Overview and Clinical Importance
Cytology and coagulation testing are fundamental diagnostic tools in veterinary medicine that provide rapid, cost-effective information for clinical decision-making. Cytology allows practitioners to differentiate inflammatory from neoplastic processes, guide treatment decisions, and stage tumors without invasive surgical biopsies. Coagulation testing is essential for diagnosing bleeding disorders, monitoring anticoagulant therapy, and assessing patients with suspected disseminated intravascular coagulation (DIC).
For the BCSE examination, this topic integrates knowledge from pathology, medicine, and diagnostics domains. Questions typically focus on proper sample collection techniques, interpretation of cytologic findings to differentiate inflammation from neoplasia, body fluid classification, and the diagnosis and monitoring of coagulation disorders including DIC.
High-YieldCytology and coagulation questions on the BCSE emphasize CLINICAL APPLICATION. Expect questions that provide clinical scenarios requiring you to select appropriate collection techniques, interpret findings, or diagnose conditions based on laboratory results.
| Feature |
FNA with Aspiration (FNAC) |
FNA without Aspiration (FNNAC) |
| Technique |
Needle attached to syringe; negative pressure applied during sampling |
Needle alone (no syringe); cells collected by capillary action and cutting motion |
| Equipment |
21-23G needle, 2-5 mL syringe |
21-25G needle only |
| Cellularity |
Generally higher cell yield |
May have lower cellularity |
| Blood contamination |
Higher risk of hemodilution |
Less blood contamination |
| Best for |
Lymph nodes, solid masses, firm tissues |
Highly vascular organs (liver, spleen, thyroid), fragile tissues |
| Cell preservation |
Good if technique is correct |
Often better preservation with less rupture |
| Technique |
Best Applications |
Key Considerations |
| Impression Smear |
Ulcerated lesions, cut surfaces of tissues, ear cytology |
Remove surface debris/blood first; blot gently; multiple impressions from different areas |
| Scraping |
Skin lesions, keratinized tissues |
Use scalpel blade held perpendicular; scrape until capillary bleeding |
| Swab Collection |
Ear canal, vaginal, nasal, fistulous tracts |
Roll (do not smear) swab across slide to preserve cells |
| Fluid Collection |
Body cavity effusions, joint fluid, CSF |
Collect into EDTA tube; make direct smears and concentrate by centrifugation |
| Lavage/Wash |
Tracheal wash, bronchoalveolar lavage, bladder wash |
Use sterile saline; rapid processing important for cell preservation |
| Type |
Predominant Cells |
Common Causes |
| Purulent/Suppurative |
Neutrophils greater than 85%; may be degenerate if septic; intracellular bacteria may be present |
Bacterial infection, foreign body, abscess, septic peritonitis |
| Pyogranulomatous |
Mixed population of neutrophils and macrophages; may see epithelioid macrophages |
Fungal infection, mycobacteria, foreign body reaction, FIP in cats |
| Granulomatous |
Macrophages predominate (greater than 70%); may form giant cells; few neutrophils |
Chronic fungal infection, mycobacteria, lipid-laden inflammation |
| Eosinophilic |
Eosinophils greater than 10-20%; often mixed with other inflammatory cells |
Parasites, allergic/hypersensitivity, eosinophilic granuloma complex, mast cell tumor |
| Lymphocytic/Plasmacytic |
Small lymphocytes and plasma cells predominate |
Chronic antigenic stimulation, immune-mediated disease, some viral infections |
| Category |
Feature |
Description |
| Nuclear Criteria |
Anisokaryosis |
Variation in nuclear size; significant if greater than 2:1 ratio between cells |
| Nuclear Criteria |
Increased N:C ratio |
Nucleus occupies greater proportion of cell than normal |
| Nuclear Criteria |
Multinucleation |
Multiple nuclei, especially if different sizes |
| Nuclear Criteria |
Prominent/multiple nucleoli |
Large, angular, or variably-sized nucleoli |
| Nuclear Criteria |
Abnormal mitotic figures |
Asymmetric, multipolar, or lagging chromosomes |
| Nuclear Criteria |
Coarse chromatin |
Irregular, clumped chromatin pattern |
| Nuclear Criteria |
Nuclear molding |
Nuclei conform to shape of adjacent nuclei |
| Cytoplasmic |
Anisocytosis |
Variation in cell size |
| Cytoplasmic |
Cytoplasmic basophilia |
Increased blue staining due to high RNA content |
| General |
High cellularity |
Cells exfoliate readily in sheets or clusters |
| General |
Cellular pleomorphism |
Variable cell morphology within population |
| Feature |
Reactive Hyperplasia |
Lymphoma |
| Cell population |
Heterogeneous; mixed small, medium, and large lymphocytes |
Monomorphic; greater than 50% intermediate to large cells in high-grade lymphoma |
| Small lymphocytes |
Predominate (greater than 50-70%) |
Minority (less than 50%) or absent |
| Plasma cells |
Often increased |
Usually absent or rare |
| Mitotic figures |
Rare to occasional |
Often frequent (greater than 3 per 5 high-power fields) |
| Criteria of malignancy |
Absent |
Variable; may see anisokaryosis, multiple nucleoli |
| Tingible body macrophages |
May be present |
Often increased (starry sky pattern) |
Part 1: Cytology
Collection Techniques
Proper sample collection is the foundation of diagnostic cytology. The goal is to obtain adequate cellularity with good cell preservation in a monolayer format suitable for microscopic evaluation. Multiple techniques exist, and selection depends on the tissue type, lesion characteristics, and clinical situation.
