Disseminated Intravascular Coagulation: The Evidence Behind the Pathway

It is late evening in the medical ICU. A 61-year-old man with diabetes was admitted this morning from Karkala with a perinephric abscess and septic shock. The drain is in and the antibiotics are running. The evening bloods are back: platelets 62, prothrombin time 4 seconds above control, INR 1.5, fibrinogen 1.4 g/L, D-dimer five times the upper limit of normal. The cannula site in his hand has started to ooze. The resident asks: is this DIC, and should we give plasma? This is an illustrative case, not a real patient.

The DIC Pathway scores the coagulation, sets the phenotype and works out the blood components and the number of units. It keeps every cut-off, every threshold and every dose. What it no longer carries is the explanation of what DIC is and how it happens, and the score tables in one piece. Those have moved here. By the end you will know why the same patient can clot and bleed at once, and what the two scores are telling you about him.

1. What DIC is

Disseminated intravascular coagulation is not a disease. It is an acquired, systemic activation of coagulation, always driven by something else, in which thrombin is generated throughout the circulation, microvascular fibrin is deposited, and platelets and clotting factors are consumed faster than they are made.

“Then why is he bleeding, if he is clotting?” This is the question every resident asks, and it is the right one. The paradox that confuses the bedside is that the same process causes both thrombosis and bleeding: clots block small vessels and cause organ failure, while the consumption that follows leaves the patient unable to stop bleeding from a cannula. Think of a fire brigade sent to a thousand small fires at once. Every engine is out, and when the big fire starts there is nothing left to send.

The 2025 ISTH definition names three strands together: coagulation activation, dysregulated fibrinolysis and endothelial injury. The 2025 update also restates DIC as an acquired, life-threatening intravascular disorder with systemic coagulation activation, dysregulated fibrinolysis and endothelial injury, and separates the haemorrhagic from the thrombotic phenotype. Our patient, with sepsis, is the thrombotic kind: microthrombi and organ failure dominate, and bleeding is less common.

2. How it happens

The mechanism comes in four steps. Each one explains a number on the report.

1. Tissue factor, exposed by injured endothelium, activated monocytes or tumour, triggers the extrinsic pathway and generates thrombin.
2. Thrombin cleaves fibrinogen to fibrin, which is laid down in the microvasculature, and activates platelets, so both are consumed.
3. The natural anticoagulants, antithrombin and protein C, are overwhelmed and depleted, and in sepsis fibrinolysis is switched off by a surge of plasminogen activator inhibitor, so the fibrin is not cleared.
4. The result is simultaneous microvascular thrombosis and a consumptive bleeding tendency: a falling platelet count and fibrinogen, a lengthening prothrombin time, and a rising D-dimer as the fibrin that is formed is eventually broken down.

Read our patient’s report against the last step. The low platelets and the falling fibrinogen are the consumption. The long prothrombin time is the factors being used up. The D-dimer is the fibrin being broken down. In sepsis, the brake on clot breakdown is on, which is why the fibrin stays in the small vessels and the kidneys and lungs suffer.

3. The ISTH overt DIC score, whole

Here is the score as the tool carried it on 4 November 2026. The tool still shows every cell, as two narrower tables. It applies only where an underlying disorder associated with DIC is present, and a total of 5 or more is compatible with overt DIC.

Score our patient. Platelets 62: 1 point. D-dimer five times the upper limit: 2 points. Prothrombin time 4 seconds above control: 1 point. Fibrinogen 1.4 g/L, above 1.0: 0 points. Total 4. That is below 5.

“So it is not DIC?” Not yet, on this score. The common mistake is to read a score below 5 as an all-clear. It is easy to see why: a number below a cut-off looks like a no. But the process evolves, and the tool tells you to repeat the tests every 6 to 12 hours in a patient at risk.

4. The SIC score finds him earlier

In sepsis there is a second score, built to catch the earlier phase. Here it is whole.

Score him again. INR 1.5, above 1.4: 2 points. Platelets 62, below 100: 2 points. His SOFA across the four organs is 2 or more in septic shock: 2 points. Total 6, with a platelet-plus-INR subtotal of 4. SIC is diagnosed at a total of 4 or more, with that subtotal 2 or more, in a patient with sepsis. He has sepsis-induced coagulopathy, though not yet overt DIC.

5. The drug that was withdrawn

“Is there not a drug that switches DIC off?” Many have been tried. Recombinant activated protein C was recommended for severe sepsis with DIC in 2009, then withdrawn worldwide in 2011 when the PROWESS-SHOCK trial found no benefit and a bleeding risk. The lesson has held since. Beyond treating the cause and supporting the patient, no specific anticoagulant has proven itself. The tool says so, and says that recombinant activated protein C is no longer used.

Back to the ICU

Should he have plasma for the ooze? The tool’s rule is to transfuse the patient, not the number: components are for the bleeding patient or one facing a procedure, and plasma for bleeding with a PT or aPTT above 1.5 times the reference. Enter his values and the tool works out whether, and how many units. What he needs most is what he already has: the drain and the antibiotics, because DIC does not resolve while its trigger runs. The resident repeated the panel at six hours. The score was 8: platelets 38, D-dimer nine times the upper limit, prothrombin time 7 seconds above control, fibrinogen 0.9 g/L. He now had overt DIC, and the tool took him to the component rules.

Try this

A woman bleeding after delivery has a fibrinogen of 3 g/L. A colleague says this is normal and reassuring. Is it? Illustrative case.

Answer. No. Fibrinogen rises to 4 to 6 g/L at term, so a fibrinogen of 3 g/L in a bleeding parturient is a warning and not a comfort. The ordinary ISTH score, built on non-pregnant thresholds, misses it; the tool uses the pregnancy-specific score instead, and the fibrinogen target in obstetric haemorrhage is higher, above 2 g/L. For the rest of that story, see Postpartum Haemorrhage: The Evidence Behind the Pathway.

Take-home points

• DIC is never the diagnosis on its own: name and treat what is driving it.
• The same process clots the small vessels and empties the stores, so the patient can thrombose and bleed at once.
• An ISTH score below 5 is not an all-clear; repeat the panel every 6 to 12 hours while the risk lasts.
• In sepsis, the SIC score finds the coagulopathy earlier than the overt DIC score.
• Transfuse for bleeding or a procedure, not for a number.

Declaration: the author built and maintains the tool. It is free to use. The figures in this article are those the tool carried in its Protocols and Evidence tabs on 4 November 2026, each from the source the tool names. The DIC Pathway is still in administrator preview, pending clinical review. The illustrative case was scored by hand from the two tables; check the tool’s result for a real patient.

References

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