Principles of effective consultation:

• Clearly understand the reason for consultation
• Understand the urgency of consultation. Urgent consultations must be seen as soon as possible.
• Personally gather the patient’s data (history/ examination/ laboratory findings). Do not rely on secondhand information.
• Communicate the recommendations as briefly as appropriate. With this one can expect optimal compliance.
• Make specific recommendations for diagnosis and treatment. Provide specific drug doses, schedules and treatment guidelines.
• Briefly address alternative diagnosis and anticipate complications.
• The attending physician has ultimate responsibility for the patient. Hence never write any orders without his/ her permission.
• Provide relevant evidence based literature or guidelines.
• Continue involvement in care of the patient as indicated.

General surgery and orthopaedics

Perioperative evaluation of bleeding risk:

History must include:

• Specific bleeding complaints
• History of bleeding with previous surgical procedures such as circumcision/dental exctraction/ child birth
• History of menorrhagia
• Family history of bleeding disorder
• Use of medications which can cause bleeding tendency

• If history is suggestive minimal chance of bleeding disorder
  • Do PT, APTT, Platelet count, LFT, RFT, Peripheral smear.
  • If all these are normal, then there is no need for further evaluation.
• If history is suggestive high chance of bleeding disorder-
  • Do PT, APTT, Platelet count, LFT, RFT, Peripheral smear
  • If all these above tests are normal: Do platelet function tests, von Willebrand workup, Factor VIII, IX, XI and XIII assay (As mild hemophilia can have normal APTT)
• If PT, APTT, Platelet count are abnormal
  • Further evaluation to identify the particular bleeding disorder

Targets of platelets for various surgical procedures

• Low risk surgery- 50,000/cmm
• High risk surgery- 1,00,000/cmm

These platelet counts must be maintained for 7 days post operatively

Note: Patients with ITP bleed less compared to other thrombocytopenia with same platelet count. Platelet transfusions are ineffective in ITP. Steroids with IVIg must be given to ITP patients to achieve satisfactory platelet counts.

Patients on antiplatelet agents undergoing surgery

• Minor procedures with least bleeding risk (Cataract surgery, endoscopies with mucosal biopsy, minor dental/ dermatological procedures)- Do without stopping.
• Neuraxial anesthesia is considered safe in patients receiving aspirin.
• Major surgeries:
  • High cardiovascular risk- Do without stopping
  • Low cardiovascular risk- Stop 7-10 days prior to surgery
  • Dual antiplatelets with high cardiovascular risk- Stop clopidogrel 5 days prior to surgery
  • Post PTCA patients. Defer surgery if possible, during the period of highest risk for in-stent thrombosis
    • Bare metal stents- 6 weeks
    • Drug eluting stents- 6 months
    • If surgery cannot be delayed, dual antiplatelets should be continued during and after the surgery.
• If patient needs emergency surgery- Platelets should be transfused at least 2 hours after the last dose of aspirin and periopertaively tranexamic acid.

For thromboprophylaxis and bridging of anticoagulation in surgical patients, refer to venous thromboembolism chapter, in coagulation disorders section.

Topical hemostatic agents

• Physical agents
  • Bone wax
  • Ostene
• Absorbable agents
  • Gelatin foams- Provide physical matrix upon which coagulation can initiate. They expand to double their volume.
  • Oxidised cellulose- Derived from wood pulp
  • Microfibrillar collagen- Bovine product
• Biological agents
  • Fibrin sealants- Composed of virally inactivated human thrombin and human fibrin
  • Applied using a dual syringe delivering device.
  • Platelet gel- It consists of platelets and fibrinogen. This is also applied through dual syringe delivering device.
• Synthetic agents
  • Polyethylene glyconhydrogels- Sprayed on to tissue where it forms cross linked polymer matrix
  • Cyanoacrylates- Liquid monomers that rapidly polymerise in the presence of water
  • Gluteraldehyde cross linked albumin- Used for sealing sutures and staple lines in complex cardiovascular procedures
• Hemostatic dressings
  • Contain combination of gauze and lyophilized fibrinogen and thrombin

Medical Oncology

Anemia in cancer patients

Causes:

 Patients may have non-cancer related causes such as megaloblastic anemia, iron deficiency, renal dysfunction etc.

