Unit 6: Hematolgical Disorders; DIC & HIT

hematopoiesis

• blood cell formation

• stem cell differentiate

  • erythrocytes

  • leukocytes

  • thrombocytes

blood contains

• plasma (clotting factors floating, liver producers)

• solutes

• serum proteins

  • coags

  • healing transport

  • osmotic pressure

• blood cells

where are globulins made

liver

what’s the main protein in blood

albumin, made in liver

what can happen with decreased proteins

third spacing

erythrocytes/RBC’s

• purpose: O2 transport

• production stimulated by: EPO

• maturation: 4-5 days

• lifespan: 120 days

• normal: 4.2-5.15

• decreases with: renal disease

thrombocytes/platelets

• purpose:clotting

• production stimulated by: thrombopoietin

• maturation: 2/3 circulate in blood, 1/3 in spleen

• lifespan: 8-12 days

• normal: 150-400k

• decreased with: used more rapidly if multiple vascular injuries or clotting stimuli

leukocytes/WBC

• purpose: fight infection and antigens

• production stimulated by: triggering mechanism within the immune response

• maturation: varies

• lifespan: varies

• normal: 4500-11,000

• decreased with: malnutrition, immune disorders, advanced age

CBC with diff includes

• basophils

• eosinophils

• neutrophils

• monocytes

• B and T lymphocytes

hemostasis

• platelets

• blood proteins

• vasculature

• balance between clotting system and fibrinolytic system

clotting cascade steps

1. vasoconstriction

2. plts get sticky —> activation —> platelet plug

2A. fibrin = cement, intrinsic & extrinsic meet at the common pathway (Factor X) —> thrombin —> fibrin

what needs to work in order for clotting factors to work

• liver

• calcium

what is Factor X

the common pathway

• can get anti factor XA lab test

• where the intrinsic and extrinsic pathway meeet

• all other anticoagulants work here !!!! besides the heparin and warfarin

anti platelets do what

makes plts less sticky

antiplt meds

pt plug inhibitors

• ASA

• clopidogrel

• ticagrelor

antiplatelet meds MOA

block plt aggregation —> prevents CLOT FORMATION

works on the plt phase —> primary hemostasis

anticoagulants do what

work on the production of fibrin

• clotting cascade inhibitor

anticoagulant meds

• heparin

• warfarin

heparin works on the

intrinsic pathway

• injury’s INSIDE the vessel/ to the blood

heparin antidote

• protamine sulfate

heparin lab to monitor

• aPTT

aPTT normal range and therapeutic range

• normal: 25-3 seconds

• therapeutic: 1.5-2.5 the normal, so 60-80 seconds

warfarin works on the

extrinsic pathway

• tissue injury OUTSIDE the vessel

• needs Vitamin K dependent factors

warfarin antidote

vitamin K

warfarin labs to monitor

• PT

• INR

INR normals and therapeutic range

normal: 1

therapeutic: 2-3

hemostasis summary

• activation of the coagulation cascade

• formulation of a stable fibrin clot

• activation of fibrinolytic system

blood clots

• stop bleeding from injured vessel

• 3 physiologic mechanisms known to trigger clotting

  • tissue injury ‘

  • vessel injury

  • FBO in bloodstream

fibrinolysis

• stimulated by clot formation & occurs 1-3 days after clot formation

• plasmin- an enzyme that digests fibrinogen & fibrin

• when plasmin digests fibrinogen—> fragments are produced that function as potent ANTICOAGULANTS

  • form FIBRIN DEGREDATION PRODUCTS (FDP’s)/ Fibrin split products (FSP’s) —> bleeding —> CAN LEAD TO DIC

coagulation pathway

• cascade theory

• initiating event

  • intrinsic pathway: injury to blood (factor XII (12)

  • extrinsic pathway: tissue injury (factor VII (7)

