Blood product transfusions

Transfusions

• Indications for red blood cell (RBC) transfusions include hemoglobin levels less than 7 g/dL, especially under 8 g/dL in cardiogenic shock cases
• Other indications are evidence of ischemia due to impaired oxygen transport, symptomatic anemia, and hypovolemic shock or bleeding
• A single unit transfusion should increase hemoglobin by 1 g/dL or hematocrit by 3%

Plasma

• Plasma provides all coagulation factors
• Administering 10-15 ml/kg of plasma will replace around 20% of a patient's clotting factors
• Plasma is given in cases of massive hemorrhage.
• Use before surgical procedures with an INR greater than 1.6
• Use when specific factor concentrates aren't available, and for plasma exchange

Platelets

• A single unit platelet transfusion typically raises the platelet count by 25-50 per unit given
• Platelets last about a week after donation
• Platelets are administered for massive hemorrhage, platelet counts below 10, and before procedures when platelet counts are below 50k
• Given for active bleeding, central nervous system or intraocular bleeding, when platelet count is below 50k
• Antiplatelet therapy and congenital platelet dysfunction/bleeding also warrant platelet transfusion

Cryoprecipitate

• Contains fibrinogen and von Willebrand Factor (vWF)
• It is administered in cases of massive hemorrhage, Hemophilia A, and von Willebrand disease (vWD)

Transfusion Considerations

• ABO antigens are codominantly inherited, meaning individuals can have blood types A, B, AB, or O, based on the presence or absence of A and B antigens
• If someone inherits both A and B alleles, both antigens get expressed, resulting in blood type AB
• Blood type O signifies the lack of both A and B antigens
• Blood type A produces anti-B antibodies and reacts with anti-A serum.
• Blood type B produces anti-A antibodies and reacts with anti-B serum.
• Blood type AB has no antibodies present and can receive both A and B blood.
• Blood type O has no antigens present and produces both anti-A and anti-B antibodies

Agglutinins

• Agglutinins are antibodies that cause clumping (agglutination) of incompatible red blood cells

Rh Factor

• The D-antigen is present in about 85% of the population (Rh+)
• Rh-negative patients only develop anti-D antibodies after exposure to Rh-positive blood, with pregnancy as a key instance
• If a mother is Rh-negative and exposed to fetal Rh-positive blood, she develops Anti-D antibodies that can cause hemolytic disease of the fetus and newborn (HDFN)
• Administering Rh immune globulin, or RhoGAM, prevents complications; this contains anti-D IgG antibodies that clear fetal Rh-positive cells from the maternal blood stream, preventing the development of maternal Rh antibodies

Type and Screen

• Cross-matching to reduce complications includes determining ABO type, Rh type, and screening for other antibodies
• Religious considerations, like those of Jehovah's Witnesses, should be respected; do not assume they will refuse blood.
• Pediatric cases require knowledge of hospital policies and ethics committee involvement
• For individuals with dietary restrictions (vegetarian, vegan, Islam, Judaism), note that heparin is derived from porcine intestinal mucosa

Thrombosis and Thrombophilia

• Thrombus: An aggregate of coagulated blood containing platelets, fibrin, and trapped cellular elements
• Thrombosis: Formation of a thrombus, leading to potential blood vessel obstruction
• Arterial thrombosis can lead to MI, stroke, and peripheral arterial thrombosis often associated with AFIB without anticoagulation
• Venous thrombosis can lead to DVT and pulmonary embolism

Outcomes of Thrombosis:

• Lysis: The fibrinolytic system can rapidly dissolve recent thrombi.
• It is less effective for older, more resistant clots
• Propagation: The thrombus grows by accumulating platelets and fibrin, which can lead to vessel occlusion
• Embolization: A portion of the thrombus breaks off and travels, resulting in blockages elsewhere
• Organization: Inflammation and fibrosis occur, which makes the thrombus firm and grayish white
• Canalization: A new lumen forms within the organized thrombus, allowing partial blood flow restoration
• Thromboembolus: A thrombus formed in one location that detaches, traveling to a distant site Venous thromboembolism (VTE): DVT, PE, cerebral venous sinus thrombosis
• Embolus: Intravascular solid, liquid, or gaseous mass carried to a distant site
• Fat embolus: Fat emboli is released into circulation following fractures of long bones, soft tissue truama or burns and may result the following:
  • Sudden onset
  • Tachypnea, Dyspnea, Tachycardia
  • Neurologic symptoms, which include Mental changes that progress to delirium or coma
  • Diffuse widespread petechiae (20-50% of cases)
  • Thrombocytopenia due to adherence of platelets to fat globules
  • Appears 1-3 days after injury and mostly obstructs microcirculation (arterioles and capillaries)
  • Usually is associated with Long bone fractures or Burns; trauma occurs in 90% of subjects with skeletal injury, but <10% of patients show clinical symptoms
  • The Fat embolus syndrome is fatal in 10% of cases. -Mechanism of injury: Fat globules present in microvasculature of lungs (ARDS) and brain (cerebral edema and small hemorrhages), followed by platelet activation and granulocyte recruitment and Free fatty acids from fat globules causing local injury to endothelium