Treatment

• Depends on cause
• Transfusion support            
• Erythropoietin
  • 10,000 IU – 3 times a week
  • Indications- Hemoglobin - < 10g/dL
  • Some suggest to avoid using EPO as it increases the risk of thrombosis and as some tumors express EPO receptors, there can be growth of these tumors

White cell changes in cancer patients:

• Neutrophilia- Seen in RCC and Hodgkin’s lymphoma
• Neutropenia- Seen in BM infiltration, hypersplenism, treatment induced, LGL leukemia
• Basophilia- Seen in myeloproliferative neoplasms
• Eosinophilia- Seen in Hodgkin’s lymphoma, T cell lymphomas, metastatic adenocarcinoma, drug allergy, opportunistic infections
• Monocytosis- Seen in carcinomas, Hodgkin’s lymphoma
• Lymphocytosis- Lymphoid malignancies, post splenectomy, opportunistic infections

Thrombocytopenia in cancer patients

• Decreased production- Chemotherapy/ radiotherapy, marrow infiltration
• Accelerated destruction- Hypersplenism, DIC, Drug related ITP (Transtuzumab, oxaliplatin), thrombotic microangiopathy

Bleeding tendency in cancer patients

• DIC
• Acquired platelet function defect
• Thrombocytopenia
• Circulating anticoagulants/ inhibitors

Thrombotic tendency in cancer patients

• Venous stasis due to bed rest, venous compression by tumor
• Increased procoagulants
• Decreased inhibitors of coagulation such as protein C and S and antithrombin
• Direct activation of coagulation by tumor cells
• Reactive thrombocytosis
• Refer to “venous thromboembolism” chapter for more details.

Rheumatology

Hematological changes in rheumatological disorders

• Anemia
  • Anemia of chronic disease
  • Iron deficiency anemia- Drug induced blood loss
  • Folate deficiency
  • Sideroblastic anemia
  • PRCA
  • Hemolytic anemia
• Thrombocytopenia
  • Immune thrombocytopenic purpura
  • TTP
• Autoimmune pancytopenia
• Coagulation problems
  • Lupus inhibitor
  • Specific factor acquired deficiency
  • DIC
• Others
  • Autoimmune myelofibrosis
  • LGL leukemia
  • Drug induced changes such as gold induced aplastic anemia
  • Cryoglobulinemia
  • Amyloidosis

Diagnostic criteria for Systemic Autoimmune diseases:

Systemic Lupus Erythematosis (American College of Rheumatology): Any 4 or more of following 11 criteria must be present: 

• Malar rash
• Discoid rash
• Photosensitivity
• Oral ulcer
• Arthritis
• Serositis
  • Pleurisy
  • Pericarditis
• Renal disorder
  • Persistent proteinuria
  • Cellular casts
• Neurologic disorder
  • Psychosis
  • Seizures
• Hematologic disorder
  • Hemolytic anemia
  • Leukopenia
  • Lymphopenia
  • Thrombocytopenia
• Immunologic disorder
  • Anti-DNA
  • Anti-Sm
  • Antiphospholipid antibodies
• Antinuclear antibody

Mixed Connective Tissue Disorder (Sharp Criteria): 

• Anti-U1RNP antibodies titer >1:4000 AND at least 4 major criteria or 
• anti-U1RNP antibodies titer > 1:1000 AND 2 major criteria among 1,2, 3 AND 2 minor criteria

Major

• Severe myositis
• Pulmonary involvement
• Raynaud’s phenomenon
• Swollen hands or sclerodactily
• Anti-ENA >1:10,000 and anti-U1RNP positive and anti-Sm negative

Minor

• Alopecia
• Leukopenia
• Anemia
• Pleuritis
• Pericarditis
• Arthritis
• Trigeminal neuropathy
• Malar rash
• Thrombocytopenia
• Mild myositis
• History of swollen hands

Note: Whenever systemic autoimmune rheumatic disease is suspected, first send Antinuclear antibody test. If it is reactive, then send anti-extractable antigen (anti-ENA) and anti-double-stranded DNA tests.

Endocrinology

Anemias due to endocrine abnormalities

Hypothyroidism

• Moderate anemia
• Concomitant drop in plasma volume makes hemoglobin concentration an unreliable indicator of red cell mass
• Anemia results due to hypoproliferation as thyroxine normally potentiates action of EPO.
• Usually macrocytic anemia. But can be normocytic/ microcytic
• Iron deficiency can occur due to menorrhagia
• Hashimoto’s thyroiditis is sometimes associated pernicious anemia
• Treatment- Thyroxine replacement

Hyperthyroidism:

• Anemia occurs due to increased plasma volume and decreased RBC survival
• Treatment- Antithyroid drugs