• final common pathway

  • prothrombin —> thrombin

  • fibrinogen —> fibrin

  • CLOT

fibrinolysis continued

• Stimulated by clot formation

  • Thrombin released

  • Stimulates conversion of plasminogen to plasmin

• Breakdown yields fibrin degradation products

(FDPs), or fibrinogen split products (FSPs)

cues to heme and immune problems

• altered O2

• bleeding

• infection

heme dx tests

• CBC with diff

• coagulation profile

• based on these findings, further testing math be required

bleeding disorders

Abnormality in stages of clotting

• Vasoconstriction

• Creation of platelet plug

• Development of clot

• Fibrinolysis

˜ Inherited or acquired

˜ Common in renal, hepatic, and gastrointestinal

disorders; malnutrition

D dimer indicates what

clot breaking down

dx of bleeding

• CBC

  • H&H

  • Fibrinogen

• FSP/FDP

• D Dimer

• PT, aPTT

nursing managment of bleeding

Assess blood loss

• Assess vital signs, hemodynamics, and

perfusion

• Assess for signs and symptoms of hypovolemia

• Administer blood products and fluids

• Administer topical agents as needed

what can we given for prolonged clotting factors

FFP

medical management of bleeding

• Whole blood

• Packed RBCs

• Leukocyte-poor RBCs

• Platelets

• Cryoprecipitate

• Albumin

• Granulocytes

• Plasma protein

• Fresh frozen plasma

whole blood

• what is it: RBC’s, plasma, clotting factors

• why do we give: restores O2 carrying capacity and intravascular volume

• indications: SEVERE hemorrhage, symptomatic anemia with major circulating volume deficit

PRBC’s

• what is it: RBC’s spun out from whole blood (leukoreduced)

• give why: restores O2 carrying capacity and intravascular volume

• indications: symptomatic anemia, acute hemorrhage

• based of H&H <7 or active bleed

platelets

• what is it: plts thatve been removed from blood

• why we give: improve plt count and hemostasis

• indications: prophylactic for <20K and for signs of bleeding with counts <50K

FFP

• what is it: plasma w/o platelets and RICH IN CLOTTING FACTORS

• why we give: replaces clotting factors

• indications:

  • deficit of coag factors

  • mass transfuions

  • DIC

  • major trauma with s/s of hemorrhage

  • elevated/prolonged PT/INR/PTT

Cryo

• what is it: coagulation factor VIII (8), with 250 mg fibrinogen and 20-30% of factor XIII (13)

• why we give: replaced selected clotting factors i

• indications:

  • inherent clotting disorders (hemophilia)

  • mass transfusions

  • hypofibrinogenemia

DIC

disseminated intravascular coagulation

Accelerated activation of clotting cascade

˜ Depletion of clotting factors

˜ Bleeding

˜ Secondary problem

bleeding with no perfusion to kidneys and brain

what is DIC cont

hematological disorder that occurs because of an acceleration in the clotting cascade. A triggering event causes the release of procoagulant factors such as: sepsis , trauma, big hemorrhage

In other words -

˜ It’s a coagulopathy in which you have both

intravascular clotting and bleeding

patho of DIC

Initiating event: procoagulants

• Stimulation of intrinsic or extrinsic pathway

• Clots in microvasculature

• Consumption of clotting factors (eating up clotting factors —> microemboli = consumptive couagulopathy

• Fibrinolysis

• FDPs: potent anticoagulants

DOC etiology

Infection

• Trauma (e.g., burns, crush)

• Obstetric conditions (e.g., abruptio placentae,

amniotic fluid embolus, retained dead fetus, PPH)

• Hematological disorders

• Oncological disorders

• Other: shock or sepsis, acute respiratory

distress syndrome

blood is an organ —> DIC = failure of organ

1st phase of DIC

thrombotic

• last hours to days

• large amounts of thrombin are produced and clots are lodged in the micro vasculature

2nd phase of DIC

fibrinolytic

• fibrinolysis now breaks down clots which releases FDP’s/FSP’s

• FDP’s are potent anticoagulants that act by impairing thrombin and decreased ability to make clots

DIC summary

Triggering event (endothelial damage or direct tissue damage)

• Activation of clotting cascade

• Excessive thrombin production leads to fibrin

deposits in the microvasculature (leads to death to

whichever organ is occluded)

• Available clotting factors are spent/consumed

• Fibrinolysis occurs, leading to FDPs (anticoagulants)

• RBCs are damaged as they try to pass blocked capillary beds (more hemolysis)

why is bleeding such a big thing in DIC

anticoagulants are floating around and there are NO CLOTTING FACTORS LEFT= bleeding !!!!

