Leukocytapheresis is a technique used to treat acute leukemia. NB: there is a contraindication to treating patients with APL (AML FAB M3) because of the risk of DIC. You should be able to check this with a blood smear. Pheresis (also referred to as apheresis) can be used for a huge number of conditions, which are outlined in exhaustive detail here.
How does it work? The concept is similar to dialysis or ECMO, except in pheresis, the plasma is siphoned off (and replacement fluid is given) and RBCs are returned to the body. There shouldn’t be any major fluid shifts like in dialysis.
Do you need a special catheter for pheresis? Ideally, pheresis is done through a peripheral IV because a lot of times these patients are thrombocytopenic, and you don’t want to delay pheresis for line placement or risk additional bleeding. However, there is such a thing as a pheresis catheter, which is a large-bore tunneled central line. Pheresis lines should be placed when multiple rounds of pheresis are expected, but to give emergent pheresis, anything from a peripheral IV to a regular central line is okay.
How much can someone improve with pheresis? Lots! Pheresis can be done when the WBC is 50-100K, but is only absolutely indicated when WBC >300K, as patients are at risk of leukostasis (if they don’t already have it). According to this review, the WBC can be expected to drop by 10-70% with the first session alone. However, it’s a game of diminishing returns. The WBC is most viscous and concentrated at the first session, so as sessions go on and the WBC improves, pheresis will become less and less effective.
You have a patient who presents with persistent bleeding, and heme/onc recommends a workup for bleeding disorders. One of the tests is a “mixing study.” This literally consists of mixing a patient’s plasma with normal plasma to see if there is a factor deficiency (aPTT corrects) or factor inhibitor (aPTT does not correct).
This is a good overview of a general approach to an abnormal PT or aPTT. (The whole PDF is a good review of workup for hypercoagulable disorders.)
Although this will likely not result in life-or-death decisions and is more a matter of intellectual curiosity, I would argue that hemoglobin is superior to hematocrit because it is directly measured and tells you about O2 delivery. Read on.
Hemoglobin is directly measured with spectroscopy (it’s a pigmented dye, so can be directly measured).
Hematocrit can be measured, but in modern times is calculated (RBC count x MCV). It represents a ratio of packed cells: total volume. Conditions that change the osmolarity of the blood will change the MCV temporarily, and affect Hct. It is affected by multiple factors:
Polycythemic or macrocytic anemias (larger MCV but less number of RBCs may show a normal Hct but low Hgb)
Microcytic anemias would show a reduced MCV and reduced RBC count, so the Hct should still be in line with the reduced Hgb
Let’s say you have the following patient: 80 year old male with COPD and diabetes who comes into the ED with dizziness and SOB. The emergency department gets a CTA, which for once, shows subsegmental PEs in his right and left lungs. He is started on a heparin drip and admitted to your team. What happens next?
The first decision you need to make is whether to start him on warfarin or a novel anticoagulant (NOAC). This category of medications includes drugs like rivaroxaban, apixaban, and dabigatran. We could have a whole discussion about when warfarin might be more preferable, or a NOAC. Parts of that discussion can be found here and here (specific to non-valvular afib).
You decide to start the patient on a NOAC. Fine. Now the question is, which one do you choose? Enter the EINSTEIN-PE trial, summarized in this 2-Minute Medicine article. This trial examined how rivaroxaban, or Xarelto, compared to lovenox + warfarin. Rivaroxaban was non-inferior and had fewer bleeding events. This supports the use of rivaroxaban for treating PE. Unfortunately, there is no such data for apixaban or dabigatran. Therefore, rivaroxaban is the NOAC of choice when treating PE.
The risk of bleeding versus the risk of clotting must always be weighed when starting or stopping a patient on anticoagulation. It can be kind of vague and theoretical, and multiple scoring systems have been developed to serve as clinical decision-making tools. Two of these are CHADS VASC (which measures risk of stroke in someone with a fib) and HAS-BLED (measures risk of bleeding in any patient started on anticoagulation.
You can’t compare any two scores directly. It’s not as though a higher CHADS VASC score “outweighs” a HAS-BLED score and thus anticoagulation should be continued.
It has been reported that HAS-BLED is more accurate in predicting risk for its group of patients. However as this paper states, HAS-BLED should not be used on its own to exclude patients from antocoagulation therapy; it allows the clinician to identify bleeding risk factors and to correct those that are modifiable, ie, by controlling blood pressure, removing concomitant antiplatelet or nonsteroidal antiinflammatory drugs, and counseling the patient about reducing alcohol intake (if excessive).
“Thus, bleeding risk assessment with HAS-BLED should not be used as an excuse not to prescribe OAC but rather to highlight those patients in whom caution with such treatment and regular review is warranted.”
Unlike most of my questions, this one is rhetorical. Putting an IVC filter in most patients is a sucky move. There is even a possible class action lawsuit against them.
The IVC filter began with an innocuous idea. The balance between bleeding-clotting is delicate, and one question that emerged was, what can we do to prevent DVT/PE in patients who are also at high risk of bleeding? Enter the IVC filter. Two commonly cited indications for an IVC filter is someone with a DVT with contraindication to bleeding, or prophylaxis in high-risk patients (trauma patients, for example).
There was a study conducted to determine efficacy, PREPIC, which is summed up neatly in this PulmCCM article–basically, the only evidence for reduced DVT was within 12 days of placement, and patients actually had a higher risk of recurrent DVTs in the future, without reduced mortality in the long run. Furthermore, patients with contraindication to anticoagulation were excluded from the study!
IVC filters cause complications. Chief among these is recurrent DVT. Instead of catching clots, the foreign material of an IVC filter may cause clots to form. Other possibilities include filter fracture (yes, pieces can actually break off if they’re left in long enough), filter migration, and rarely, IVC perforation with retroperitoneal bleeds. And just because an IVC filter is billed as “retrievable” does not mean that it can be easily removed. A lot of times, the filter is not removed soon enough, exposing patients to greater risk of complications.
Thus, whenever it can be shown that someone with an IVC filter doesn’t actively have a DVT/PE, they should be referred to a surgeon to have the filter removed.
Hgb <7.0: give 1-2 units of packed red blood cells (although there are certain conditions in which patients should be transfused when Hgb <8.0)
Plts <10,000 or plts <50,000 and the pt is actively bleeding: give 5-10 units of platelets. In pts with heme malignancies with abnormal CBCs, this threshold still applies.
When pts have DIC and low fibrinogen (<80-100 mg/dl): give 5 bags of cryoprecipitate (in addition to fibrinogen, also contains assorted things like von Willebrand factor, factor VIII, factor XIII).
When pts with liver disease are bleeding, need emergent warfarin reversal, are actively bleeding in DIC, or you are desperate for a last-ditch effort to stop bleeding: give fresh frozen plasma. (these are all C recommendations, by the way). Do NOT give FFP for the sole purpose of a volume expander–consider albumin instead.