Fine Needle Aspiration (FNA)
Fine needle aspiration is the most commonly used technique for sampling masses and lymph nodes. It involves inserting a fine gauge needle (typically 21-25 gauge) into the lesion and collecting cells either with or without applying negative pressure via an attached syringe.
Comparison of FNA Techniques
High-YieldFor lymph nodes specifically, FNAC (with aspiration) produces more diagnostic samples with higher cellularity compared to non-aspiration techniques. For highly vascular organs like the spleen, non-aspiration may reduce hemodilution.
MEMORY AID - FNA Technique Steps
"RAPID" - Restrain patient, Aim needle into lesion, Perform 3-4 rapid passes in multiple planes, Immediately expel onto slide, Dry and stain for examination
Proper FNA Technique Steps
1. Stabilize the mass between fingers or use ultrasound guidance
2. Insert needle into lesion perpendicular to skin
3. Redirect needle 3-4 times in short, rapid strokes using a multi-plane cutting motion
4. If using aspiration, apply negative pressure ONLY while needle is in tissue; release before withdrawal
5. Withdraw needle and expel contents onto glass slide
6. Prepare at least 4-5 slides from each lesion; examine 1-2 stained slides to confirm adequate cellularity before submission
Other Collection Techniques
Smear Preparation Techniques
The squash prep (also called compression smear) is ideal for most FNA samples. Place a small drop of material near one end of a clean glass slide, then place a second slide perpendicular on top. Allow the material to spread by capillary action, then gently pull the slides apart horizontally. This creates a monolayer of cells with minimal rupture.
High-YieldNever use excessive pressure when making smears - this ruptures cells and creates thick, unreadable preparations. The weight of the spreader slide alone should provide sufficient pressure.
Inflammatory vs. Neoplastic Cytology
One of the most critical skills in cytology is differentiating inflammatory processes from neoplasia. This distinction directly impacts treatment decisions and prognosis.
Characteristics of Inflammation
MEMORY AID - Degenerate vs Non-Degenerate Neutrophils
"SEPTIC makes neutrophils SICK" - Swollen (karyolysis), Indistinct nuclear margins, Cytoplasm pale/vacuolated, Karyorrhexis (nuclear fragmentation). Non-degenerate neutrophils retain segmented nuclei with distinct margins - indicates sterile inflammation.
High-YieldDegenerate neutrophils with intracellular bacteria indicate SEPTIC inflammation. However, absence of visible bacteria does not rule out infection - some bacteria are difficult to see on cytology.
Criteria of Malignancy
Neoplastic cells display cytologic criteria of malignancy that reflect their uncontrolled growth and genetic instability. These criteria are divided into nuclear, cytoplasmic, and general features. The more criteria present, the higher the confidence in a malignancy diagnosis.
Cytologic Criteria of Malignancy
MEMORY AID - Criteria of Malignancy
"MALIGNANT Has Big Problems" - Multinucleation, Anisokaryosis/Anisocytosis, Large nucleoli, Increased N:C ratio, Giant cells, Nuclear molding, Abnormal mitoses, N chromatin coarse, Tremendous pleomorphism, Hypercellularity, Basophilic cytoplasm, Prominent nucleoli
High-YieldA SINGLE criterion of malignancy is NOT diagnostic. Look for THREE OR MORE criteria before diagnosing malignancy. Some benign conditions (reactive mesothelial cells, activated macrophages) can show mild atypia.
