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
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.
Here are the transfusion guidelines for different patients:
stable CAD: 7.0-8.0
anemia with sx: 8.0
asx, stable pts in ICU: 7.0
acute UGIB: 7.0
One of the landmark papers that helped determine the benefits of low-threshold vs high-threshold transfusions was the TRICC trial. This trial randomized over 800 hemodynamically stable ICU patients with Hgb <9 to a goal of Hgb 7-9 or Hgb 10-12. There was no statistically significant difference in 30-day mortality, though it was very close to being significant for the more conservative group (Hgb 7-9) (22.2 vs. 28.1, p=0.05). Subgroup analysis showed lower mortality when using goal Hgb 7-9 among patients with APACHE II <20 (8.7% vs. 16.1%, p=0.03) and in patients younger than 55 (5.7 vs. 13.0 p=0.02). Although there was no noted difference in mortality among patients with cardiac disease, the authors acknowledge a high rate of refusal to participate among patients with cardiac disease, possibly affecting the results. That is one of the reasons there is a slightly higher transfusion goal set for cardiac patients.
NB: CAD is still a gray area, and some attendings may still prefer to transfuse asymptomatic patients with a history of CAD for a Hgb <8.0. However, trials on restrictive transfusion did use 7 as a threshold…
In practical terms, total iron binding capacity=transferrin. Why?
TIBC refers to the amount of iron in the serum + the amount of iron that could theoretically still be bound to transferrin. Transferrin is usually only 25-30% saturated at any given point.
Knowing the molecular weight of the transferrin (80 kDa) and that each molecule of transferrin can bind 2 atoms of iron, TIBC and transferrin concentration is interconvertible. If you want to get into the mechanics of it, here is a somewhat dotty conversation from the UK. I have to admit I still didn’t understand it after reading those series of equations.
If it is possible to order transferrin and TIBC separately, transferrin may be useful as a marker of nutritional status or liver status, since it is produced in the liver.
Side note: ferritin, which is completely different, is usually correlated with how much iron is stored in tissues. However, because it’s an acute phase reactant, it may be falsely elevated in inflammation or anemia of chronic disease.