DIC assessment

• Overt bleeding or oozing

• Occult bleeding

• Signs of platelet deficiency

  • Petechiae

  • ecchymosis

• Decreased perfusion to organs

  • Changes in mental status

  • Infarction of tissue in digits and nose (necrosis)

what labs will be decreased with DIC

• platelets

• fibrinogen

• coagulation factors

• H&H

labs that will elevated or HIGH with DIC

• FSP/FSP

• D dimer

labs that will be PROLONGED (elevated/high) with DIC

• PTT

• PT/INR

• normal INR is 1

• thrombin

DIC tx

• CORRECT THE UNDERLYING CAUSE

• Administer blood and components

  • Platelets

  • Fresh frozen plasma

  • Cryoprecipitate

  • Packed RBCs

• Stop abnormal coagulation

• Heparin: controversial when experiencing more hemorrhage than thrombosis

why may we give heparin in DIC

prevents thrombin and fibrin formation —> stops it from getting broken down in the first place

• don’t give to active bleeding

• overall prevents new from forming, overall less clot breakdown happens overall

stopping the unwanted clotting and control bleeding

Platelets

• Highest priority

  • Fresh Frozen Plasma (FFP)

• For Fibrinogen replacement

• Contains all clotting factors and antithrombin III

• Cryoprecipitate

  • When plasma is frozen, Factor VIII is inactivated so you'll need to replace through cryoprecipitate

• PRBCs

  • To replace losses

• FFP + Cryo for DIC

other tx for DIC

• Tranexamic acid TXA, (anti-fibrinolytic)-for extreme hemorrhage, but causes thrombotic events (MI and renal artery occlusion)-should be used with Heparin —> prevents plasmin from breaking down fibrin

˜ Antithrombin III (inhibits thrombin, factor Xa, common pathway)-

prevents development of fibrin clot.

• prevents more fibrin production in the 1st place

heparin

a Thrombin Inhibitor

• Thought is to block the clotting process

• Controversial (might work or make bleeding

worse)

antithrombin III

Synthetic Antithrombin III inhibits thrombin

• May shorten course of DIC and improve survival

rates

transexamic acid

• Inhibits fibrinolysis by interfering with plasmin activity

• For severe hemorrhage with DIC

• Risk thrombotic events-MI and renal

artery occlusion

nursing managment of DIC

Assess and prevent

• Conduct frequent laboratory analysis

• Administer blood products

• Assess circulation

• Oral care and skin care

• Relieve pain

• Assess for complications: shock, multisystem

organ failure, impaired circulation

prevent and treat hypothermia

• Keep pt covered during transfusion

• Warmed blankets and/or Bair Hugger as needed

• Utilization of fluid warmers or a rapid transfuser that provides warming

ionized calcium

• Blood transfusions include citrate. It binds to calcium in the patient’s blood causing hypocalcemia (tetany, laryngospasm)

  • Chvosteks & Trousseaus

• Follow up CBC and DIC panel

• multiple blood transfusions can cause low Ca+

• citrate builds up with multiple transfusions and lowers Ca+, checking the ionized shows the free floating ca in blood and gives more accurate levels

thrombocytopenia

Decreased platelets

• Less than 100,000/microliter

  • Risk for bleeding

• Treated with platelet transfusions

HIT

heparin induced thrombocytopenia

• side effect

what is HIT

• Can occur (as a delayed onset) even after

heparin discontinuation

HIT type 1

• Type 1-non-immune, direct effect of Heparin on platelets-DC the Heparin immediately

