

Lymphoma, gastric lymphoma, what's that associated with? What other disease? What types of patients get gastric lymphoma?

AIDS patients. And malt lymphoma. is associated with H. pylori. This is actually pretty cool.

This is one cancer we can treat with an antibiotic. Because if we give the right triple therapy to treat the H. pylori, the malt lymphoma often goes away also.

Okay, so some other random stomach stuff. Do you all remember what mentrieres is? So it's a protein-losing enteropathy. So we might see that foamy P. And also on EGD, we might see enlarged rugae in the stomach.

Gastric varices, different from esophageal varices, these are often associated with splenic vein thrombosis, and it can happen after chronic pancreatitis. Diap... I can't even say this.

Someone pronounce this word for me. Thank you. And what is this associated with? If a patient has this, what are they going to come see you for? This is also on your differential for hematemesis.

Because that's where a vessel erodes into the stomach, and so the bleeding occurs, and we can have hematemesis. So that's what that is. Okay, so we talked about gastric ulcers, but if the mid-epigastric pain gets better with eating, what type of ulcer are we likely dealing with?

It's at the top of the slide. Duodenal, good. And these are more likely to be associated with H. pylori. Healthy patients, we can just go ahead and try them on a trial of medical management.

But we want to make sure that they're not bleeding occultly, so we'll want to do an occult blood test, fecal occult blood test. And then they're... A variety of tests we can do for H.

pylori. Which is the best one? Don't look at the slide.

Or look at it. So the best test is with endoscopy, we can do a CLO test. And again, this is best because we actually have tissue.

And we can exclude something scarier, like cancer, attributing to the problem. So the treatment here is our triple therapy with a PPI and antibiotics. And the breath and stool antigen tests can be done after therapy to make sure that we've cured the process.

So what are we worrying about if we treat our H. pylori and the pain doesn't get better? It's a medication refractory ulcer. Or there's lots of ulcers, or there's ulcers in weird places in the duodenum.

It's all in your ellison. So we're going to worry about DE syndrome here if the ulcers are refractory. There's still symptoms. There's still ulcers after treatment. And the best test for this is a secretin stimulation test.

And we find high gastrin even when we administer secretin. That's supposed to suppress it. So we treat this with surgical resection if we can find the tumor. And even though the ulcers are in the duodenum, the cancer or the tumor is actually more likely to be in the pancreas.

And more importantly, what else do we look for if we've diagnosed ZE syndrome in a patient? There's a syndrome that this pancreatic tumor is associated with, MEN1. So what else are we looking for? Here's the pancreas.

What are the other two things we look for? Pituitary and parathyroid. Good.

Very good. So in a patient with bilious vomiting, postprandial pain, and they just won the biggest loser and lost a buttload of weight, what are we worried about? I got pimped on this in the OR and got it wrong. It was very sad. So this is SMA syndrome.

Have you guys read about this? So SMA syndrome happens after rapid weight loss because the duodenum is compressed in that area between the abdominal aorta and the SMA. So that compression can cause pain after you eat when blood flow is trying to rush to the area. The treatment really is by restoring weight and nutrition, if possible. A Roux-en-Y surgery is a more drastic and last resort option.

So as far as pancreatic problems are concerned, mid-epigastric pain that radiates straight through to the back, what do we worry about? Pancreatitis. And what are the two most common etiologies?

Drinking and eating at McDonald's, right? Gallstones and alcohol-induced. I've read books where one or the other is listed as number one.

I'm not sure what the right answer is. I think it depends on your patient population. Here it's probably gallstones.

So how do we diagnose pancreatitis? What's the test of choice? So CT is the best imaging test. We can take a look at the amylase and lipase levels because those will both be elevated.

And the treatment for pancreatitis is mainly supportive. So NG suction if they're nauseous, NPO to give them bowel rest. IV hydration and just watching them.

Bad prognostic factors are things that we look for upon admission and then 48 hours later. And you can see those listed on the slide. The questions that I think are the most difficult about pancreatitis are the complications.

So what are some common complications of pancreatitis? Huh? Pseudocysts, sure. What else?

Third spacing of fluid, sure, that counts too. Hemorrhage and abscess, absolutely. So pseudocyst, remember, because it's pseudo, it doesn't have any cells.

