1. Reactive thrombocytosis
- Platelets are an acute phase reactant - you will see them up in infection, inflammation
- Bleeding - platelets generally go up in bleed; they only go down in profound hemorrhage s/p many many units of transfusion
- Iron deficiency
- Cancer
- Splenectomy (transiently will go up over 1,000.000) - sickle cell patients tend to run high because of autoinfarction of spleen, 5 or 600,000
- These conditions rarely push your platelets above 1,000,000
2. Primary thrombocytosis
- You will see numbers >1-1.5 million
- Essential thrombocythemia
- Polycythemia vera
3. RBC mass
- 71 mL/kg is the normal blood volume.
- 29-33 mL/kg is the normal RBC mass
- Fick principle - take aliquot of blood label with chromium 51, inject back, then take another aliquot, measure chromium 51, then you can determine the total rbc mass.
4. Reactive erythrocytosis
- You expect to see decreased epo
- Chronic hypoxemia (COPD, R to L cardiac shunt etc)
- Renal (RCC, PCKD)
- Hepatocellular CA that makes epo
- Chronic carbon monoxide poisoning (ie smokers) - can get a CO test
- Some inherited Hb mutations that cause left shift of your oxyhemoglobin disassociation curve, so you've got a relative hypoxemia.
5. Primary erythrocytosis
- Expect to see increased epo
- P.Vera (High rbc, wbc, platelets, big spleen)
6. Reactive left shift (i.e. infection)
- Reminder cell line progeny: Blasts -> promyelocytes -> myelocytes -> metas -> bands -> polys
- Polys and bands will be way up, occasionally metas and myelocytes will be up a bit but you will almost never see promyelocytes or blasts.
- NO changes in eos and basos.
- Changes you will see in the polys-- toxic granulation, vacuolated neutrophils, dhole bodies (typically sepsis, sometimes G-CSF recipients)
7. CML left shift
- You'll see a more disorderly left shift
- Some polys, less bands, few metas, tons of myelocytes, lots of basos, increased eos, some promyelocytes and blasts.
- Neutrophils are pale, NOT toxic granulations. Work perfectly well, no infection risk so long as you have enough polys.
8. Myelodysplastic vs myeloproliferative
- Myeloproliferative - you make more cells, but the cells are functional. Look in the BM- all wbc, its CML, all cell lines up, its P.vera. Myelofibrosis ia type of myeloproliferative-- clonal production of megakaryocytes that elaborate cytokines (particularly FGF) induce filling of the marrow with fibroblasts, collagen.
- Myelodysplastic- you make a lot of cells, but the cells don't work well; your marrow is full of wbc but you're still getting infections. <20% blasts is MDS, >20% blasts is AML.
9. Phosphodiesterase inhibitors
- Nonselective: caffeine, theophylline, IBMX
- PDE 3 inhibitors: milrinone, cilastazol, imarinone, enoximone.
- PDE 4 inhibitors: rolipram, ibudilast, roflumilast
*PDE4 is in immune cells, so PDE4-I are often used as anti-inflammatories esp in people with inflammatory lung diseases (asthma, copd)
- PDE 5 inhibitors: dipyridamole aka persantine, all the viagra-type drugs (sildenafil, tardalafil, etc)
- PDE 10 inhibitors: papaverine (opium alkaloid antispasmotic). Treats GI/ureter spasm, can induce smooth muscle relaxation in coronary and cerebral vessels (has been used to treat subarachoid hemmorhage, angina). Can be directly applied to blood vessels in microsurgery to relax them to facilitate vascular anastomoses.
- Also, forskolin is an Adenylyl cyclase activator.
10. Prinzmetal's angina
- Tends to occur at the same time every day; often between the hours of midnight and 8 AM.
- Diagnosed clinically but can also be diagnosed with ergonovine infusion in cath lab
- Tx with calcium channel blockers
Thursday, May 8, 2014
Wednesday, May 7, 2014
1. Reasons to want a shorter heparin drip time while bridging to warfarin
- HIT (white clot syndrome) - worse than other drug-induced thrombocytopenia because HIT makes you hypercoagulable-- you shower platelet fragments everywhere and clot. Typically appears on day 5 or 10 when you start heparin (assuming no recent exposure to heparin/HIT)
- Pragmatic reasons (prevent coumadin hostages)
2. Reasons to want a longer heparin drip while bridging to warfarin
- Patient has increased risk of warfarin skin necrosis (i.e. protein C deficiency) - get big swaths of soft tissue necrosis
- Remember that just because the INR is 2 doesn't mean you're anticoagulated - factor 7 has a shorter half life and so your INR will change rapidly with coumadin, but 2, 5, and 10 are still high. So when someone comes back 2 days after you just d/c-ed them after 2 days on a heparin drip with a worse clot than they were admitted for, its not failure of coumadin, it's a failure of you properly anticoagulating them.
3. HIT
- HIT doesn't usually drop your platelets <50 - if you have platelets below that its not HIT. Or not just HIT.
- If you diagnose it, the patient is committed to 3 months of anticoagulation even if they didn't clot on it. The data shows a 50% chance of clotting in the first week
- FDA approved anticoagulants for HIT- direct thrombin inhibitors like argatroban and leparudin; factor Xa like fonda and rivaroxaban have been used but are not FDA approved for this purpose.
- PFA-4 - sensitive but not specific. Serotonin release assay - specific, takes a week to do. Don't go randomly sending off PF4-4 in people unless you have a reason to suspect HIT-- if it comes back falsely elevated (which is not uncommon) you've bought them 3 months of anticoagulation, so you don't want to be wrong.
- It's especially bad to be wrong about HIT in people who may need CT surgery-- cardiac surgeons don't want to use anything other than heparin in the bypass circuit, it works, can reverse with protamine before you return the blood to the patient, and so if the patient is carrying a HIT diagnosis then everything gets more complicated. The good news is that there's some data that you can use it during surgery even in people with HIT, and some data that heparin is OK 3-6 months after HIT but you'd rather not have to go there.
4. Blood s/p centrifugation:
- Plasma
- Buffy coat (bottom of plasma) = platelets, should not have any red cells, which is important, this means you don't have to cross-match platelets.
- Red cells
If you spin down plasma in the cold you get cryoprecipiate
5. Platelets
- A "six pack" of platelets- buffy coat from 6 different donors, pooled into one bag.