Hypopituitarism

• Mild anemia (Hemoglobin around 10gm/dL)
• Usually normocytic normochromic anemia
• Bone marrow- Hypoplastic
• Treatment- Replacement of thyroid, adrenal and gonadal hormones

Decreased androgens

• Average fall in hemoglobin after orchiectomy- 1.2gm/dL
• Testosterone stimulates EPO production and also has direct action on the marrow
• Treatment- Testosterone supplementation

Addison’s disease

• Causes normocytic normochromic anemia
• Anemia may be masked by decreased plasma volume
• Occurs because glucocorticoids normally enhance the effect of EPO
• Pernicious anemia can occur in patients with autoimmune adrenal insufficiency 

Hyperparathyroidism

• Causes normocytic normochromic anemia
• Cause is not known
• Resolves after parathyroidectomy

Nephrology

Anemia with renal failure

Causes include:

• HUS/TTP
• Iron deficiency- due to GI bleeding, frequent blood draws, hemodialysis
• Folate deficiency
• Hyperparathyroidism
• Aluminium toxicity
• Decreased erythrocyte survival due to uremic acidosis
• Anemia of chronic disease due to concomitant inflammation
• PRCA due to EPO use
• Multiple myeloma
• Systemic vasculitis
• Anemia of renal disease
  • Occurs due to failure of erythropoietin production, presence of dialysable inhibitor of erythropoiesis and increased hepcidin levels.
  • Results in normocytic normochromic anemia with low reticulocyte count
  • BMA- 
    • Normocellular/ mildly hypocellular
    • Relative erythroid hypoplasia
    • Bone marrow fibrosis (osteitisfibrosa) in some cases.
    • May show renal osteodystrophy due to secondary hyperparathyroidism
  • S. EPO- Normal (which is disproportionate to anemia)
  • Treatment
    • Rec Erythropoietin- 5-75 units/kg/week-SC given in 2-3 divided doses
    • Intravenous iron helps in decreasing EPO requirement
    • Avoid EPO once hemoglobin level reaches 10gm/dL
    • Impaired response suggests alternate causes for anemia and associated iron deficiency.
    • Transfusions if there is acute blood loss
    • Folic acid supplementation- As folic acid is a dialysable molecule
    • Propyl hydroxylase inhibitors: Stabilize HIF alpha proteins and enhance endogenous EPO production.

Thrombocytopenia with renal failure

• TTP/HUS and other microangiopathies
• DIC
• Renal allograft rejection
• Adverse reaction to drugs such as heparin

Hemostatic Disturbance in CRF

Causes:

• Platelet dysfunction due to
  • Increased levels of platelet inhibitory prostacyclins (PGI₂) which are released from endothelium
  • Reduced expression of procoagulant anionic phospholipids on platelet surface
  • Accumulation of platelet toxic materials in the plasma such as Guanidosuccinic acid and Phenolic acids
  • Acquired storage pool disease
• Hypocoagulability
  • Dysfunctional vWF
  • Decreased production of thromboxane
  • Decreased factor XII, XI, prothrombin

Clinical features

• Bleeding- Ecchymosis, purpura, epistaxis, bleeding from puncture sites

Treatment

• Correction of anemia
• Hemodialysis- Improves platelet function
• DDAVP (Vasopressin) – 0.3 – 0.4 µg/kg – IV. Improved platelet signal transduction, along with increased vWF levels
• Other measures which can be useful
  • EPO
  • Cryoprecipitate
  • Conjugated estrogens- 0.6mg/kg- OD for 5 days. Mechanism of action is not known.
  • Tranexamic acid

Hematological problems during renal transplantation

Anemia

• Early post-transplant (<6 months)
  • Post operative hemorrhage
  • Hemolytic anemia- Secondary to
    • Passenger lymphocyte syndrome- Due to antibodies from donor’s B lymphocytes
    • HUS/MAHA- Due to use of calcineurin inhibitors
  • Infections
    • Bacterial sepsis
    • Viral infections- CMV, EBV, Parvovirus
  • Medications- Some of the immunosuppressive drugs
  • Additional causes in renal transplant patients
    • Iron deficiency
    • Prior uremia
    • Bone disease
• Late post-transplant anemia(>6months)
  • Infections- EBV, Parvo, CMV
  • Drug effect by myelosuppression
  • Alloimmune hemolytic anemia due to antibodies
  • Rejection
  • Post-transplant lymphoproliferative disease
  • Anemia of chronic disease
  • Iron deficiency
  • Renal failure