If you see cells on a cyst on the pancreas, it's probably cancer. Hemorrhage and abscess, third spacing, which can progress to ARDS, is another complication. So chronic pancreatitis, really these patients usually present with malabsorptive symptoms.

And what I want you guys to remember about it is that chronic pancreatitis can predispose to splenic vein thrombosis, which then leads to what? Gastric varices. Good. So cancer of the pancreas, adenocarcinoma is the most common. And these are sad cases because they usually don't present with symptoms until it's pretty advanced.

And really, you have the best chance of getting caught early if the tumor is in the head of the pancreas. because you might have some obstructive symptoms. So some random vocab words to remember. Covocier's sign?

Is that how you say that? C word? What's that sign?

Palpable non-tender gallbladder, and it also might be associated with obstructive symptoms, itching and jaundice. What's Trousseau's sign? No.

This one's migratory thrombophlebitis. There may be a different trousseau, but the trousseau sign associated with pancreatic cancer is thrombophlebitis in different vessels that migrates around. So we diagnose pancreatic cancer with an endoscopic ultrasound, an FNA.

We always want to get a tissue diagnosis. And for you guys, what's important is when do we do surgery? Or I should say, when is surgery not contraindicated? When is a pancreatic tumor deemed resectable? Mainly, it can't be invading into important stuff.

So we don't want to have mets outside the abdomen because the whipple won't be curative. We don't want extension into the SMA or the portal vein or mets into the liver or elsewhere. So resectable lesions are really pretty well confined to the pancreas and the immediately surrounding areas like the duodenum.

Okay, so endocrine pancreas, insulinoma, usually diagnosed clinically with Whipple's triad. What's that? Oh, you guys are getting sleepy, I'll tell you. So symptoms like sweating, being shaky, hungry, even seizures from hypoglycemia, low blood glucose level, and then the symptoms that get better after we give glucose.

So on labs, how we can tell it from a big faker, is their insulin levels are high, but their C-peptide levels are high, and their pro-insulin levels are also high. So those second two lab tests are really how we can tell the real deal from the surreptitious insulin administrators. So a glucagonoma, then, is an endocrine tumor that makes glucagon, and the symptoms there are hyperglycemia, diarrhea, and weight loss.

And you probably won't see this picture, but glucagonoma has a characteristic rash. Does anyone remember the name of it? It's on this guy's butt cheeks right here. I think that's his butt, I'm not sure.

So it's called necrolytic migratory erythema. In case you see it in a clinical vignette on a super hard question, at least you've heard it once. So somatostatinoma, these are the worst tumors to have because they're more commonly malignant, and they present basically with malabsorptive symptoms.

And then a VIPOMA, the symptoms are kind of like carcinoid syndrome. Watery diarrhea, flushing, and then hypokalemia and dehydration from the diarrhea. So the treatment there is like with carcinoid syndrome.

We give octreotide. So gallbladder. You saw lots of gallbladder pathology on your general surgery rotation.

The characteristic symptoms of right upper quadrant pain goes to the shoulder or the back. Nausea, vomiting, fever. After you eat some McDonald's. What's that usually? What gallbladder problem is that?

Is it cholecystitis or is it symptomatic gallstones? And fever. Fever really can help us make that determination.

A white blood cell count would also be helpful because you're more likely to see leukocytosis and cholecystitis, but fever can also give you that clue. So the best first test is an ultrasound. That's what I've got shown to the side.

And we treat it by taking the gallbladder out. I'm sure you guys saw a lot of those. So the only time you put a percutaneous cholecystostomy is if the patient is too unstable to go to surgery. So in a patient with right upper quadrant pain, high bilirubin, and ALK-FOS, what are we thinking of there?

So it's obstructive symptoms, right, with the high bilirubin and alkaline phosphatase. So yeah, choledoco. So that's where the stone is.

So we've got a blockage of the common bile duct, and we can usually see the stone on ultrasound. And treatment is similar. We take the stone out.

So if your patient in your clinical vignette has this pentad of right upper quadrant pain, fever, jaundice, hypotension, and altered mental status, it's a complication of choledocolithiasis, or it gets infected, ascending cholangitis. Good. So we've got to treat them with antibiotics to cure the infection, and then we also have to take the stone out with ERCP. So for choledococysts, if you had some experience with PD surge, you might have seen some of this. There's a whole spectrum of types, but I would really remember type 1 and type 4 because the treatments are very different.