- More commonly, one donor will get platelet pharesis to pull a lot of platelets from one guy
6. Plasma
- FFP has all factors
- Cryo is rich in factor 8, vWF, and fibrinogen (good for DIC)
- Prothrombin factor concentrate: designed to reverse warfarin, so rich in factors 2, 7, 9, 10.
7. T+S vs T+C
- Screen: run recipient plasma against a few red cells of known antigenicity
- If its positive, you run a panel - trying to identify what the antibody that the patient is reacting against.
- Crossmatch - Indirect coombs-- looking for antibodies in the serum of the recipient that will react with the donor cells
8. Treatments for hemophilia:
- Hemophilia A (factor 8 deficiency): Recombinant factor 8: #units/kg * 2 = % rise in factor (So to go from 0 to 80% factor 8, then you'll need 40 U/kg)
- Hemophilia B (factor 9 deficiency) Prothrombin factor concentrate (contains 2, 7, 9, and 10)
9. Transfusion reaction
- Immediate: Wrong type-- circulating anti-A or anti-B antibodies immediately attack transfused blood. Complement, cytokine release, anaphylaxis. maybe ATN, maybe death.
- Delayed: people can develop new antibodies against blood. Not life threatening (no anaphylaxis, ATN, etc). Person is fine, then a few days later, Hb drops because they've developed new antibodies.
10. Platelet transfusion:
- Theoretically: 1 unit = 5,000-10,000 bump. But the more times you've been transfused, the less of a bump you get due to antibodies. Big spleen = you will also get less of a bump.
- "Pooled platelets are random donor platelet concentrates obtained from units of whole blood that are pooled at the time of transfusion. Single donor platelets are collected by apheresis using a cell separator. This technique allows the simultaneous collection of several units of platelets during a single donation. An average single donor platelet collected by apheresis will contain an equivalent of 6-7 units of random donor platelets. The recommended platelet transfusion dose is 1 unit per 10 kilograms of body weight when using random pooled platelets1 or one unit of single donor platelets per transfusion episode. The recommended dose is targeted to elevate the platelet count to adequate hemostatic levels (40,000-50,000/μL). Occasionally ABO antibodies can reduce platelet survival. Clinical factors such as fever, sepsis, splenomegaly, active bleeding, use of amphotericin, veno-occlusive disease, DIC, early post hematopoietic stem cell transplant period and some dialysis procedures are associated with decreased survival of transfused platelets2,3,4. Immune refractoriness, caused by allo- or auto-antibodies with specificities to the HLA or rarely, HPA antigens, can also complicate platelet transfusion support2,3,4." {source: institute for transfusion medicine}
- HIT (white clot syndrome) - worse than other drug-induced thrombocytopenia because HIT makes you hypercoagulable-- you shower platelet fragments everywhere and clot. Typically appears on day 5 or 10 when you start heparin (assuming no recent exposure to heparin/HIT)
- Pragmatic reasons (prevent coumadin hostages)
2. Reasons to want a longer heparin drip while bridging to warfarin
- Patient has increased risk of warfarin skin necrosis (i.e. protein C deficiency) - get big swaths of soft tissue necrosis
- Remember that just because the INR is 2 doesn't mean you're anticoagulated - factor 7 has a shorter half life and so your INR will change rapidly with coumadin, but 2, 5, and 10 are still high. So when someone comes back 2 days after you just d/c-ed them after 2 days on a heparin drip with a worse clot than they were admitted for, its not failure of coumadin, it's a failure of you properly anticoagulating them.
3. HIT
- HIT doesn't usually drop your platelets <50 - if you have platelets below that its not HIT. Or not just HIT.
- If you diagnose it, the patient is committed to 3 months of anticoagulation even if they didn't clot on it. The data shows a 50% chance of clotting in the first week
- FDA approved anticoagulants for HIT- direct thrombin inhibitors like argatroban and leparudin; factor Xa like fonda and rivaroxaban have been used but are not FDA approved for this purpose.
- PFA-4 - sensitive but not specific. Serotonin release assay - specific, takes a week to do. Don't go randomly sending off PF4-4 in people unless you have a reason to suspect HIT-- if it comes back falsely elevated (which is not uncommon) you've bought them 3 months of anticoagulation, so you don't want to be wrong.
- It's especially bad to be wrong about HIT in people who may need CT surgery-- cardiac surgeons don't want to use anything other than heparin in the bypass circuit, it works, can reverse with protamine before you return the blood to the patient, and so if the patient is carrying a HIT diagnosis then everything gets more complicated. The good news is that there's some data that you can use it during surgery even in people with HIT, and some data that heparin is OK 3-6 months after HIT but you'd rather not have to go there.
4. Blood s/p centrifugation:
- Plasma
- Buffy coat (bottom of plasma) = platelets, should not have any red cells, which is important, this means you don't have to cross-match platelets.
- Red cells
If you spin down plasma in the cold you get cryoprecipiate
5. Platelets
- A "six pack" of platelets- buffy coat from 6 different donors, pooled into one bag.
- More commonly, one donor will get platelet pharesis to pull a lot of platelets from one guy
6. Plasma
- FFP has all factors
- Cryo is rich in factor 8, vWF, and fibrinogen (good for DIC)
- Prothrombin factor concentrate: designed to reverse warfarin, so rich in factors 2, 7, 9, 10.
7. T+S vs T+C
- Screen: run recipient plasma against a few red cells of known antigenicity
- If its positive, you run a panel - trying to identify what the antibody that the patient is reacting against.
- Crossmatch - Indirect coombs-- looking for antibodies in the serum of the recipient that will react with the donor cells
8. Treatments for hemophilia:
- Hemophilia A (factor 8 deficiency): Recombinant factor 8: #units/kg * 2 = % rise in factor (So to go from 0 to 80% factor 8, then you'll need 40 U/kg)
- Hemophilia B (factor 9 deficiency) Prothrombin factor concentrate (contains 2, 7, 9, and 10)
9. Transfusion reaction
- Immediate: Wrong type-- circulating anti-A or anti-B antibodies immediately attack transfused blood. Complement, cytokine release, anaphylaxis. maybe ATN, maybe death.
- Delayed: people can develop new antibodies against blood. Not life threatening (no anaphylaxis, ATN, etc). Person is fine, then a few days later, Hb drops because they've developed new antibodies.
10. Platelet transfusion:
- Theoretically: 1 unit = 5,000-10,000 bump. But the more times you've been transfused, the less of a bump you get due to antibodies. Big spleen = you will also get less of a bump.