Lymph Node and Mass Cytology
Normal Lymph Node Cytology
Normal lymph nodes contain a heterogeneous population of lymphoid cells. Small, mature lymphocytes predominate (75-90%), with smaller numbers of medium and large lymphocytes, plasma cells, and occasional macrophages. The background contains lymphoglandular bodies (small, light blue cytoplasmic fragments).
Reactive Hyperplasia vs. Lymphoma
High-YieldThe "50% rule" for lymphoma: High-grade lymphoma is diagnosed when greater than 50% of cells are intermediate to large lymphocytes. Low-grade/small cell lymphoma is challenging to diagnose cytologically and may require flow cytometry or PARR testing.
MEMORY AID - Lymphoma Diagnosis
"LARGEly Monotonous" - Large cells, Anisokaryosis, Round nuclei with multiple nucleoli, Greater than 50% intermediate/large cells, Elevated mitotic rate, Monotonous (monomorphic) population
Metastatic Disease in Lymph Nodes
Metastatic neoplasia appears as a foreign cell population within the lymph node that differs from normal lymphoid cells. The background lymphoid population may be normal or reactive.
High-YieldMast cell tumor metastasis to lymph nodes can be challenging to diagnose because normal lymph nodes contain resident mast cells. Look for CLUSTERS of mast cells or mast cells with criteria of malignancy (poor granulation, multinucleation).
Body Fluid Cytology
Body cavity effusions (pleural, peritoneal, pericardial) provide valuable diagnostic information when analyzed systematically. Classification is based on total protein concentration and nucleated cell count, which reflects the underlying pathophysiology.
Effusion Classification
MEMORY AID - Effusion Classification
"LOW protein, LOW cells = pure Transudate (decreased oncotic pressure)" and "HIGH protein, HIGH cells = Exudate (inflammation/infection)" - Modified transudate falls in between!
High-YieldTraditional veterinary classification based solely on protein and cell count has significant limitations (only 55-75% accuracy). For difficult cases, measuring effusion lactate dehydrogenase (LDH) provides better discrimination (greater than 94% accuracy).
Special Effusion Types
MEMORY AID - Chyle vs Pseudochyle
"CHYLE = True TRIGLYCERIDES elevated" - Chyle: TG effusion greater than serum, Chol effusion less than serum. Pseudochyle: TG normal/low, Chol elevated (chronic effusions with cell breakdown)
| Tumor Type |
Cytologic Features in Lymph Node Metastasis |
| Carcinoma |
Clusters/sheets of epithelial cells with cell-to-cell adherence; criteria of malignancy present; may see secretory vacuoles |
| Mast Cell Tumor |
Round cells with purple cytoplasmic granules; granules may be sparse in poorly differentiated tumors; eosinophils often present |
| Melanoma |
Round to spindle cells; may contain brown-black melanin pigment (not all melanomas pigmented); marked anisocytosis |
| Sarcoma |
Spindle cells that exfoliate poorly; may see wispy cytoplasmic tails; difficult to diagnose on cytology |
| Histiocytic Sarcoma |
Large round cells with abundant blue cytoplasm; may be phagocytic; marked pleomorphism |
| Type |
Protein (g/dL) |
TNCC (cells/uL) |
Common Causes |
| Pure Transudate |
Less than 2.5 |
Less than 1,000-1,500 |
Hypoalbuminemia (PLE, PLN, liver failure), early right heart failure |
| Modified Transudate |
2.5-5.0 |
1,000-7,000 |
Right heart failure, portal hypertension, neoplasia, liver disease, chronic inflammation |
| Exudate |
Greater than 3.0 |
Greater than 5,000-7,000 |
Septic peritonitis/pyothorax, FIP, neoplasia, hemorrhage, chyle, uroabdomen, bile peritonitis |
| Type |
Diagnostic Features |
Causes |
| Septic Effusion |
Degenerate neutrophils with intracellular bacteria; glucose less than 50 mg/dL; effusion glucose less than blood glucose by greater than 20 mg/dL |
GI perforation, bite wounds, post-surgical, hematogenous spread |
| Chylous Effusion |