Thrombocytopenia

• Drug induced thrombocytopenia
  • Tacrolimus/ Cyclosporine A induced microangiopathy
  • Azathioprine induced bone marrow suppression
• Immune thrombocytopenia
• Transplant associated HUS/MAHA
• Infections- Bacterial sepsis, HHV-6, CMV and other herpes viruses
• Graft Vs Host disease due to passenger lymphocytes (Presentation and manifestations are similar to transfusion related GVHD)

Neutropenia

• Myelosuppressive drugs- Azathioprine, ganciclovir, MMF, sirolimus, interferon
• Infections- CMV, sepsis
• Post transplant lymphoproliferative disease

Hepatology

Anemia in liver disorders

Possible mechanisms

• Abnormal protein synthesis resulting in increased membrane cholesterol and phospholipids.
• Iron, Vitamin B12 and Folic acid deficiency
• Hemolytic anemia due to marked increase in membrane cholesterol (Zieve’s syndrome)
• Hypersplenism associated with portal hypertension.
• Anemia of chronic disease- Bone marrow hypoproliferation due to absence of erythropoietic factor or direct alcohol suppression
• Blood loss from GIT
• Alcohol induced sideroblastic anemia
• Hemodilution due to fluid retention in cirrhosis
• Bone marrow suppression by hepatitis viruses/ alcohol
• Drug induced- Ribavarine induced hemolysis, interferon induced BM suppression

Coagulation defect in hepatic diseases

Introduction:

• All coagulation factors except vWF are synthesized in liver along with antithrombin III, protein C, protein S, Alpha- 2 plasmin inhibitor, and plasminogen
• Thrombopoietin is also synthesized in liver
• PT and APTT are prolonged in CLD, but they do not correlate with bleeding tendency as activity of anticoagulants such as Protein C and Protein S are also reduced. Hence most of the patients are in a “rebalanced” hemostasis.
• Total thrombin generation test is usually normal in them.
• So no need to correct prolonged PT or APTT if patient is not bleeding.

Causes for abnormalities of hemostasis in chronic liver diseases

• Deficient biosynthesis
  • Deficiency of fibrinogen; prothrombin; coagulation factors V, VII, IX, X, XI, XII, XIII; prekallinkrein; high molecular weight kininogen
  • Defieiciency ofantiplasmins, antithrombin, proteins C and S
• Aberrant biosynthesis
  • Abnormal fibrinogen, factor V, factor VII
  • Abnormal inhibitory analogs of prothrombin, factors VII, IX, and X
• Deficient clearance of
  • Hemostatic products (e.g., fibrin monomers, fibrin degradation products,  platelet factor-3)
  • Activated coagulation factors (IXa, Xa, XIa)
  • Plasminogen activators
• Accelerated destruction of coagulation factors
  • Disseminated intravascular coagulation
  • Localized intravascular coagulation (hepatic cell necrosis)
  • Abnormal fibrinolysis
• Thrombocytopenia
  • Hypersplenism (portal hypertension)  
  • Folic acid/ Vitamin B12 deficiency
  • Chronic ethanol intoxication
  • Disseminated intravascular coagulation
  • Autoimmune thrombocytopenia associated with viral hepatitis or primary biliary cirrhosis
  • Direct BM toxicity by alcohol/ hepatitis virus
  • Decreased hepatic synthesis of TPO
• Platelet dysfunction
  • Acute and chronic ethanol intoxication
  • Effects of products of fibrinogen degradation, bile salts, abnormal HDLs, increased nitric oxide and prostacyclin
  • Uremia
  • Inhibitory factors including high density lipoprotein and apolipoprotein E
  • Decreased synthesis of platelet GP 1b
  • Storage pool deficiency

Treatment

• RBC transfusion to maintain adequate hemoglobin
• Platelet transfusion if there is bleeding due to thrombocytopenia
• Eltrombopag is useful, especially in case of HCV associated thrombocytopenia.
• Maintain platelet count >50,000/cmm, prior to any invasive procedures
• Vitamin K supplementation (PO/IV)- 10-20mg
• FFP- 10-20ml/kg
  • Given in case of major hemorrhage and prior to major invasive procedures
  • Do follow up CBC, PT, APTT and fibrinogen to assess the response
  • Repeat transfusion if required every 12 hrly
• Use tranexamic acid cautiously, as there is increased risk of thrombosis
• Liver transplantation

Factors that increase thrombosis risk in CLD patients

• Increased vWF
• Decreased ADAMTS13
• Increased factor VIII
• Decreased protein C, protein S and antithrombin
• Reduced plasminogen
• Increased PAI-1