- "Pooled platelets are random donor platelet concentrates obtained from units of whole blood that are pooled at the time of transfusion. Single donor platelets are collected by apheresis using a cell separator. This technique allows the simultaneous collection of several units of platelets during a single donation. An average single donor platelet collected by apheresis will contain an equivalent of 6-7 units of random donor platelets. The recommended platelet transfusion dose is 1 unit per 10 kilograms of body weight when using random pooled platelets1 or one unit of single donor platelets per transfusion episode. The recommended dose is targeted to elevate the platelet count to adequate hemostatic levels (40,000-50,000/μL). Occasionally ABO antibodies can reduce platelet survival. Clinical factors such as fever, sepsis, splenomegaly, active bleeding, use of amphotericin, veno-occlusive disease, DIC, early post hematopoietic stem cell transplant period and some dialysis procedures are associated with decreased survival of transfused platelets2,3,4. Immune refractoriness, caused by allo- or auto-antibodies with specificities to the HLA or rarely, HPA antigens, can also complicate platelet transfusion support2,3,4." {source: institute for transfusion medicine}
Tuesday, May 6, 2014
1. Platelet bleeding is nuisance bleeding- immediate bleed, petechiae, nosebleeds, menorrhagia, rarely requires transfusions, rarely life threatening
2. Clotting factor bleed is delayed bleed (i.e. at dentist, initially you don't bleed but you do later)
3. Bleeding time (platelet function)
- BP cuff on arm, blow it above venous pressure
- Cut a few mm on volar surface of arm, every 15 seconds dab blood with filter paper. Stop the clock when the filter paper stops absorbing blood. Normal = 2-8 minutes.
- Won't run if platelet <50K; even with PFA-100, you expect worse function with lower counts
4. ITP
- Larger platelets, sort of like retics
- Can have low platelets, but normal clinical appearance
- Typically low numbers imply poor function, but these people may have normal function and thus be fine with procedures, so its good to run PFA-100/bleed time
5. Causes of platelet dysfunction (congenital)
- vWF - platelet dysfunction AND low factor VIII (20-30% of function) but not low enough to have clinically significant hemophilia-like picture (hemophiliacs have 0-1% of factor VIII function)
- Can treat vWF with intranasal DDAVP - useful in young women with very heavy periods because of vWF
- Others (rare): glanzmann's, storage pool disease.
6. Causes of platelet dysfunction (acquired)
- Uremia (although this is plus minus)
- Aspirin (pepto-bismol is a salicylate, sominex has a salicylate, many cough/cold medicines, alka-seltzer is aspirin with antacid). Effect of aspirin lasts as long as the platelet (most platelets have a 9-10 day lifespan, but given different ages of platelets in your blood, real effect is probably around 5 days.
- Drugs: NSAIDs, guaifenasin, 3rd generation penicilins: ticaricillin, piperacillin, 3rd generation cephalosporins
- Myeloproliferative disorders (p. vera, essential thrombocythemia)- lots of platelets that don't work
- Myeloma- abnl protiens made by myeloma coats platelets and affects function
7. Isolated prolonged PTT
- Deficiency: 8, 9, 11, 12-- Factor 12 def are not associated with bleeding, 11 is (rare) and 8 and 9 are.
- Inhibitor - iatrogenic (drawing blood above a heparin drip, backflow from a citrated/heparainated tube into your syringe that gets pushed into another tube) vs true (see below)
- Differentiate between the two: mixing study. If you mix pt's plasma with normal, if it works then you know its a deficiency; if it doesn't, there's a deficiency.
8. Inhibitor:
- lupus anticoagulant (not associated with bleeding)
- acquired factor inhibitors-- acquired factor 8 inhibitors as a sequelae of drugs or viral illnesses, has high mortality rate. Tx with immunosuppressants (steroids, rituximab, cyclophosphamide to block generation of inhibiting antibody) and give activated recombinant factor 7 to stop the bleeding.
9. Isolated prolonged INR
- likely vit K deficiency from antibiotics or decreased nutrition
- Transfuse FFP - as close to surgery as you can as the factors begin degrading immediately.
- Factor VII - half life around 6 hours
- In someone on warfarin, all drugs interact with it so any new drugs means you have to monitor the INR again
- Generally all antibiotics will prolong INR just because of gut flora effects
- Be careful of rapid correction with vitamin K if you overshoot the INR; if someone has an INR of 5-6, 2.5 mg of vit K PO will bring someone down to a safer level, at which point you can readjust the warfarin. But if someone is slightly high, don't go crazy with the vitamin K because if you overcorrect they may clot off whatever you were trying to keep from clotting off with the warfarin in the first place.
10. Vitamin K
- NOT IM don't give people with coagulopathy IM injection; they may get site hematomas that lead to neuropathy etc
- IV, SubQ, PO
- Takes around 24 hrs to work
2. Clotting factor bleed is delayed bleed (i.e. at dentist, initially you don't bleed but you do later)
3. Bleeding time (platelet function)
- BP cuff on arm, blow it above venous pressure
- Cut a few mm on volar surface of arm, every 15 seconds dab blood with filter paper. Stop the clock when the filter paper stops absorbing blood. Normal = 2-8 minutes.
- Won't run if platelet <50K; even with PFA-100, you expect worse function with lower counts
4. ITP
- Larger platelets, sort of like retics
- Can have low platelets, but normal clinical appearance
- Typically low numbers imply poor function, but these people may have normal function and thus be fine with procedures, so its good to run PFA-100/bleed time
5. Causes of platelet dysfunction (congenital)
- vWF - platelet dysfunction AND low factor VIII (20-30% of function) but not low enough to have clinically significant hemophilia-like picture (hemophiliacs have 0-1% of factor VIII function)
- Can treat vWF with intranasal DDAVP - useful in young women with very heavy periods because of vWF
- Others (rare): glanzmann's, storage pool disease.
6. Causes of platelet dysfunction (acquired)
- Uremia (although this is plus minus)
- Aspirin (pepto-bismol is a salicylate, sominex has a salicylate, many cough/cold medicines, alka-seltzer is aspirin with antacid). Effect of aspirin lasts as long as the platelet (most platelets have a 9-10 day lifespan, but given different ages of platelets in your blood, real effect is probably around 5 days.
