Lab value interpretation Flashcards Preview

minor allergic reaction (hives, etc) 1:100

anaphylaxis 1: 1600 

fever 1:300 (FNHTR)

volume overload 1:700 (TACO)

lung injury 1:10,000

symptomatic bacterial sepsis 1:10,000

wrong blood transfused 1:14,000

wrong ABO group tranfused: 1:40 000

fatal acute hemolytic reaction: 1:600,000

viral: HIV (1:8 M); Hep B (1:2M); Hep C (1:7M), Malaria (1:4M), bacteria (1:2,500)

Minimum effective dose

single unit, reassess symptoms after= 1 unit

acute hemolytic transfusion reaction (AHTR) - ABO incompatability -> intravascular hemolysis, complement activation

fever, chills, hypotension, acute renal failure (b/c of antibodies <3 glomerulus), DIC 

stop transfusion, notify bank and  check for clerical error, maintain BP with a lot of IV fluids, maintain urine with diuretics to avoid fluid overload

febrile nonhemolytic transfusion reaction (FNHTR)

alloantibodies to WBC, platelets, etc -> release of cytokines

0-6 hrs post ransfusion

fever, rigors, facial flushing, headache, myalgia, etc

rule out hemolytic reactions or infection

if T< 38C - continue transfusion but decrease rate and give antipyretics

if T>38C - stop transfusion, give antipyretics and anti-histomaines

Transfusion-Related Acute Lung Injury (TRALI)

new-onset acute lung injury during transfusion or w/i 6 hrs of transfusion

severe hypoxemia, pulmonary edema on CXR, etc - > pathogenesis uncertain

resolves in 24-72 hrs, do supportive therapy (oxygen)

bacterial infection

Transfusion Associated Circulatory Overload (TACO)

impaired cardiac function and excessive rapid transfussion

transfuse at lower rate, give diuretics and oxygen

Hyperkalemia

due to increased K+ release from stored RBCs (shorter life cycle -> lyse and release K+

Dilutional Coagulopathy

with massive transfusions (>10 units) : RBCs don't contain clotting factors, fibrinogen, platelets etc - give FP (plasma), platelets and cryoprecipitate

Delayed Hemolytic Reactions

alloantibodies to minor antigens such as Rh, Kell, Duffy

at transfusion time antibodies low, but level increases once in recipient body

anemia and mild jaundice (increased bili from RBC lysis)

no treatment, but important for future transfusion

5-7 daus

Transfusion Associated Graft Vs Host Disease

transfused T-lymphoctes recognize and react against host

4-30 days post transfusion

usually if immune system already severely impaired

can give irradiated blood products with no T-cells

Iron overload 

since adding more Hb (with Fe2+) in RBCs

Viral infection riks (HBV, HCV, HIV, EBV, CMV, etc)

* ALWAYS EXAMINE PATIENT POST TRANSFUSION IF HAS FEVER OR OTHER SIGNS

* RN will collect blood sample and send ot lab - they will run all the necessary tests automatically

* watch for signs of acute transfusion reactions: hives/itching, fever, hypotension, pain, red urine (AHTR - acute hemolytic transfusion response), shortness of breath or hypoxia (TRALI = transfusion related acute lung injury), ...

after transfusion, group and screen is outdated - have to order a new one!

Red cell distribution width (RDW) is a parameter that measures variation in red blood cell size or red blood cell volume. RDW is elevated in accordance with variation in red cell size (anisocytosis), ie, when elevated RDW is reported on complete blood count, marked anisocytosis (increased variation in red cell size) is expected on peripheral blood smear review.

anisocytosis

(think anise and how it can have different pods)

poikilocytosis

think poi = small; kilo - 10000 => small and big!

poikilocyte - abnormally shaped RBC - sickle, target, etc

Bite and blister cells suggest hemolysis, in particular oxidative injury to the RBCs.  Both are present in glucose-6-phosphate dehydrogenase deficiency (G6PD deficiency)

G6PD is an enzyme in cytoplasm of RBCs, whose job is to help reduce hemoglobin which has become chemically oxidised (lost electrons). If G6PD is impaired, Hgb becomes more oxidized until it precipiates wihtin the RBC. The spleen is able to "fix" some of these cells by "pitting out" the lump of precipitated Hgb - leaves RBC looking like it was bitten (bite cell) or as if it had a blister with an empty area underneath (blister cell). RBCs too damaged to survive, and may lyse within spleen or circulation. 