Geriatrics

• Old age generally means, age >65 years.
• Hematopoietic changes associated with ageing
  • Diminished bone marrow cellularity
  • Reduced CD34 mobalization
  • Decreased stem cell telomeres
  • Reduced hematopoeitic cell proliferative capacity
  • Reduction in lymphocyte function
  • Reduced response to vaccination
  • There is no change in WBC and platelets in old age.
• Anemia in old age:
  • Hemoglobin <13gm/dL in men and <12gm/dL in women is called anemia
  • 11% of old age people are anemic
  • Development of unexplained anemia (Unexplained anemia of elderly)
    • Accounts for 30-40% of total anemia cases in elderly
    • Occurs due to inappropriately low EPO response, inflammatory cytokines due to occult inflammation, decreased response to EPO, androgen deficiency and early myelodysplasia.
    • Give trial of Iron, B12 and folic acid.
    • If no improvement EPO can be given.
• Common causes of cytopenia in elderly
  • Megaloblastic anemia
  • MDS
  • Hematological neoplasm
  • Autoimmune diseases
  • Consuptive coagulopathy
  • Systemic inflammation
  • Alcohol
  • Splenomegaly
  • Thyroid dysfunction
  • HIV
  • Idiopathic
• Indications for BM aspiration in elderly
  • Unexplained requirement of frequent blood transfusions
  • Unexplained MCV- >97
  • Platelet count <1,20,000/cmm
  • ANC <1000/cmm
  • Suspicious peripheral smear
• Whenever elderly patients need intense chemotherapies, PS score must be measured. Intense chemotherapy must be administered only of performance score is ≥2

Neonatology

Normal hematological parameters in neonates:

• Normal CBC values have been included in physiology section
• Erythropoietin levels are undetectable in infants as it does not cross placenta and fetal kidney produces very little erythropoietin. Source of EPO for infant is amniotic fluid and liver.
• Reticulocyte count is <1% by 6^th day of life
• Placenta and umbilical cord contain 75-250ml of blood at term which is approximately 1/4^th to 1/3^rd of fetal blood volume. Infants held below the level of placenta can receive half of the placental blood volume (30-50ml) in 1 minute. With delayed cord clamping volume of blood in newborns may be increased from 72ml/Kg to 93ml/Kg.
• Hemoglobin falls rapidly from 2^nd week till 6-9 weeks. Nadir hemoglobin is seen at 2 months of age.
• Red cell life span is 60-80 days
• Factor levels are usually 60% of adults.
• Levels of vitamin K dependent factors are reduced in first 3-4 days of life. Hence prophylactic vitamin K should be given to all neonates.

Causes of neonatal anemia:

• Decreased production
  • Bone marrow failure- Diamond blackfan syndrome, CDA, Sideroblastic anemia, Fanconi anemia
  • Anemia of prematurity
  • Infections- Parvovirus, HIV, Syphilis, rubella, sepsis
  • Transcobalamin II deficiency
  • Maternal nutritional deficiency- Vitamin B12/ Iron
  • Bone marrow infiltration- Leukemia, neuroblastoma, osteopetrosis, etc
• Increased destruction:
  • Immune hemolysis- Hemolytic disease of newborn, drug induced immune hemolysis
  • Enzyme deficiencies
  • Membrane defects
  • Unstable hemoglobin, alpha thalassemia
  • Extracorpuscular causes- Microangiopathic hemolytic anemia, sepsis, congenital TORCH infection
• Blood loss anemia
  • Iatrogenic- from lab draws
  • Obstetric accidents
  • Malformations of placenta/ cord
  • Feto-maternal or twin-twin transfusion syndromes
  • Internal hemorrhage- Intracranial, intrahepatic, cephalohematoma, subglial hemorrhage

Causes of neonatal thrombocytopenia:

• ARDS
• Sepsis
• Small for date babies
• Trisomy syndromes
• Immunological- Alloantibodies (NAIT), auto-antibodies, drug induced antibodies
• Hypersplenism
• Cavernous hemangioma  - Kasabach merit syndrome
• DIC
• Post procedure following exchange transfusions
• Congenital thrombocytopenia- TAR, CAMT
• Bone marrow infiltrations- Congenital leukemia etc
• Drugs:
  • Suppressing platelet production- Maternal ingestion of ethanol, thiazide, chlorpropamide, tolbutamide, estrogen, steroids, alkylating agents
  • Damaging platelets directly
  • Provoking formation of platelet antibodies- Material ingestion of quinine, quinidine, hydralazine, antibiotics
• Maternal infection with Toxoplasma, CMV, Rubella, Herpes virus, Hepatitis, Varicella etc
• Infants born to women with chronic ITP, Pre eclampsia, SLE and other autoimmune diseases