Milky/opaque appearance; triglycerides greater than serum; cholesterol less than serum; predominantly small lymphocytes and lipid-laden macrophages |
Thoracic duct rupture/obstruction, neoplasia (lymphoma, thymoma), heart failure, idiopathic |
| Hemorrhagic |
PCV similar to peripheral blood (greater than 10%); erythrophagia and hemosiderin if chronic; no platelets if true hemorrhage |
Trauma, coagulopathy, splenic/hepatic neoplasia rupture, anticoagulant rodenticide |
| Uroabdomen |
Creatinine and potassium greater than serum (effusion:serum ratio greater than 2:1 for creatinine) |
Bladder rupture, ureteral avulsion, urethral tear |
| Bile Peritonitis |
Green-tinged fluid; bilirubin greater than serum (effusion:serum ratio greater than 2:1); bile pigment in macrophages |
Gallbladder rupture, bile duct injury, necrotizing cholecystitis |
| FIP Effusion (cats) |
Yellow, viscous, high protein (greater than 3.5 g/dL); pyogranulomatous; protein:globulin ratio less than 0.8 |
Feline infectious peritonitis (coronavirus mutation) |
| Pathway |
Factors Involved |
Clinical Significance |
| Extrinsic Pathway |
Tissue Factor (TF), Factor VII |
Initiates coagulation in vivo; measured by PT/INR; sensitive to vitamin K deficiency and warfarin |
| Intrinsic Pathway |
Factors XII, XI, IX, VIII |
Amplification pathway; measured by PTT/aPTT; sensitive to heparin and factor deficiencies (hemophilia) |
| Common Pathway |
Factors X, V, II (prothrombin), I (fibrinogen) |
Final common steps; defects prolong both PT and PTT; Factor XIII cross-links fibrin |
| Test |
Pathway Assessed |
Normal Range (Dog) |
Causes of Prolongation |
| PT |
Extrinsic + Common (VII, X, V, II, I) |
6-10 seconds |
Vitamin K deficiency/antagonism, liver disease, DIC, factor VII deficiency |
| PTT/aPTT |
Intrinsic + Common (XII, XI, IX, VIII, X, V, II, I) |
10-20 seconds |
Heparin, hemophilia A (VIII) or B (IX), von Willebrand disease (severe), DIC, lupus anticoagulant |
| ACT |
Intrinsic + Common (similar to PTT but less sensitive) |
60-110 seconds (dog) |
Severe factor deficiencies, severe thrombocytopenia, heparin therapy, DIC |
| Thrombin Time |
Fibrinogen to fibrin conversion |
Variable by lab |
Hypofibrinogenemia, dysfibrinogenemia, heparin, FDPs |
Part 2: Coagulation
The Coagulation Cascade
The coagulation cascade is a series of enzymatic reactions that ultimately converts soluble fibrinogen into insoluble fibrin, forming a stable blood clot. Understanding the cascade is essential for interpreting coagulation tests and diagnosing bleeding disorders.
Pathways of Coagulation
While the cascade is traditionally divided into intrinsic and extrinsic pathways, in vivo coagulation is primarily initiated by tissue factor (extrinsic pathway). The intrinsic pathway amplifies thrombin generation. Both pathways converge at the common pathway with activation of Factor X.
MEMORY AID - Coagulation Factor Numbers
"1972 and 8 to 12" - Extrinsic: Factor 7 (plus TF). Intrinsic: 12, 11, 9, 8 (descending pairs). Common: 10, 5, 2, 1 (descending). Remember: Higher numbers activate lower numbers!
MEMORY AID - PT vs PTT
"PeT = exTrinsic (factors 7, TF)" and "PTT = inTrinsic (factors 12, 11, 9, 8)". Both measure common pathway (10, 5, 2, 1). "PT is shorter test time, PTT is longer"
Vitamin K-Dependent Factors
Factors II, VII, IX, and X require vitamin K for their synthesis in the liver. Vitamin K deficiency (dietary, malabsorption, anticoagulant rodenticide toxicity) or antagonism (warfarin) leads to deficiency of these factors.
MEMORY AID - Vitamin K-Dependent Factors
"1972" or "2, 7, 9, 10" - Also remember Protein C and Protein S (natural anticoagulants) are vitamin K-dependent!
High-YieldAnticoagulant rodenticides inhibit vitamin K epoxide reductase, preventing recycling of vitamin K. Factor VII has the shortest half-life (6 hours in dogs), so PT prolongs FIRST, followed by PTT 24-48 hours later.
