Q5 LONG ANSWER 10M ★ High-yield

Define disseminated intravascular coagulation. Describe its causes, pathogenesis, clinical features and laboratory findings.

Pathology · 2nd Professional — Para-Clinical

Definition

Disseminated intravascular coagulation (DIC) is an acquired disorder in which widespread activation of coagulation forms microthrombi throughout the microcirculation, consuming platelets and clotting factors and so producing a bleeding tendency.

Also called a consumption coagulopathy or defibrination syndrome
Always secondary to another disease — it is never a primary diagnosis, and treating it means treating the cause

CLINICAL PEARL

DIC is the paradox of pathology: a clotting disorder that presents with bleeding. Thrombi form everywhere, consuming platelets and factors faster than they can be replaced; the fibrinolysis they provoke then degrades what remains. The patient therefore thromboses and bleeds at the same time.

Causes

Group	Examples
Obstetric — the commonest group in India	Abruptio placentae, amniotic fluid embolism, retained dead fetus, septic abortion, eclampsia, HELLP syndrome
Infection	Gram-negative sepsis (endotoxin), meningococcaemia, falciparum malaria, severe viral infection
Malignancy	Acute promyelocytic leukaemia, mucin-secreting adenocarcinoma of pancreas, stomach and prostate
Massive tissue injury	Trauma, extensive burns, major surgery, heat stroke
Miscellaneous	Snake bite (viper), incompatible blood transfusion, severe liver disease, acute pancreatitis, giant haemangioma

Pathogenesis

Two triggers, alone or together:

→ 1.
Release of tissue factor — from damaged tissue, placenta, tumour or monocytes stimulated by endotoxin → 2.
Widespread endothelial injury — exposing subendothelial collagen → Systemic activation of the coagulation cascade → Fibrin microthrombi throughout the microcirculation → Two consequences follow simultaneously: → ischaemia of tissues, and microangiopathic haemolysis as red cells are sheared → consumption of platelets and clotting factors, with secondary fibrinolysis → bleeding

Clinical Features

From thrombosis	From bleeding
Acute renal failure (cortical necrosis)	Petechiae, purpura and ecchymoses
Respiratory failure	Oozing from venepuncture sites, cannulae and surgical wounds
Confusion, coma, convulsions	Gastrointestinal and genitourinary bleeding
Skin necrosis, digital gangrene	Intracranial haemorrhage
Waterhouse–Friderichsen syndrome	Postpartum haemorrhage

Laboratory Findings

Test	Result	Reason
Platelet count	Low	Consumed in microthrombi
Prothrombin time (PT)	Prolonged	Consumption of factors
Activated partial thromboplastin time (aPTT)	Prolonged	Consumption of factors
Fibrinogen	Low	Consumed and degraded
D-dimer and fibrin degradation products	Raised — the most useful single test	Secondary fibrinolysis of cross-linked fibrin
Peripheral smear	Schistocytes (fragmented red cells), helmet cells	Microangiopathic haemolysis
Antithrombin III	Reduced	Consumed

No single test is diagnostic — the diagnosis rests on the combination, in a patient with an appropriate underlying illness
A falling platelet count and a rising D-dimer in a sick patient is the earliest and most useful pattern

DIC Compared with Other Causes of Bleeding

Feature	DIC	Liver disease	Vitamin K deficiency	Primary fibrinolysis
Platelets	Low	Low (hypersplenism)	Normal	Normal
PT and aPTT	Prolonged	Prolonged	Prolonged	Prolonged
Fibrinogen	Low	Low in late disease	Normal	Low
D-dimer	Raised — the discriminator	Normal or mildly raised	Normal	Normal (no cross-linked fibrin)
Schistocytes	Present	Absent	Absent	Absent
Factor VIII	Reduced — it is consumed	Normal or raised — it is not made in the liver	Normal	Normal

Factor VIII separates DIC from liver disease — it is the one clotting factor not synthesised by hepatocytes, so it is normal in liver failure and low in DIC. A genuinely useful test when both are possible

Applied Aspects

Treat the underlying cause — nothing else works: deliver the uterus in obstetric DIC, give antibiotics and source control in sepsis, and treat the leukaemia
Support with fresh frozen plasma, cryoprecipitate and platelets where there is active bleeding; fibrinogen below 1 g/L needs cryoprecipitate
Heparin is reserved for cases in which thrombosis dominates — digital gangrene, purpura fulminans — and is dangerous where bleeding predominates
Acute promyelocytic leukaemia characteristically presents with DIC, which worsens when chemotherapy lyses the cells; ATRA (all-trans retinoic acid) differentiates the cells rather than lysing them and has transformed the outcome
Snake bite is an important cause in rural India; viper venom activates coagulation directly, and the 20-minute whole blood clotting test is a simple bedside indication for antivenom
Chronic, low-grade DIC in malignancy may present only as migratory thrombophlebitis or non-bacterial thrombotic endocarditis
Purpura fulminans — extensive skin necrosis from dermal vessel thrombosis, seen in meningococcaemia and in severe protein C deficiency
Renal cortical necrosis from obstetric DIC is an important cause of irreversible renal failure in India, and is largely preventable by good obstetric care
Never treat the laboratory result alone — a low platelet count and prolonged times in a patient who is not bleeding and has no thrombosis need the cause addressed, not blood products
Serial measurements matter more than any single value, because the trend distinguishes evolving DIC from a stable abnormality
Tranexamic acid is generally avoided, since inhibiting fibrinolysis in the presence of widespread microthrombi may worsen organ ischaemia
Prognosis depends almost entirely on the underlying cause — obstetric DIC often resolves completely once the uterus is emptied, whereas DIC in established sepsis carries a very high mortality
The mortality of DIC is that of the disease that caused it, which is why it is described as a marker of severity as much as a diagnosis
A normal D-dimer makes significant DIC very unlikely, which gives the test real value in excluding the diagnosis in a bleeding patient

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