- Drugs: NSAIDs, guaifenasin, 3rd generation penicilins: ticaricillin, piperacillin, 3rd generation cephalosporins
- Myeloproliferative disorders (p. vera, essential thrombocythemia)- lots of platelets that don't work
- Myeloma- abnl protiens made by myeloma coats platelets and affects function
7. Isolated prolonged PTT
- Deficiency: 8, 9, 11, 12-- Factor 12 def are not associated with bleeding, 11 is (rare) and 8 and 9 are.
- Inhibitor - iatrogenic (drawing blood above a heparin drip, backflow from a citrated/heparainated tube into your syringe that gets pushed into another tube) vs true (see below)
- Differentiate between the two: mixing study. If you mix pt's plasma with normal, if it works then you know its a deficiency; if it doesn't, there's a deficiency.
8. Inhibitor:
- lupus anticoagulant (not associated with bleeding)
- acquired factor inhibitors-- acquired factor 8 inhibitors as a sequelae of drugs or viral illnesses, has high mortality rate. Tx with immunosuppressants (steroids, rituximab, cyclophosphamide to block generation of inhibiting antibody) and give activated recombinant factor 7 to stop the bleeding.
9. Isolated prolonged INR
- likely vit K deficiency from antibiotics or decreased nutrition
- Transfuse FFP - as close to surgery as you can as the factors begin degrading immediately.
- Factor VII - half life around 6 hours
- In someone on warfarin, all drugs interact with it so any new drugs means you have to monitor the INR again
- Generally all antibiotics will prolong INR just because of gut flora effects
- Be careful of rapid correction with vitamin K if you overshoot the INR; if someone has an INR of 5-6, 2.5 mg of vit K PO will bring someone down to a safer level, at which point you can readjust the warfarin. But if someone is slightly high, don't go crazy with the vitamin K because if you overcorrect they may clot off whatever you were trying to keep from clotting off with the warfarin in the first place.
10. Vitamin K
- NOT IM don't give people with coagulopathy IM injection; they may get site hematomas that lead to neuropathy etc
- IV, SubQ, PO
- Takes around 24 hrs to work
Monday, May 5, 2014
1. Types of cardiac imaging
- Bright blood: +/- gadolinium
- Dark blood (no contrast)
- Phase contrast for flow (no contrast)
- MRangiography (+/- contrast)
2. NSF: nephrogenic systemic fibrosis.
- Gadolinium given to patients in ESRD who can't clear it, contrast accumulates in skin and can cause fibrosis/strictures/contractures in joint and skin or excess laxity.
- No treatment. Only thing is prevention - do not give to anyone with GFR<30. If you dialyze them right after, the first dialysis takes them off 50%, second dialysis to 96%. However there is no change in the rate of development of NSF if you dialyze them. If their GFR is 30-60, and they're on dialysis, the recommendation is to reduce the gadolinium dose and dialyze them twice afterwards.
3. High signal on T1- fat, melanin (ie melanoma)
- High signal on T2- fluid
4. Viability imaging: images acquired 10 minutes after contrast injection. Assess the degree of damage and to what extent it can be recovered with revascularization interventions.
- Normal myocardium: wash in wash out
- ischemic myocardium: wash in slower (stenotic vessels), still wash out normally
- Infarcted myocardium: contrast washes in slow, and does not wash out, contrast becomes trapped inside
- If the infarcted wall is <50% of the total thickness of the heart muscle, then there is enough tissue left for revascularization to be successful. If its >50%, there is not enough tissue left over for revascularization to be successful. See following study in NEJM:
- Vasodilate, inject gadolinium, first pass (stress image)
- Do it again later (rest image)
- Comparing the two, you can identify reversible damage/potential ischemia in times of stress.
- Adenosine: potent vasodilator
7. No reflow phenonmonon
- Microvascular disease, small vessels are damaged too
- Gadolinium is unable to reach certain part of tissue
- Implies MI within last 7 days, poor prognostic indicator as even the small vessels are affected.
8. TAVR vs open aortic valve repair: PARTNER trial 20% reduction in mortality and improved QoL compared to medical therapy alone.
9. When you do a TAVR, you don't replace the old valve, you just pop the new one into it, and crush the old valve open. First complication you think of? Strokes, and as you can see from PARTNER trial above the risk of stroke is significant. Second complication you think of? occluding the coronary ostia....
- Heart block with need for pacemaker placement. Increased risk in people with RBBB. PARTNER trial showed similar risk of heart block comparing surgery and Sapien valve, higher risk with CoreValve.
- Paravalve regurg-- higher risk in people with heavily calcified annulus, prosthesis too small, not opening the balloon enough during the valvuloplasty (but if you open it too much you risk valve rupture! Devastating complication). Paravalve regurg assoc with worse outcomes. PARTNER trial data- mild paravalve regurg in ~40%, moderate/severe in ~10% at 2 years. Regurg is assoc with increased mortality (HR >2), however its not controlled for degree of co-morbidity.
- Bright blood: +/- gadolinium
- Dark blood (no contrast)
- Phase contrast for flow (no contrast)
- MRangiography (+/- contrast)
2. NSF: nephrogenic systemic fibrosis.
- Gadolinium given to patients in ESRD who can't clear it, contrast accumulates in skin and can cause fibrosis/strictures/contractures in joint and skin or excess laxity.
- No treatment. Only thing is prevention - do not give to anyone with GFR<30. If you dialyze them right after, the first dialysis takes them off 50%, second dialysis to 96%. However there is no change in the rate of development of NSF if you dialyze them. If their GFR is 30-60, and they're on dialysis, the recommendation is to reduce the gadolinium dose and dialyze them twice afterwards.
3. High signal on T1- fat, melanin (ie melanoma)
- High signal on T2- fluid
4. Viability imaging: images acquired 10 minutes after contrast injection. Assess the degree of damage and to what extent it can be recovered with revascularization interventions.
- Normal myocardium: wash in wash out
- ischemic myocardium: wash in slower (stenotic vessels), still wash out normally
- Infarcted myocardium: contrast washes in slow, and does not wash out, contrast becomes trapped inside
- If the infarcted wall is <50% of the total thickness of the heart muscle, then there is enough tissue left for revascularization to be successful. If its >50%, there is not enough tissue left over for revascularization to be successful. See following study in NEJM:
N Engl J Med. 2000 Nov 16;343(20):1445-53.
The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction.