So type 1 is the most mild kind. It's just where you have fusiform dilation of the common bile duct, and we treat it with just excision. of that cyst done early in life by a pediatric surgeon.

Type 4 is the most bad. It's the most complicated. It's also called Carulli's disease, and that's where the cysts are far into the liver, into the intrahepatic ducts.

So for those, we can't just excise them because they're in the liver. We need a total liver transplant. And cholangiocarcinoma is pretty rare.

The risk factors are... primary sclerosan cholangitis, which is associated with ulcerative colitis, and then some other random things. Cancer, like most cancers in the GI tract, is treated with surgery, and maybe we add radiation afterwards. Okay, so if we order some LFTs and we see our AST is twice our ALT, what's causing that hepatitis?

Alcohol, absolutely. And what if they're, oh, just kidding, supposed to be ALT greater than AST, but they're both super high, like in the thousands. So reverse that little crocodile mouth. ALT is higher, but they're both in the thousands. It's not alcohol, it's a virus.

So viral hepatitis has higher levels of your liver enzymes, and the ALT is usually higher. So if they're both really high, but it's after hemorrhage or surgery, particularly cardiovascular surgery, what might be causing the elevated liver enzymes? Hurt of shock liver? So hypotension can cause liver injury, which leads to elevated liver enzymes as well. So in terms of cirrhosis, that can lead to portal hypertension and cause problems for our patients.

Medical treatment is usually tried first. Somatostatin is one of the medications of choice. And those vasoconstrict to decrease the portal pressure.

Again, we talked about esophageal varices already and that you don't need to treat them prophylactically. And TIPS is a surgical procedure that can be done that's really good at relieving portal hypotension, but what complication can it cause? So it makes the portal hypertension worse, I mean better.

What does it make worse associated with cirrhosis? What? Encephalopathy. Good.

It worsens encephalopathy. Because it prevents the clearance of ammonia. So we'll have higher ammonia levels, which worsens the hepatic encephalopathy.

And what do we treat hepatic encephalopathy with? Lactulose. So we poop it out, or the patients poop it out when they take lactulose. Some risk factors to remember for hepatocellular carcinoma.

The main one is if you're a chronic hepatitis B carrier. Hepatitis C carries a risk. to a smaller extent, and then cirrhosis for any reason can predispose you for HCC. AFP is the tumor marker to remember for hepatocellular carcinoma, and diagnosis is typically with a CT or MRI.

And the treatment depends on if there's one lesion or multiple. If there's one, it's easier to take it out surgically. If there are multiple, then we've got to look at some other options. Okay, so some random liver stuff.

If you're a woman on OCPs, either got a palpable abdominal mass or spontaneous rupture and hypotension, what might that be from? Hepatic adenoma. Hepatic angioma is the most common benign lesion in the liver, but this sudden rupture and the association with oral contraceptives should make us think hepatic adenoma in this case. Typically, we diagnose it either with ultrasound or MRI, and the treatment? Stock the OCPs.

So surgery really isn't needed unless it's super large or the woman wants to become pregnant, because pregnancy can increase estrogen as well, and estrogen is what makes these tumors grow. So the other benign liver tumor that's also more common in women but less likely to provide a problem when it ruptures is what? It's like hepatic adenoma, but different in that it's less dangerous, less likely to rupture. That's focal nodular hyperplasia. So that's the second most common benign liver tumor.

Okay, so let's talk about bugs. A bacterial abscess is most commonly caused by what bacteria? Okay, so the big three are E. coli, bacterioides, and enterococcus.

This is an example of something that's in surgical recall that actually might be on your shelf, so that's good to know. We treat this by drainage and IV antibiotics. So contrast that with this next patient who has pain in the right upper quadrant around the liver, profuse sweating, hard core chills, their liver is enlarged and palpable.

This isn't a bacterial abscess, but an amoebic one. So this is an amoebic abscess. It's a really profound fevers and chills.

They're sicker than somebody with just a bacterial liver abscess. And how do we treat these? Do we drain it? No. So this is the second abscess in the body that's not preferentially treated by drainage.

The first was a lung abscess. The second is an amoebic liver abscess. So treatment of choice is metronidazole.