Air Embolus

• Requires 100mL.
• Pressurized air embolus (deep water scuba diving) is caused by ascending too quickly, leading to rapid decompression

Amniotic Fluid Embolism

• Characterized by amniotic fluid or tissue fluid leading to intense inflammatory response (RARE → HIGH mortality rate)

Virchow's Triad

• Virchow's Triad consists of Endothelial Injury, Circulatory Stasis and Hypercoagulability; that leads to thrombosis and are worsened by:
  • Cancer, COVID, Pregnancy Circulatory status
  • Turbulent flow leads to arterial thrombosis result of turbulence around an aneurysm or at bifurcation sites
  • Stasis (slowed flow) is a major factor for venous thrombosis
  • Venous stasis caused by Prolonged immobilization, Foreign bodies, CHF, Pregnancy, Dehydration, Atrial fibrillation, Valve stenosis, Ventricular dysfunction, Polycythemia/sickle cell Endothelial Injury
  • Injury to the inner lining of blood vessels from surgery, trauma, or high blood pressure makes clot formation more likely.
  • Caused by Atherosclerosis, Hyperlipidemia Phlebitis/vasculitis Foreign body, Trauma and Bacterial infection. Hypercoagulability
  • Increased tendency for blood to clot due to genetic disorders, cancer, pregnancy, medications caused by:
  • Factor V Leiden which is autosomal dominant, and occurs in 2-15% of Caucasians Mutation → abnormal factor V not deactivated by protein C. A heterozygous risk of DVT by 4–6-fold and homozygous Condition → single greatest risk factor 50- to 100- fold risk increase for DVT
  • Protein C or S deficiency found in neonates, and occurs with: Severe congenital protein C deficiency → rare (1-2 neonates for every 1 million births) leading abnormally high numbers of clots → death. Symptoms appear soon after birth with a wide-spreading clot, that requires treatment with Protein C concentrate (Ceprotin)

Hyperhomocysteinemia

• Marked hyperhomocysteinemia has Plasma homocysteine level >100 µmol/L is found in Pediatrics
• Caused by Homozygous for cystathionine-beta-synthesis deficiency; that may lead to Severe developmental disability Lens and skeletal defects or Atherosclerotic and thromboembolic disease
• Moderate elevation: 16-100 µmol/L caused by Heterozygous enzyme deficiency of B12, Folic acid, or Pyridoxine (B6).
  • Homocysteine is normally metabolized which, deficiencies in these vitamins lead to elevated homocsyteine levels, increasing cardiovascular disease.
• Mild/moderate shows Homocysteine toxicity results in direct damage to endothelium, increased loss of thrombolysis
• Homocysteine toxicity: direct damage to endothelium, increased platelet adhesion → loss of thrombolysis
• Homocysteine causes an Independent risk factor for CAD, PVD, DVT, and Antithrombin deficiency

VTE (Venous Thromboembolism)

The most common of VTE is; Deep vein thrombosis (DVT)

• Deep vein thrombosis (DVT) (large vessels) enters right side of heart; and is - Asymptomatic in 50% cases or Impaired venous valve function.
• Results in Pulmonary Embolism(90% cases) (CT angiography) Risk Factor Advanced age, Sickle cell disease, Genetics + Males higher risk Obesity, Smoking, Immobilization, Prolonged bed rest, Flight travel
• Flight Travel Risks*:
  • Asymptomatic(higher)
  • 4hr: 1/4600

  • 8hr: 1/200 risk factor Foreign body, Estrogen: hormone replacement therapy is a DVT RiskFactor

DVT (Deep Vein Thrombosis) Pathogenesis

DVT Causes:

• Stasis
• Injury
• Hypercoagulability, oral Contraceptivse and smoking
• Advanced Age
• Late pregnancy Clinical Findings:
• Majority (90%) =legs vs 10% pelvis Superficial
• *Thrombi →found in saphenous Symptoms
• Local congestion
• Swelling
• Pain
• Tenderness along venous course
• Rarely embolize
• Local edema
• Impaired venous drainage Deep
• Thrombi → larger veins popliteal, femoral, iliac Symptoms
• Swelling→ unilateral
• Pain, Erythema, & Tenderness Pulmonary Embolism