BACKGROUND:
Recent studies indicate that magnetic resonance imaging (MRI) after the administration of contrast material can be used to distinguish between reversible and irreversible myocardial ischemic injury regardless of the extent of wall motion or the age of the infarct. We hypothesized that the results of contrast-enhanced MRI can be used to predict whether regions of abnormal ventricular contraction will improve after revascularization in patients with coronary artery disease.
METHODS:
Gadolinium-enhanced MRI was performed in 50 patients with ventricular dysfunction before they underwent surgical or percutaneous revascularization. The transmural extent of hyperenhanced regions was postulated to represent the transmural extent of nonviable myocardium. The extent of regional contractility at the same locations was determined by cine MRI before and after revascularization in 41 patients.
RESULTS:
Contrast-enhanced MRI showed hyperenhancement of myocardial tissue in 40 of 50 patients before revascularization. In all patients with hyperenhancement the difference in image intensity between hyperenhanced regions and regions without hyperenhancement was more than 6 SD. Before revascularization, 804 of the 2093 myocardial segments analyzed (38 percent) had abnormal contractility, and 694 segments (33 percent) had some areas of hyperenhancement. In an analysis of all 804 dysfunctional segments, the likelihood of improvement in regional contractility after revascularization decreased progressively as the transmural extent of hyperenhancement before revascularization increased (P<0.001). For instance, contractility increased in 256 of 329 segments (78 percent) with no hyperenhancement before revascularization, but in only 1 of 58 segments with hyperenhancement of more than 75 percent of tissue. The percentage of the left ventricle that was both dysfunctional and not hyperenhanced before revascularization was strongly related to the degree of improvement in the global mean wall-motion score (P<0.001) and the ejection fraction (P<0.001) after revascularization.
CONCLUSIONS:
Reversible myocardial dysfunction can be identified by contrast-enhanced MRI before coronary revascularization.
5. Takosubo stress-induced cardiomyopathy: physical or psychological stressor leading to acute MI picture (elevated troponins, wall motion abormalities, clinical symptoms) in the setting of normal coronaries. Perhaps some people are more sensitive to this, may have to do with variable AChR in the myocardial tissues.
6. Stress perfusion studies- Vasodilate, inject gadolinium, first pass (stress image)
- Do it again later (rest image)
- Comparing the two, you can identify reversible damage/potential ischemia in times of stress.
- Adenosine: potent vasodilator
7. No reflow phenonmonon
- Microvascular disease, small vessels are damaged too
- Gadolinium is unable to reach certain part of tissue
- Implies MI within last 7 days, poor prognostic indicator as even the small vessels are affected.
8. TAVR vs open aortic valve repair: PARTNER trial 20% reduction in mortality and improved QoL compared to medical therapy alone.
N Engl J Med. 2010 Oct 21;363(17):1597-607. doi: 10.1056/NEJMoa1008232. Epub 2010 Sep 22.
Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery.
Leon MB1, Smith CR, Mack M, Miller DC, Moses JW, Svensson LG, Tuzcu EM, Webb JG, Fontana GP, Makkar RR, Brown DL, Block PC, Guyton RA, Pichard AD, Bavaria JE, Herrmann HC, Douglas PS, Petersen JL, Akin JJ, Anderson WN, Wang D, Pocock S; PARTNER Trial Investigators.
BACKGROUND:
Many patients with severe aortic stenosis and coexisting conditions are not candidates for surgical replacement of the aortic valve. Recently, transcatheter aortic-valve implantation (TAVI) has been suggested as a less invasive treatment for high-risk patients with aortic stenosis.
METHODS:
We randomly assigned patients with severe aortic stenosis, whom surgeons considered not to be suitable candidates for surgery, to standard therapy (including balloon aortic valvuloplasty) or transfemoral transcatheter implantation of a balloon-expandable bovine pericardial valve. The primary end point was the rate of death from any cause.
RESULTS:
A total of 358 patients with aortic stenosis who were not considered to be suitable candidates for surgery underwent randomization at 21 centers (17 in the United States). At 1 year, the rate of death from any cause (Kaplan–Meier analysis) was 30.7% with TAVI, as compared with 50.7% with standard therapy (hazard ratio with TAVI, 0.55; 95% confidence interval [CI], 0.40 to 0.74; P<0.001). The rate of the composite end point of death from any cause or repeat hospitalization was 42.5% with TAVI as compared with 71.6% with standard therapy (hazard ratio, 0.46; 95% CI, 0.35 to 0.59; P<0.001). Among survivors at 1 year, the rate of cardiac symptoms (New York Heart Association class III or IV) was lower amongpatients who had undergone TAVI than among those who had received standard therapy (25.2% vs. 58.0%, P<0.001). At 30 days, TAVI, as compared with standard therapy, was associated with a higher incidence of major strokes (5.0% vs. 1.1%, P=0.06) and major vascular complications (16.2% vs. 1.1%, P<0.001). In the year after TAVI, there was no deterioration in the functioning of the bioprosthetic valve, as assessed by evidence of stenosis or regurgitation on an echocardiogram.
CONCLUSIONS:
In patients with severe aortic stenosis who were not suitable candidates for surgery, TAVI, as compared with standard therapy, significantly reduced the rates of death from any cause, the composite end point of death from any cause or repeat hospitalization, and cardiac symptoms, despite the higher incidence of major strokes and major vascular events. (Funded by Edwards Lifesciences; ClinicalTrials.gov number, NCT00530894.).
JACC Cardiovasc Interv. 2013 May;6(5):452-61. doi: 10.1016/j.jcin.2012.11.014. Epub 2013 Apr 17.
Coronary obstruction following transcatheter aortic valve implantation: a systematic review.
Ribeiro HB1, Nombela-Franco L, Urena M, Mok M, Pasian S, Doyle D, DeLarochellière R, Côté M, Laflamme L, DeLarochellière H, Allende R, Dumont E,Rodés-Cabau J.
OBJECTIVES:
This study sought to evaluate, through a systematic review of the published data, the main baseline characteristics, management, and clinical outcomes of patients suffering coronary obstruction as a complication of transcatheter aortic valve implantation (TAVI).
BACKGROUND:
Very few data exist on coronary obstruction after TAVI.
METHODS:
Studies published between 2002 and 2012, with regard to coronary obstruction as a complication of TAVI, were identified with a systematic electronic search. Only the studies reporting data on the main baseline and procedural characteristics, management of the complication, and clinical outcomes were analyzed.