Don't drain it first. OK, the last one. I always miss this one on the Q bank. It's usually a patient from Mexico or or somewhere else in South America or somewhere in South America. And they come in with right upper quadrant pain and lots of liver cysts on an ultrasound.

Yes, so this is Echinococcus. And the mode of transmission here, how do people get it? I think it's dog poo, but I'm not sure.

Could be fish also. Could be fish also. So that's where I read that this cysts come from. It's from dog feces.

The laboratory findings that are characteristic here, you see eosinophilia because it is a parasite. And there's something called the Cassoni skin test that's positive just because of the high amounts of IgE and the eosinophils from the reaction to the parasite. So the treatment is important. Surgery or no surgery? 50-50.

We do do surgery. So we give albendazole for medication, and we have to be very careful during surgery. Because if... one of these little cysts opens or breaks during removal, it can cause an anaphylactic reaction and even death for the patient. So we do do surgery, but we have to be very careful to remove this cyst in one piece.

All right, so some spleen stuff. Remember, after a splenectomy, you want to make sure to check the platelets. They can be high after splenectomy.

It's not a huge deal. You just have to give aspirin for preventing clots. And prophylactic penicillin is important for people after a splenectomy because of its role in immune function.

Also remember the big three vaccines we need to give a patient after we've removed their spleen. ITP, we talked about this a little bit already. The buzzwords you look for in the clinical vignette is that only the platelets are low. Everything else is fine.

COAG's are fine. Isolated decrease in platelets usually means ITP. Hereditary spherocytosis, you can also have splenomegaly.

because those abnormally round red blood cells are being taken up by the spleen. So the treatment there is going to be splenectomy as well. A little bit on trauma, traumatic splenic rupture. We talked about this already a little bit. We want to consider it if there's a left lower rib fracture and intra-abdominal bleeding.

And Kerr's sign we already talked about. That's left shoulder pain because of irritation in the left hemidiaphragm. All right. So. We'll probably get to talk about the appendix and then it will be nine o'clock.

But I will have all the rest of these slides posted if you guys want to take a look at them later. Because I know nobody's brain can work after nine if the review is supposed to go from seven to nine. So we'll talk about the appendix and then we'll stop. OK, so what if we have a patient with pain that starts kind of peri-emphilically and then moves to the right lower quadrant and becomes more sharp? What's that?

Softball, right? That's appendicitis. Good. So when do we go to surgery in a patient with appendicitis? Not a trick question.

If we think they have appendicitis. Yeah, if they have a strong clinical picture, we really don't technically need imaging. At UH, they typically get a CT anyway, but really you don't need it to justify surgery.

How would your management change if the appendix were either perforated or had an abscess? Exactly. So we want to make sure we drain the abscess and give antibiotics first, particularly antibiotics that are going to cover E. coli and bacterioides, because those are the most common bugs.

And then we'll do an appendectomy after they've been stabilized. So stabilize first and then take out the appendix. So carcinoid tumor.

Anyone know the number one site for carcinoid tumor? Appendix, good. So, conveniently placed on this slide. And what are the symptoms for carcinoid syndrome?

Flushing, diarrhea, that's pretty much it. Some wheezing too, wheezing. So when do they happen?

What has to happen to the carcinoid tumor before we get carcinoid syndrome? It's metastatic already. to the liver or beyond, right?

Because serotonin is metabolized by the liver on first-pass metabolism. So if it's just in the GI tract, the serotonin... and would be denatured before it gets out. So what else are we looking for in a patient with carcinoid syndrome? There's a particular nutritional deficit that patients with carcinoid syndrome often have.

It's a vitamin that they become deficient in. Nice and very good. Why?

Yes. Close. Serotonin and niacin are both made from tryptophan.

Good. So, yes. So if all of our tryptophan is being used to make serotonin, there's none left to make niacin.

And high five for that at almost nine o'clock. Very good. And remember from way back in the day, the cardinal symptoms of niacin deficiency are diarrhea, dementia, and dermatitis.

So that's another sneaky medicine thing that they can throw into your surgery shelf. Okay, so if our carcinoid tumor is bigger than two centimeters at the base of the appendix or with positive lymph nodes in the area, what surgery do we do? A big one, right, a hemicolectomy.

So we're going to take out more than just the appendix. If it's smaller than two centimeters in the tip of the appendix and no nodes are positive, we can just take out the appendix itself. Okay, what time is it? How many slides more can I do? Probably do one or two more.