• pH will increase when Heparin is stopped

• directly damages the platelets

HIT type 2

• immune mediated and has life and limb

threatening thrombotic complications

• platelets start clumping together

• plts attacked, stopping the Heparin doesn’t help

HIT type 2 continued

HIT is an immune response to Heparin

• Usually occurs 5-10 days after receiving heparin therapy

• The immune response causes a >50% decrease of the highest platelet count after

heparin started.

examples: platelets before starting Heparin 300,000. five days later after therpay was started plts count now at 140,000.

just find half of the OG lab level, if less than or equal to that it’s HIT type2

HIT etiology

• Heparin binds to platelets, specifically Platelet

Factor 4 (PF4)

• This forms an antigenic complex on the surface of the platelets

  • Some people develop an antibody to this

• If your body develops an antibody, it means

your body sees your platelets as foreign (seen more with Enoxaparin)

• Macrophages begin to eat platelets

risk factors for HIT

• 10-fold higher with unfractionated heparin v.

LMWH (Lovenox)

• Major Surgery

HIT complications

HYPERCOAGULABILITY (more with Type 2 HIT) & THROMBOSIS as opposed to bleeding, even though platelet count is low

WILL ACTUALLY CLOT MORE even though plts are low, not a bleeding risk

• start clumping like crazy together, so count drops overall becuase they’re being used up in clots and consumed not becuase of BLEEDING!!!

thromboembolic complications of HIT

• DVT

• PE

• MI

• CVS (stroke)

• arterial occlusion

• DIC maybe

HIT Dx

A 50% decrease ( 300,000 —> 150, 000) from the highest level after heparin is started AND –a new thrombus OR – an anaphylactoid reaction after a heparin bolus

• withdraw heparin

HIT treatment

• Discontinue ALL Heparin

• Administer meds that inhibit thrombin formation or cause direct thrombin inhibition

  • Argatroban (Novastan)

  • Bivalirudin (Angiomax)

• Warfarin, LMWH, Aminocaproic acid, and

platelets are AVOIDED

Can exacerbate thrombosis

blood product administration

• As needed

• PRBCs

  • Symptomatic anemia

• Platelets

  • Thrombocytopenia

• With signs of bleeding or counts low enough for spontaneous bleed with a sneeze

meds that are thrombolytics/fibrinolytics (plasminogen activators)

known as clot busters “-ase”

• atleplase

• stretokinase

meds that work on the common pathway

• rivroxaban

• dabigatran

• apixaban

• enoxaparin

• endoxaban

• fondaparinux

when do you when to make the switch from Heparin to Warfarin

pt will be on a heparin drip

• will start Warfarin PO at the same time

• wont d/c the Heparin drip til Warfarin reaches therapeutic level INR of 2-3

what do you for all types of blood transfusion reactions

• STOP THE INFUSION

• aspirate any blood left in the line, dont want any more going into the patient and then flush with NS

• send back to blood bank

• get VS

• notify the MD

• get and type and screen

• and tx the type of transfusion reaction (ex: febrile give antipyretics, support the s/s)

acute hemolytic reaction

• most dangerous

• cause: ABO incompatibility —> wrong blood

• onset is immediate

• can lead to shock, DIC, KF

acute hemolytic reaction s/s

• fever and chills

• LOWER BACK PAIN/FLANK PAIN

• chest tightness

• hypotension

• tachy

• dark urine

• impending doom feeling

febrile nonhemolytic reaction

• most common

• cause: WBC in donor blood → immune response

• onset: within a few hours

febrile non hemolytic reaction s/s

• FEVER

• chills

• headache

• malaise

• no hemolysis→ not life threatening

allergic reaction blood transfusion

• sensitivity to donor plasma proteins

• onset: during transfusion

allergic reaction transfusion s/s

• ITCHING

• hives

• flushing

anaphylactic reaction

• severe allergy from hypersensitive often IgA

• onset is immediate

• will see airway swelling

• wheezing

• dyspnea

• hypotension

• shock

• life threatening

circulatory overload reaction

• too much volume too fast

• occurs during or shortly after

• s/s include→ HTN, JVD, crackles, dyspnea, pulmonary edema

with what blood product do you see more reactions with

FFP