RESULTS:
A total of 18 publications describing 24 patients were identified. Most (83%) patients were women, with a mean age of 83 ± 7 years and a mean logistic European System for Cardiac Operative Risk Evaluation score of 25.1 ± 12.0%. Mean left coronary artery (LCA) ostium height and aortic root width were 10.3 ± 1.6 mm and 27.8 ± 2.8 mm, respectively. Most patients (88%) had received a balloon-expandable valve, and coronary obstruction occurred more frequently in the LCA (88%). Percutaneous coronary intervention was attempted in 23 cases (95.8%) and was successful in all but 2 patients (91.3%). At 30-day follow-up, there were no cases of stent thrombosis or repeat revascularization, and the mortality rate was 8.3%.
CONCLUSIONS:
Reported cases of coronary obstruction after TAVI occurred more frequently in women, in patients receiving a balloon-expandable valve, and the LCA was the most commonly involved artery. Percutaneous coronary intervention was a feasible and successful treatment in most cases. Continuous efforts should be made to identify the factors associated with this life-threatening complication to implement the appropriate measures for its prevention.
10. Other complications of TAVR: - Heart block with need for pacemaker placement. Increased risk in people with RBBB. PARTNER trial showed similar risk of heart block comparing surgery and Sapien valve, higher risk with CoreValve.
- Paravalve regurg-- higher risk in people with heavily calcified annulus, prosthesis too small, not opening the balloon enough during the valvuloplasty (but if you open it too much you risk valve rupture! Devastating complication). Paravalve regurg assoc with worse outcomes. PARTNER trial data- mild paravalve regurg in ~40%, moderate/severe in ~10% at 2 years. Regurg is assoc with increased mortality (HR >2), however its not controlled for degree of co-morbidity.
Friday, May 2, 2014
1. Algorithm for who gets a CXR:
- + findings on exam: breath sound changes, crackles, egophany
- High fever as long as you don't think it's flu (What makes you think its the flu - flu season, unvaccinated)
- Immunocompromised
- Any SOB.
- Heart failure & COPD - exam is really unreliable in people with COPD because they have bullae and its hard to hear the pathology
- Abnormal vital signs.
2. Who do you treat even if the CXR is negative
- Pneumonia is a clinical diagnosis - if someone's clinical picture looks like pneumonia, still treat it even if the CXR is negative
- Get the CXR anyways so you can establish a baseline (in case they dont get better you can see the changes over time), and to look for complications (parapneumonic effusion - needs to be tapped to check for superinfection)
3. Tx: when to treat beyond azithro+ceftriaxone
- Upper lobe, reticulonodular, chronic, cavitary: TB
- Cavitary, post-viral: Staph (+ vanc)
- Aspiration risk: anaerobes (+ clinda)
- Diffuse, known HIV risk factors: PCP (+bactrim/steroids)
- HCAP risk factors (recent hosp, nursing homes): pseudomonas
4. Acute bacterial pneumonia in HIV+ looks just like acute bacterial pneumonia in everyone else.
- Abrupt in onset, fever, focal (NOT diffuse) infiltrate = data says its overwhelmingly normal CA bacterial pneumonia, so you treat as you would treat anyone else.
- Don't add coverage for PCP or staph. Don't bronch him.
5. 90% of the lung infections in AIDS are one of the following:
- Bacterial pneumonia: acute (<1 week), any CD4 count, lobar consolidation, injection drugs. Dx c sputum cx/gram stain, blood cx. Treat empirically
- PCP: subacute (weeks to months), CD4 <200, b/l diffuse perihilar, symeeetric homogenos. Clues: elevated LDH, more hypoxia than expected from CXR. Dx with BAL, silver stain, DFA for PCP
- TB: subacute, weeks to months, any CD4. When CD 4 <200 it can present in any way possible on CXR. Pleural effusion often present. Dx with sputum smear and cx.
6. Headache in an HIV+ patient (with a clean CT scan and exam)
- MRI much more sensitive than CT in AIDS patients.
- Meningitis: cryptococcal most common meningitis in AIDS patients-- presents with neg exam, neg CT, neg MRI, subacute/indolent course -- this agent is not very virulent, doesn't affect normal people, and people can have it for weeks and look fine, no meningeal signs. Dx with serum cryptococcal antigen or fungal cx. LP will be normal 1/3 of the time-- so if you're gonna tap someone, you have to specifically request testing for cryptococcus). Can also do serum cryptococcal antigen- 95% sensitive. No substitute for CSF but if you can't get an LP you can use it.
- Encephalitis
7. Headache, HIV+, focal neuro signs/seizures => mass lesion:
- Toxo: serum toxo IgG: not 100% sensitive, and only proves past exposure not current infection. Biopsy isn't very sensitive (often necrotic). The way to deal with this is to treat it. All of the following criteria must be fulfilled to just do empiric toxo treatment and not work up futher: 1) not on bactrim prophy as it works well to prevent toxo 2) + toxo IgG 3) Multiple ring enhancing lesions 4)no meningeal signs. The danger is not in overtreating but missing something else which needs different treamtn.
- Primary CNS lymphoma (assoc w EBV 100% of the time in AIDS patients, other people with primary CNS lymphomas not always assoc with EBV, happens in people with CD4s of 0)
- PML (progressive mulitfocal leukoencephalopathy - can see in MRI): caused by JC virus. Treat with HAART, no specific treatment for it ?
8. Before you get an LP
- CT
- Coags!! Coags!!! Coags!!!! Prevent epidural hematoma.
9. Insulin pump
- cons- need frequent needle changes (q2-3 days), need training on carb counting and input, possib of DKA if pump malfunctions, cost (>6,000$), tethered to device
- pros- less glucose variability, better lifestyle, don't have to carry around a kit
10. New insulins
- inhaled
- oral
- plant based
- artificial pancreas
- + findings on exam: breath sound changes, crackles, egophany
- High fever as long as you don't think it's flu (What makes you think its the flu - flu season, unvaccinated)
- Immunocompromised
- Any SOB.
- Heart failure & COPD - exam is really unreliable in people with COPD because they have bullae and its hard to hear the pathology
- Abnormal vital signs.