PT/PTT/ACT Interpretation
Coagulation Test Overview
Pattern Interpretation
MEMORY AID - PT First, PTT Later
In anticoagulant rodenticide toxicosis: "Factor 7 has 7-hour half-life" (actually about 6 hours in dogs). PT prolongation occurs within 24-36 hours. PTT prolongation follows 48-72 hours post-ingestion when factors IX and X become depleted.
High-YieldA shortened PT or PTT may indicate a HYPERCOAGULABLE state. In one study, dogs with shortened PT or PTT had significantly more thrombosis, higher suspicion of pulmonary thromboembolism, and elevated D-dimers compared to dogs with normal values.
D-Dimers and Fibrinogen
D-Dimers
D-dimers are fibrin degradation products formed when cross-linked fibrin is broken down by plasmin. Their presence indicates that both coagulation AND fibrinolysis have occurred, making them a marker of thrombotic activity.
High-YieldD-dimers are MORE SENSITIVE than fibrin degradation products (FDPs) for detecting DIC and thromboembolic disease. FDPs may be negative even when D-dimers are elevated.
Fibrinogen
Fibrinogen (Factor I) is the substrate for fibrin clot formation and an acute phase protein. Its concentration provides information about both coagulation status and inflammation.
MEMORY AID - Fibrinogen in DIC
"DIC has a BIPHASIC pattern" - Early DIC: fibrinogen may be NORMAL or INCREASED (acute phase response exceeds consumption). Late DIC: fibrinogen DECREASED (consumption exceeds production). Track trends over time!
Disseminated Intravascular Coagulation (DIC)
DIC is a complex syndrome characterized by systemic activation of coagulation leading to widespread microvascular thrombosis, followed by consumption of clotting factors and platelets resulting in bleeding. It is always SECONDARY to an underlying disease process.
Underlying Causes of DIC
DIC can occur secondary to numerous conditions that trigger systemic coagulation activation:
DIC Diagnostic Criteria
There is no single gold-standard diagnostic test for DIC. Diagnosis is based on the presence of an underlying disease that predisposes to DIC combined with multiple abnormal hemostatic parameters.
High-YieldDIC DIAGNOSIS requires: (1) Underlying disease known to cause DIC, PLUS (2) THREE OR MORE abnormal hemostatic parameters. A validated canine DIC scoring system using PT, aPTT, D-dimer, and fibrinogen has 83-91% sensitivity and 77-90% specificity.
MEMORY AID - DIC Diagnosis Criteria
"3 Strikes Rule" - Need 3 or more abnormalities from: Thrombocytopenia, Prolonged PT, Prolonged PTT, Elevated D-dimers, Decreased fibrinogen, Decreased antithrombin. PLUS an underlying predisposing disease!
DIC Phases
MEMORY AID - DIC Phases Clinical Signs
"CLOT then BLEED" - Early hypercoagulable phase: Catheter thrombosis, Livedo reticularis, Organ dysfunction (acute kidney injury, respiratory distress), Thromboembolism. Late consumptive phase: Bleeding from ALL sites, oozing from venipuncture, petechiae.
Cytology Key Points
- FNA with aspiration generally provides higher cellularity for lymph nodes; non-aspiration technique is preferred for highly vascular organs to reduce hemodilution
- Proper smear preparation (gentle squash prep) is critical for maintaining cell morphology and creating readable monolayers
- Three or more criteria of malignancy must be present to diagnose neoplasia; single criteria may be seen in reactive/inflammatory conditions
- Degenerate neutrophils with intracellular bacteria indicate septic inflammation; non-degenerate neutrophils suggest sterile inflammation
- High-grade lymphoma shows greater than 50% intermediate to large lymphoid cells with monomorphic appearance; reactive hyperplasia shows heterogeneous population with small lymphocytes predominating
- Body fluid classification (transudate/modified transudate/exudate) guides differential diagnosis; special fluid types (chyle, septic, hemorrhagic) require specific testing
Coagulation Key Points
- PT measures extrinsic pathway (Factor VII + common pathway); PTT measures intrinsic pathway (Factors XII, XI, IX, VIII + common pathway)
- Vitamin K-dependent factors (II, VII, IX, X) are affected by rodenticide toxicosis; Factor VII has shortest half-life, so PT prolongs FIRST