D-dimer is a breakdown product of formed blood clot (thrombus). If your patient has elevated D-dimer, this means the patient has clotted somewhere in the body

Schistocytes are fragmented RBCs, similar to schizophrenia ("split" mind). Usually get schistocytes due to membrane damage as RBCs pass narrowed vessels. Vessels can be narrowed either by clot (fibrin strands stretching and occluding lumen) or shearing b/c of abnormal turbulent flow like atherosclerosis. 

polychromasia = "bluish-purple" discoloration of immature RBCs due to their immaturity (remember basophilic erythrocyte -> polychromatic erythrocyte (greyish purple cytoplasm) -> normocyte ->reticulocyte (pink cytoplasm)

sign of immature RBC b/c cytoplasm not quite pink, meaning some organelle material left over ie. cell not fully developed and organelles not fully extruded

Target cells = RBCs with "bull's eye", caused by relative excess of membrane to cytoplasm. The excess membrane piles up in the centre of the RBC on the glass slide (since there is indent in the middle) and causes target appearance. Target cells can be seen in conditions with too much membrane - ex. liver disease, or too little cytoplasm - thalassemias (low content inside, low cytoplasm)

eliptocytes ar eelongated "pencil shaped" RBCs, commonly seen in iron deficiency and hereditary RBC syndromes (like hereditary elliptocytosis).

 hypersegmented neutrophil is a clinical laboratory finding. Normal 3-5 lobes, hypersegmented 6+ lobes.

Hypersegmented neutrophils have classically been thought to be pathognomonic of the class of anemias called megaloblastic anemias (anemias caused by failure of bone marrow blood-forming cells to make DNA, often caused by vitamin B12 or folate deficiencies, or DNA-replication poisons).

Mixing studies are tests performed on blood plasma used to distinguish factor deficiencies from factor inhibitors, such as lupus anticoagulant, or specific factor inhibitors, such as antibodies directed against factor VIII. Mixing studies take advantage of the fact that factor levels that are 50 percent of normal should give a normal Prothrombin time (PT) or Partial thromboplastin time (PTT) result.

"Mixing studies are very helpful, and very simple. In a mixing study, normal plasma with normal amounts of factors (i.e. by definition 100% factor activity is considered normal) is added to patient plasma in a 50-50 mix. If the patient’s plasma has a factor deficiency, the normal plasma will supply enough of that factor to give you a final factor percentage of at least 50%. Since you only need 40-50% of any factor to have a normal PTT, the mix will “correct”: i.e. it will give you a normal PTT."

Lupus anticoagulant is a condition characterized by the presence of antibodies to phospholipids.  These antibodies interfere with intrinsic coagulation cascade in vitro, in the laboratory test tube, and cause the PTT to be prolonged. Mr. White’s lab test results are perfectly compatible with a lupus anticoagulant. But his history is completely wrong for lupus anticoagulant: in vivo (that is to say, in the patient) lupus anticoagulant antibodies actually produce a pro-coagulant state leading to vascular thromboses, e.g. DVT, stroke, etc. In pregnant patients they can cause pregnancy loss by producing vascular occlusion in the placenta. The name “lupus anticoagulant” is very confusing because it is NOT an anticoagulant in the patient, and most patients do NOT have lupus (although many patients with lupus do have a lupus anticoagulant). 

D-dimer is a molecule which is formed when the body begins to break down fibrin clot. The formation of thrombus is always faster than the destruction of thrombus, so it’s not as if the thrombus will be broken down before it has plugged whatever vascular hole required it in the first place. But to prevent the thrombus from growing too big, the body begins breaking it down as soon as it has formed. The enzymes responsible for fibrinolysis, such as plasmin, act like scissors cutting the fibrin clot into pieces. One of the pieces that plasmin cuts off the fibrin clot is called D-dimer (which, unsurprisingly, is a dimer of the D domain of fibrin). If a patient has an elevated D-dimer level, this is proof that the patient has clotted somewhere in his or her body... because you have to form clot before your plasmin enzymes can cut D-dimers off it. As you will appreciate, there are physiologic clots (e.g. a vascular wound that generates a thrombus) and pathologic clots (e.g. a DVT), and D-dimer does not tell us which is which. An elevated D-dimer may be a “good” thing or a “bad” thing, depending on whether we want the patient to clot somewhere or not. All we can say with an elevated D-dimer is that clotting has taken place, somewhere in the patient.