2. Who do you treat even if the CXR is negative
- Pneumonia is a clinical diagnosis - if someone's clinical picture looks like pneumonia, still treat it even if the CXR is negative
- Get the CXR anyways so you can establish a baseline (in case they dont get better you can see the changes over time), and to look for complications (parapneumonic effusion - needs to be tapped to check for superinfection)
3. Tx: when to treat beyond azithro+ceftriaxone
- Upper lobe, reticulonodular, chronic, cavitary: TB
- Cavitary, post-viral: Staph (+ vanc)
- Aspiration risk: anaerobes (+ clinda)
- Diffuse, known HIV risk factors: PCP (+bactrim/steroids)
- HCAP risk factors (recent hosp, nursing homes): pseudomonas
4. Acute bacterial pneumonia in HIV+ looks just like acute bacterial pneumonia in everyone else.
- Abrupt in onset, fever, focal (NOT diffuse) infiltrate = data says its overwhelmingly normal CA bacterial pneumonia, so you treat as you would treat anyone else.
- Don't add coverage for PCP or staph. Don't bronch him.
5. 90% of the lung infections in AIDS are one of the following:
- Bacterial pneumonia: acute (<1 week), any CD4 count, lobar consolidation, injection drugs. Dx c sputum cx/gram stain, blood cx. Treat empirically
- PCP: subacute (weeks to months), CD4 <200, b/l diffuse perihilar, symeeetric homogenos. Clues: elevated LDH, more hypoxia than expected from CXR. Dx with BAL, silver stain, DFA for PCP
- TB: subacute, weeks to months, any CD4. When CD 4 <200 it can present in any way possible on CXR. Pleural effusion often present. Dx with sputum smear and cx.
6. Headache in an HIV+ patient (with a clean CT scan and exam)
- MRI much more sensitive than CT in AIDS patients.
- Meningitis: cryptococcal most common meningitis in AIDS patients-- presents with neg exam, neg CT, neg MRI, subacute/indolent course -- this agent is not very virulent, doesn't affect normal people, and people can have it for weeks and look fine, no meningeal signs. Dx with serum cryptococcal antigen or fungal cx. LP will be normal 1/3 of the time-- so if you're gonna tap someone, you have to specifically request testing for cryptococcus). Can also do serum cryptococcal antigen- 95% sensitive. No substitute for CSF but if you can't get an LP you can use it.
- Encephalitis
7. Headache, HIV+, focal neuro signs/seizures => mass lesion:
- Toxo: serum toxo IgG: not 100% sensitive, and only proves past exposure not current infection. Biopsy isn't very sensitive (often necrotic). The way to deal with this is to treat it. All of the following criteria must be fulfilled to just do empiric toxo treatment and not work up futher: 1) not on bactrim prophy as it works well to prevent toxo 2) + toxo IgG 3) Multiple ring enhancing lesions 4)no meningeal signs. The danger is not in overtreating but missing something else which needs different treamtn.
- Primary CNS lymphoma (assoc w EBV 100% of the time in AIDS patients, other people with primary CNS lymphomas not always assoc with EBV, happens in people with CD4s of 0)
- PML (progressive mulitfocal leukoencephalopathy - can see in MRI): caused by JC virus. Treat with HAART, no specific treatment for it ?
8. Before you get an LP
- CT
- Coags!! Coags!!! Coags!!!! Prevent epidural hematoma.
9. Insulin pump
- cons- need frequent needle changes (q2-3 days), need training on carb counting and input, possib of DKA if pump malfunctions, cost (>6,000$), tethered to device
- pros- less glucose variability, better lifestyle, don't have to carry around a kit
10. New insulins
- inhaled
- oral
- plant based
- artificial pancreas
Thursday, May 1, 2014
1. Transient global amnesia
- Processing is normal but people fail to make new memories
- Resolves within 24 hours
- Cause unknown.
2. Findings on radiograph that help with TB
- Upper lobe disease: TB goes to your lower lobes first because you ventilate it more, then they multiply, go to your hilar nodes, then thoracic duct and go systemic. It settles in the upper lobes because they are oxygen loving and you perfuse your upper lobes less and thus extract less oxygen from the air.
- Reticular nodular
- Cavitary
- If you don't have any of the signs, odds of TB<1%. Unless someone has a low CD4 count; they get a primary active TB when they inhale it for the first time (TB goes to lower lobes and immediately prevails). HIV with normal CD4 count presents like anyone else with TB.
- Key TB risk factors: recent active exposure and foreign-born (asia/africa). Other risk factors are less specific.
3. Dx TB
- Sputum for AFB (bronch if you need to) - stain and culture.
- Treat for CAP until you're sure its TB
- Quantiferon uses a specific antigen that doesn't cross-react with BCG.
- Don't start TB meds until you're sure it's TB
4. Respiratory viruses
- Only virus that cause high fever is influenza (adeno, others don't)
- If you're not in flu season, having a high fever tells you something. You should be thinking bacterial pneumonia rather than respiratory viruses.
- If you come in with a 102 degree fever and a cough in July, you get a CXR. Because respiratory viruses don't happen
5. High fever + diarrhea
- Salmonella, shigella, campylobacter
- High fever rarely occurs in viral gastroenteritis
6. Risk factors for aspiration = people with difficulty swallowing
- Neurological - dementia/stroke
- ENT problems
- Drugs/alcohol
- IV drug use
7. PCP pneumonia
- Diffuse homogenous alveolar filling space
- When you treat it with bactrim, DON'T FORGET STEROIDS. Because it'll lyse the cells and create such a bad ARDS that you won't be able to oxygenate through.
- If someone comes in and you suspect PCP, and labs come back with HIV+ and a low CD4, keep them on their drugs and send them to get a bronch for definitive diagnosis. Because it may be PCP, fungal, MAI, they can all present similarly.
- Physical exam is not good at detecting this, if you suspect it you need a bronch.
8. Healthy people with cough and low grade fever for a week, yellowish sputum => viral bronchitis. No evidence that people with viral bronchitis get better with antibiotics.
9. Viral flu: people tend to get sick really fast, spike a fever really fast, and then slowly get better. Bacterial pneumonia can also present like that, and can also present with slowly increasing fever over time. Viral flu does NOT present with slowly increasing fever over time.
10. Incidence of DM is very high among Scandinavian countries and extremely low in Asian/Indian populations (600 fold difference in incidence) that seems more a function of geography/environment than genetics. Icidence is increasing over time, mostly in very young kids in Finland, preteens in US
- Processing is normal but people fail to make new memories
- Resolves within 24 hours
- Cause unknown.
2. Findings on radiograph that help with TB
- Upper lobe disease: TB goes to your lower lobes first because you ventilate it more, then they multiply, go to your hilar nodes, then thoracic duct and go systemic. It settles in the upper lobes because they are oxygen loving and you perfuse your upper lobes less and thus extract less oxygen from the air.