- D-dimers indicate active thrombosis AND fibrinolysis; elevated D-dimers support DIC diagnosis and screen for thromboembolism
- Fibrinogen may be increased (acute phase response, early DIC) or decreased (consumptive DIC, liver disease); track trends over time
- DIC diagnosis requires: underlying predisposing disease PLUS three or more abnormal hemostatic parameters (prolonged PT, prolonged aPTT, thrombocytopenia, elevated D-dimers, decreased fibrinogen, decreased antithrombin)
- DIC has biphasic presentation: early hypercoagulable phase (may have shortened PT/PTT) followed by late hypocoagulable/consumptive phase (prolonged times, bleeding)
| PT |
PTT |
Differential Diagnoses |
| Prolonged |
Normal |
Early vitamin K deficiency/antagonism (factor VII affected first due to short half-life), early liver disease, isolated factor VII deficiency (rare) |
| Normal |
Prolonged |
Hemophilia A (factor VIII deficiency), Hemophilia B (factor IX deficiency), von Willebrand disease (severe), factor XI or XII deficiency, heparin therapy, lupus anticoagulant |
| Prolonged |
Prolonged |
Common pathway defect (X, V, II, I), severe vitamin K deficiency/antagonism, severe liver disease, DIC, warfarin overdose, massive transfusion dilution |
| Shortened |
Normal/Shortened |
May indicate hypercoagulable state; associated with increased thrombosis risk; often seen in early DIC (hypercoagulable phase) |
| Application |
Clinical Significance |
| DIC Diagnosis |
Elevated D-dimers support DIC diagnosis; sensitivity 85%, specificity 77-97% depending on cutoff; part of DIC scoring systems |
| Thromboembolism |
In dogs: D-dimer greater than 500 ng/mL has 100% sensitivity, 70% specificity for PTE. At greater than 1000 ng/mL: 80% sensitivity, 94% specificity |
| Rule-out Test |
Normal D-dimers have high negative predictive value - help rule OUT thrombotic disease when clinical suspicion is present |
| Cats (ATE) |
Less reliable in cats; only 50% of cats with arterial thromboembolism have elevated D-dimers |
| Fibrinogen Level |
Interpretation |
| Increased |
Acute phase response (inflammation, infection, neoplasia); pregnancy; postoperative period; hypercoagulable states; early DIC (before consumption) |
| Decreased |
DIC (consumptive coagulopathy); severe liver disease (decreased production); massive hemorrhage; hyperfibrinolysis; rare hereditary deficiency |
| Normal Range |
Dogs: 100-300 mg/dL; Cats: 50-300 mg/dL (varies by method and laboratory) |
| Category |
Examples |
| Sepsis/Infection |
Bacterial sepsis, pyometra, septic peritonitis, parvovirus, leptospirosis, cytauxzoonosis (cats), severe pneumonia |
| Neoplasia |
Hemangiosarcoma, mammary carcinoma, lymphoma, hepatocellular carcinoma, disseminated histiocytic sarcoma |
| Trauma/Surgery |
Major trauma, extensive surgery, burns, heat stroke |
| IMHA |
Immune-mediated hemolytic anemia (high thrombotic risk) |
| Pancreatitis |
Severe acute pancreatitis releases tissue factor |
| Other |
Snake envenomation, SIRS, anaphylaxis, liver disease, GDV, obstetric complications |
| Parameter |
Expected Finding in DIC |
Points (Scoring) |
| Platelet Count |
Decreased (thrombocytopenia less than 150,000/uL) |
+1 |
| PT |
Prolonged (greater than 25% above upper reference limit) |
+1 |
| PTT/aPTT |
Prolonged (greater than 25% above upper reference limit) |
+1 |
| Fibrinogen |
Decreased (less than 100-150 mg/dL) OR variable (may be increased early) |
+1 if low |
| D-dimers |
Elevated (indicates fibrinolysis) |
+1 |
| Antithrombin (AT) |
Decreased (consumed by excess thrombin) |
+1 if low |
| Schistocytes |
Present on blood smear (RBC fragmentation from microthrombi) |
Supportive |
| Phase |
Characteristics |
Laboratory Findings |
| Hypercoagulable (Early) |
Excessive thrombin generation; microvascular thrombosis; organ dysfunction; may see thrombosis of IV catheters |
PT/PTT may be SHORTENED or normal; platelets mildly decreased; fibrinogen normal/elevated; D-dimers elevated; hypercoagulable on TEG |
| Hypocoagulable (Late) |
Consumption of factors and platelets; secondary fibrinolysis; clinical bleeding (petechiae, ecchymoses, hemorrhage from venipuncture sites) |
PT and PTT prolonged; severe thrombocytopenia; hypofibrinogenemia; D-dimers markedly elevated; hypocoagulable on TEG |