Obstetrics

(Individual diseases during pregnancy are discussed under those diseases itself)

Hematology related physiological changes during pregnancy

• Dilutional anemia is seen, as plasma volume increases to approximately 50% greater than pre-pregnancy value, but RBC mass increases by 20-30%.
• Platelet count decreases to 1.2 to 1.5lac/cmm
• EPO levels are high (150% of pre-pregnancy levels)
• CRP increases
• ESR increases
• 1gm of iron is required during normal pregnancy
  • 300mg- For fetus and placenta
  • 500mg- For maternal RBC mass expansion
  • 200mg- Lost by excretion
• Folate requirement doubles during pregancy (400microgram to 800microgram per day)
• B-12 deficiency is rare during pregnancy, as B-12 deficiency leads to infertility
• Von Willebrand factor levels rise in 3^rd trimester of pregnancy
• Levels of Vitamin K dependent factors, factor VIII and fibrinogen are increased

Anemia during pregnancy

• Defining anemia in pregnancy- Hemoglobin levels <11gm/dL in first and second trimester and less than 10.5 gm/dL in third trimester 
• Hemoglobin should be measured at booking and at 28 weeks of gestation
• Anemia is seen in 50% of pregnant woman
• May be associated with significant fetal and maternal complications
• Iron deficiency and folic acid deficiency are the most common causes
• S. Ferritin must be measured in women with known hemoglobinopathy to identify concomitant iron deficiency and exclude iron overload.

Thrombocytopenia during pregnancy

• Seen in 10% of pregnancies
• Platelet count of <1lac/cmm, is considered as thrombocytopenia in pregnancy
• Target platelet counts
  • Neuraxialanaesthesia- >80,000/cmm
  • Delivery (Vaginal/LSCS)- >50,000/cmm
• Common causes include
  • Gestational thrombocytopenia
  • Megaloblastic anemia
  • Immune thrombocytopenic purpura
  • APLA and SLE
  • Eclampsia/ HELLP syndrome
  • Acute fatty liver of pregnancy
  • Thrombotic thrombocytopenic purpura
  • Disseminated intravascular coagulation
  • Drug induced thrombocytopenia
  • Type IIb von Willebrand disease
  • Splenic sequestration
  • Marrow infiltration and marrow failure
• Evaluation must include
  • Peripheral smear examination
  • Reticulocyte count
  • DCT
  • Coagulation profile
  • VWD testing
  • Liver function tests
  • APLA work up
  • ANA profile
  • Thyroid function test
  • Viral screening- HIV, HBV, HCV, and CMV
• For details of each of disorders refer to respective sections in platelet disorders, Microangiopathic hemolytic anemia etc.

Recent advances:

Rivaroxaban vs placebo for extended antithrombotic prophylaxis after laparoscopic surgery for colorectal cancer 

PROphylaxis of venous thromboembolism after LAParoscopic Surgery for colorectal cancer Study II (PROLAPS II) was a randomized, double-blind, placebo-controlled, investigator-initiated, superiority study aimed at assessing the efficacy and safety of extended prophylaxis with rivaroxaban after laparoscopic surgery for colorectal cancer. All patients received antithrombotic prophylaxis with low-molecular-weight heparin from surgery to randomization. VTE occurred in 11 of 282 patients in the placebo group compared with 3 of 287 in the rivaroxaban group. Major bleeding occurred in none of the patients in the placebo group and 2 patients in the rivaroxaban group.

https://doi.org/10.1182/blood.2022015796

Aspirin or Low-Molecular-Weight Heparin for Thromboprophylaxis after a Fracture

This trial enrolled patients 18 years of age or older who had a fracture of an extremity. Patients were randomly assigned to receive low-molecular-weight heparin (enoxaparin) at a dose of 30 mg twice daily or aspirin at a dose of 81 mg twice daily while they were in the hospital. A total of 12,211 patients were randomly assigned to receive aspirin (6101 patients) or low-molecular-weight heparin (6110 patients). Thromboprophylaxis with aspirin was noninferior to low-molecular-weight heparin in preventing death and was associated with low incidences of deep-vein thrombosis and pulmonary embolism and low 90-day mortality. 

https://doi.org/10.1056/NEJMoa2205973