- Reticular nodular
- Cavitary
- If you don't have any of the signs, odds of TB<1%. Unless someone has a low CD4 count; they get a primary active TB when they inhale it for the first time (TB goes to lower lobes and immediately prevails). HIV with normal CD4 count presents like anyone else with TB.
- Key TB risk factors: recent active exposure and foreign-born (asia/africa). Other risk factors are less specific.
3. Dx TB
- Sputum for AFB (bronch if you need to) - stain and culture.
- Treat for CAP until you're sure its TB
- Quantiferon uses a specific antigen that doesn't cross-react with BCG.
- Don't start TB meds until you're sure it's TB
4. Respiratory viruses
- Only virus that cause high fever is influenza (adeno, others don't)
- If you're not in flu season, having a high fever tells you something. You should be thinking bacterial pneumonia rather than respiratory viruses.
- If you come in with a 102 degree fever and a cough in July, you get a CXR. Because respiratory viruses don't happen
5. High fever + diarrhea
- Salmonella, shigella, campylobacter
- High fever rarely occurs in viral gastroenteritis
6. Risk factors for aspiration = people with difficulty swallowing
- Neurological - dementia/stroke
- ENT problems
- Drugs/alcohol
- IV drug use
7. PCP pneumonia
- Diffuse homogenous alveolar filling space
- When you treat it with bactrim, DON'T FORGET STEROIDS. Because it'll lyse the cells and create such a bad ARDS that you won't be able to oxygenate through.
- If someone comes in and you suspect PCP, and labs come back with HIV+ and a low CD4, keep them on their drugs and send them to get a bronch for definitive diagnosis. Because it may be PCP, fungal, MAI, they can all present similarly.
- Physical exam is not good at detecting this, if you suspect it you need a bronch.
8. Healthy people with cough and low grade fever for a week, yellowish sputum => viral bronchitis. No evidence that people with viral bronchitis get better with antibiotics.
9. Viral flu: people tend to get sick really fast, spike a fever really fast, and then slowly get better. Bacterial pneumonia can also present like that, and can also present with slowly increasing fever over time. Viral flu does NOT present with slowly increasing fever over time.
10. Incidence of DM is very high among Scandinavian countries and extremely low in Asian/Indian populations (600 fold difference in incidence) that seems more a function of geography/environment than genetics. Icidence is increasing over time, mostly in very young kids in Finland, preteens in US
Wednesday, April 30, 2014
1. Stable angina - 3% risk per year of progression to MI/death
2. Treatment for angina:
- Decrease O2 demand: b-blockers, ca-channel blockers
- Increase O2 supply: nitrates
- Anticoagulate: aspirin, plavix in people s/p stent or who can't take aspirin
- Statin
- ACE/ARB in diabetics or people with HF
3. STEMI vs NSTEMI
STEMI = transmural ischemia or infarction
NSTEMI = subendomyocardial ischemia
4. Chest pain in the ER
- Around 15% of people with chest pain in the ER are having an MI
- New 1mm ST elevation: 80% prevalence of MI
- New ST depression/inversion: 20%
- No new changes in patient with known CAD: 4%
- No new changes in a patient without known CAD: 2%
5. Utility of physical exam findings for diagnosing MI {JAMA}
6. Cardiac enzymes
- Troponin and CKMB are both very sensitive and specific for MI. CKMB is not useful after 24 hours.
- Renal insufficiency can cause falsely elevated troponin, but even in people with high baseline troponin it should still rise and fall in acute MI
7. GERD vs MI
- Most helpful history: pain that is recurrent (>1/month), persists for several hours, awakens someone at night, provoked by recumbency, assoc with heartburn/regurg is much more likely to be GERD
- Symptoms that are NOT helpful for distinguishing the two (surprisingly): radiation to L arm, exacerbation with exercise, relief with nitroglycerin.
- Repeat: relief with nitroglycerin is useless in differentiating angina from GERD or other causes of chest pain
8. When to scope someone with GERD:
- Symptoms of complicated disease (dysphagia, extra-esophageal symptoms, bleeding, weight loss, chest pain of unclear etiology)
- Risk for Barett's (long standing reflux symptoms)
- Patients require long-term treatment
- Poor response to treatment
9. When to get pH monitoring:
- GERD sx + normal endoscopy
- Monitoring therapy in refractory cases
10. Surgery:
- Limited role
- ONe study found a higher mortality of those treated with surgery at 11 years than those treated medically, #needed to harm = 8.3
2. Treatment for angina:
- Decrease O2 demand: b-blockers, ca-channel blockers
- Increase O2 supply: nitrates
- Anticoagulate: aspirin, plavix in people s/p stent or who can't take aspirin
- Statin
- ACE/ARB in diabetics or people with HF
3. STEMI vs NSTEMI
STEMI = transmural ischemia or infarction
NSTEMI = subendomyocardial ischemia
4. Chest pain in the ER
- Around 15% of people with chest pain in the ER are having an MI
- New 1mm ST elevation: 80% prevalence of MI
- New ST depression/inversion: 20%
- No new changes in patient with known CAD: 4%
- No new changes in a patient without known CAD: 2%
5. Utility of physical exam findings for diagnosing MI {JAMA}
- Troponin and CKMB are both very sensitive and specific for MI. CKMB is not useful after 24 hours.
- Renal insufficiency can cause falsely elevated troponin, but even in people with high baseline troponin it should still rise and fall in acute MI
7. GERD vs MI
- Most helpful history: pain that is recurrent (>1/month), persists for several hours, awakens someone at night, provoked by recumbency, assoc with heartburn/regurg is much more likely to be GERD
- Symptoms that are NOT helpful for distinguishing the two (surprisingly): radiation to L arm, exacerbation with exercise, relief with nitroglycerin.
- Repeat: relief with nitroglycerin is useless in differentiating angina from GERD or other causes of chest pain
8. When to scope someone with GERD:
- Symptoms of complicated disease (dysphagia, extra-esophageal symptoms, bleeding, weight loss, chest pain of unclear etiology)
- Risk for Barett's (long standing reflux symptoms)
- Patients require long-term treatment
- Poor response to treatment
9. When to get pH monitoring:
- GERD sx + normal endoscopy
- Monitoring therapy in refractory cases
10. Surgery:
- Limited role
- ONe study found a higher mortality of those treated with surgery at 11 years than those treated medically, #needed to harm = 8.3
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