Is supported by data from the PLADO study + others (see refs) which show that giving more than a standard dose of platelets (1 pool/unit* in an adult) did not ⬇️ bleeding incidence
2/ Each platelet exposure has (uncommon but significant) risks of allergic reaction, virus transmission and...
Each exposure to platelets is also another potential exposure to HLA antigens which the recipient does not have
3/ This may not have a big impact for many patients but for those awaiting transplants (haem or solid organ @BukuRenal) it increases the chance of graft rejection.
Why does this happen?
4/ Standard platelet transfusion are not HLA-matched, and this is fine because most of us will never need platelets, and if we do, it is often a 'one-off' during critical illness
Even for haematology patients who receive many platelets, HLA sensistization is not often a problem
5/ With each platelet transfusion however the chance increases of the immune system becoming 'aware' of these non-self antigens
5/ When this occurs, antibodies can form against those HLA antigens. Again, for many of us that is not an issue as our body will never 'see' those antigens again.
If however the patient needs a solid organ transplant for example, there is a risk of rejection of that organ...
6/ ...when it is introduced to the body
➡️ acute rejection.
In bone marrow transplants, antibodies against HLA on the donated bone marrow stem cells can prevent the stem cells engrafting/'moving in' to the recipient marrow space/their new home
7/ SO platelet transfusions can be critical for patients w. low platelet counts and bleeding/procedure but are often given when not indicated. And please only give one unit & review, as evidence says that 2 pools do not help more than 1 ➕ is an unnecessary blood product exposure
8/ *FACT: Platelets are prescribed as a 'pool because it us a single dose made from multiple donors. Single donor units aka apheresed units are available and reduce HLA exposure for those at risk
Ref; Dose of Prophylactic Platelet Transfusions and Prevention of Hemorrhage | NEJM nejm.org/doi/full/10.10…
Febrile neutropenia is a common and serious complication of chemotherapy treatment and can rapidly progress to life-threatening severe sepsis. Patients with bone marrow failure conditions (e.g. AML, Myelodysplastic syndrome) are also at risk.
2/ Outcomes have improved with increased recognition of the importance of prompt treatment and better supportive care, driven by initiatives such as the Surviving Sepsis Campaign.
🔥IV antibiotics must be given within one hour in all suspected neutropenic sepsis 🔥
3/ Patient education is crucial, as is a failsafe, 24/7 contact line for prompt assessment and treatment in secondary care: once there, antimicrobials should be given within the hour.
🔬History, examination, imaging and cultures are then used to pinpoint the source.
The risk of venous thromboembolism (VTE) is up to 7 x higher in patients with cancer, and contributes to morbidity and mortality
Overall prognosis is worse in patients with cancer and VTE, compared to those with cancer and no VTE
2/ The treatment of VTE in cancer is complex due to concerns around;
-Interactions with anti-cancer treatment 💊
-Timing of surgery and procedures 🪚 (no scalpel emoji)
-Low platelet counts due to treatment 🩸
-Higher risk of bleeding related to some cancers 🩹
3/ LMWH was traditionally the treatment of choice, with data from the CLOT study (2003) showing improved efficacy vs warfarin & no ⬆️ bleeding risk
It is a useful option as no monitoring (usually) required, less interactions and short T1/2. It is however given by injection...
1/ Antidote news! There has been promise recently regarding antidotes being developed for DOACs. Before we get onto that, a quick summary of what we have so far...
2/ In the case of bleeding while on warfarin, this should be stratified by severity. Usual rule is if life/limb/sight threatening bleeding, prothrombin complex concentrate + vit K is used. If not, vitamin K +- pause/cessation of warfarin is advised.
3/ Warfarin works by inhibiting vitamin K-dependent clotting factor production. These factors are II, VII, IX and X. The 'antidote' is prothrombin complex concentrate (e.g beriplex) which is a concentrated 'soup' of factors II, VII, IX and X (and some protein C and S)
1/19. When considering whether a patient is at risk of bleeding before a procedure/surgery or if a patient is bleeding and you want to assess if there are any 'correctable' clotting abnormalities, a thorough approach is needed to ensure all factors are identified.
2/19. The patient might have a PT of 19 seconds but this will probably make little/no difference in terms of bleeding risk, but the clopidogrel they have continued to take without telling the nurses/medical staff really will. I.e the coagulation screen isn't the whole picture..
3/19. The 3 main elements are platelets, fibrinogen and clotting factors.
Platelet function depends on platelet number and function. Count can be reduced by many causes. Major surgery can occur with a platelet count of 50x10^9 or more (BSH guidelines. Note neurosurgery >100)
1/7. Prothrombin time (PT) measures the extrinsic coagulation cascade. The only 'major' clotting factor in the extrinsic pathway is factor VII. This is the clotting factor with the shortest half life, and explains why the PT is so often prolonged in unwell patients
2/7. It also makes a long PT relatively easy to investigate and manage. The absolute majority of patients with a long PT will either be vitamin K deficient, have factor VII deficiency due to consumption in sepsis/bleeding or liver disease.
3/7. Warfarin and the DOACS (to a varying degree) will represent most of the rest of prolonged PT results. Factor VII deficiency is incredibly rare, and will have been present from birth, therefore if the patient has had a normal PT in the past...