• dyspnea + tachycardia

• R/o PE and VTE
• *90% case→emboli originate deep veins
• Lungs findings: 65% Bilateral vs 25% Right only and Left 10% and Lower > upper 4x
• Mech: Thrombi obstruction= Primary vs Vaso constriction(Low O), Secondary Severity
• Sig rise in P (>25mm)= 30-50% blocked
• RV->CO, central venous and right atrial pressure increase

Arterial Hypoxemia

Arterial Hypoxemia occurs due to ventilation-perfusion (V/Q) Exact Mechanisms:

• Increased alveolar dead space (vent present, perfusion absent
• "R to L Shunting
• *Right-to-left shunting can occur in lung regions:partial atelectasis
• Hypoxemia :improve with deep breathing
• Bronchoconstriction : Plate 5ht and PG Clinical Presentation:
• 60-80% Pulmonary eboli small and Symptomatic
• Undergo become and the Organized into vascular wall
• Symptoms*
  • "chest pain and dyspnea and Tachypnea and syncope and 15% with Death"

Pulmonary Embolism:

• The Most Common Cardiovascular Collapse→≥60% Scenarios:
  • "PE in Hopitalized patients but was fine"
  • Obstructive PE ( most cause Death)
  • Chronic Heart and lung, inmmobilzaion→ PE → Death Saddle Lodged @ bifurcation pulmonary ( obstructed)
  • 50% trunk blocked- > death
  • Rt v→Rt Ventric Failure and Shock
• If not deadly PE*
• Symptoms include include*

Hypo Tension and impaired and pale Weaken and sweat IIPulmonary with fluid but not embolism

• "Pulmonary Infarction

• 15% of cases in chest

• *Plead effisun, pneumonia - Cough IIi Congestive Atelectasis

*Impaired lung Tachnea Chest CT ray shows and hypuxima Lab Tests:

• "If embolism suspected d-dimer
• Air

Air Embolism

Air embolism often casured bu Neck to the lung Quantities: 100 ml → Effect Phisycal → blood side lungs Gas dissolved rapid decent ascent Clincial presentation Thromboemblotic is dervived by tromobus Causes

• Pathways*→PE,
• asymto Symptoms:
• Ultrasound alteration
• 20-30 Classical symptoms
• Major patient at risks
• *Surgery (trauma) with old patient:
• High chance without surgery

Surgery Considerations

• Clinical Checklist*

high<+ * Ultrasound and low * Doppler.

Other factors:

• Plasma: d-dimer elevation

• Contrast more accurate>
• Patient likely will have it
• Dye hypertonic

Heparin, Pulmonary, and Anticoagulation

Hepatotoxic

• Pulmonary: movement the lungs, and lodges

• "Dvt Is lower
• PE is 20% cases
• Other sources are less with pelvus Risk Factors:
• Heart Failure and women: Chemical
• 5ht 40%

Clinical features

• "Can Asymptomatic
• *Acute dyspnea often"
• Symptoms: Acute pain"

Benign White Blood Cell Disorders

• Benign White Blood Cell disorders*: Absolute *→ ↓ Neutrophil (Bands+ANC < 1500)
• B1= Low or No Disease or Immune
• Infect*:
• -gram fungal*
• 1= History/Diagnosis* =
• w differential*
• BM* Markers

Drug Causes

• Drug Causes*:
• *Sulfonamides drugs, GI medicine (citi), Anti
• Deficiency (vitamine B12) and Auto or infections
• Causes of hyper= viral or lung
• Lymphocytopenia

Infectious and inflammatory and CML:

• test 1: -Peripheral test abnormal Wbc (blast)
• -phylly 1 :genetic testing*
• • Bone is if high etc* L: *platelet ↓<150K *platelet

→Causes Risk bleeding increases = causes ↓ production and Increase in the spleen

• BM (Bone Marrow)* Impaired
• *Genetic and abornmitaes -Increase in storage and auto.

Infection-Induced TPO

Infection can attack trans

• Diagnosis*
• History, with BM Treatment:
• IVIG and
• Anti-p > can causes infection
• Can cuase Spleen removals. Infection with a

Anemia HUS

• Causes E Coli Infection

DIC:

• auto
• Derminty Diagnosis:
• History and Physical
• Test ANA. and HIV is SH
• PT PTT -If it doesn’t go with the other is dis-chord-

. Summary

• Acute/Chronic is the leukemia -Proliferation or my-Loid is the plasma related

Benign White Blood Cell Disorders

• Benign White Blood Cell disorders
• absolute count 600
• Causes of Neutropenia
• -gram is can test drug induced with infection etc*
• L= lymphocyte↑ and Causes increase virous bone* L is the platelet and
• It’ is* thrombocytopenia
• -- auto increases spleen.

Overview of indications for transfusions of red blood cells, plasma, and platelets. Includes transfusion guidelines based on hemoglobin levels, clotting factors, and platelet counts. Also covers usage in hemorrhage and surgical procedures.