So in terms of small bowel obstruction, I can just point out the highlights here. Remember that the symptoms for small bowel obstruction, pain, constipation, obstipation, not passing gas, and vomiting because nothing's going through. And again, what you need to remember is when do we do surgery? This is a surgery shelf, or at least it's supposed to be. So surgery is indicated in small bowel obstruction.

If there are peritoneal signs, rigidity, rebound tenderness, that kind of stuff. Or if conservative management doesn't cause improvement within 48 hours. Differences between post-op ileus and Ogilvy syndrome, I remember being important for the surgery shelf.

Radiographically, they're different in that post-op ileus has dilated loops of small bowel all the way through with air fluid levels. Because it's kind of a general stasis of stuff through your bowel. Whereas Ogilvy syndrome...

Really the highest points of dilation, or the biggest points of dilation, are in the colon, or cecum. So the thing to remember about Ogilvy syndrome is the threshold for treating is greater than 10 centimeters of dilation. And you can either decompress from above with an NG tube, below with a colonoscope, or you can give them neostigmine, because that kind of gets stuff moving through the bowel.

The thing that makes this scary, and I had a patient who we gave neostigmine to when I was a third year, is that neostigmine can cause bradycardia. So you really have to have somebody ACLS certified standing by the patient's bedside while you're giving that treatment. And this is a good slide to end on because you probably will see some kind of chest X-ray or abdominal X-ray on your shelf.

So I kind of want to point out some of the high-yield stuff that you might see. So what... What do we have going on in this one?

Can you even tell me what they noticed about this first abdominal x-ray? So we kind of see some dilated loops here. And can you see on this x-ray, do these little markings, these little segmental markings go all the way through or do they go halfway through? All the way. And from gross anatomy, does that mean it's small bowel or a large bowel?

Small, right? Because the pleca go all the way around the whole diameter, circumference of the bowel. If we were in large bowel, the haustra only go halfway through.

So this is a small bowel obstruction, and we can see the transition point or the blockage is probably somewhere like right here, right? Because there's poop in the lower part of the intestine. There's no air down here, but in the small bowel, we see the dilated loops up from the point of distension. So let's compare that to this picture. What do you think we have going on here?

Lots of air, right? Lots of dilation pretty much all the way through, right? It's pretty uniformly dilated. There's air throughout all of the intestine all the way down to the rectum down here, air in the rectum.

So what condition would most likely cause the second picture that we just talked about? It's a post-op ileus. Good.

And as a bonus, what electrolyte should you check if you see this abdominal x-ray? Potassium, because low potassium can contribute to ileus. Good. All right. So what about this thing?

Can you see how big this part is right here? What part of the intestine do you think this is? That's cecum.

That's a big, ginormous cecum. So what is this picture? This is Ogilvy's.

So this is the characteristic abdominal x-ray of Ogilvy's. The cecum is really massively dilated. I don't have a ruler or anything, but I bet it's bigger than 10 centimeters, so we would be treating this pseudo-obstruction. Okay, so lastly, we've seen this picture before.

Does this picture make you nervous down here? Yes. Where are we going with this chest x-ray? To the OR. This is free air under the diaphragm, so maybe a perforated small bowel obstruction.

Maybe diverticulitis gone awry. So something super bad here. And this barium study, they might describe it as a bird's beak.

So this is a volvulus. Sequel or sigmoid? Sequel. Sequel. So the bird's beak is a sequel volvulus.

This coffee bean sign here is a sigmoid volvulus. So the kind of crease in the coffee bean, can this kind of look like a coffee bean? Right? This crease here is the mesenteric artery. That's the kind of focal point for the twist.

So this is a sigmoid volvulus. This is a sequel volvulus. Those are kind of the abdominal x-rays, at least, that you would want to be able to identify correctly on your test. And I think that brings us right to 9 o'clock. So I'm sorry we couldn't get through everything.

I guess I talk a lot and we couldn't go through all of surgery in two hours, but I will post these slides tomorrow morning. Dr. Henze will send you the link and the file. So if you have any questions, email me. You know, I'm a fourth year, so I don't have anything to do. And thanks for coming, and I wish you luck on Friday.

Thank you. Thank you. Thanks, Harlingen.