What then are the causes of Disseminated Intravascular Coagulopathy? The commonest are bacterial infections
Dr Emmanuel Enabulele
In our last outing on disseminated intravascular coagulation, we dealt with its most acute dramatic form in Obstetrics that was ultimately fatal. Today we will be talking about some of the subtle, insidious or chronic form of this condition. It must be stated that DIC is not a primary disease or lesion on its own but results from assault on the body by just any disease condition that can trigger it.
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Thus even when the primary disease that triggered it has been removed, its progression to fatality may remain unchecked. Secondly, it is a known fact that the presence of DIC increases the possibility of death beyond that usually caused by the primary disease that triggered it.
What then are the causes of DIC? The commonest are bacterial infections. In this arena, the ENDOTOXINS in GRAM NEGATIVE cell walls are the worst culprits. These toxins do not cause the shock in SEPTICAEMIA, a situation where multiplication of bacteria in the blood is very rapid; they also trigger disseminated intravascular coagulation. Gram positive bacteria, viruses, protozoans (single cell organisms….remember amoeba?), and fungal infections are all triggers of DIC.
Severe TRAUMATIC events leading to soft tissue injury and blood vessels disruption, brain injuries, burns and conditions of low body temperature known as HYPOTHERMIA can all trigger DIC. On the other hand extreme body temperatures as a result environmental heat bad enough to cause heat stroke, in this case known as HYPERTHERMIA can trigger DIC. That reminds one of the difficulty we are facing now with the current heat wave and the collapsed power sector. This is definitely not the best of times. Sorry for the digression.
Some cancers apart from the tissue damage they cause in the process of their local and distant spread also produce TUMOUR FACTORS that trigger DIC. In some cases DIC may be the first sign of an undiagnosed underlying cancer. To be added to this list is VASCULO TOXIN from snake bite VENOM. This is usually obvious if the reptile is seen, and may be catastrophic if the victim is unaware that he/she has been bitten by a venomous snake.
All in all, just any disease condition that is capable of causing tissue damage; from severe blood transfusion reaction, liver failure, organ damage as in inflammation of the PANCREASE to organ transplant rejection can all trigger DIC.
The most important symptom of DIC is excessive bleeding or hemorrhage that occurs throughout the body. This can be provoked or unprovoked. The severity may vary from minor skin discoloration under skin to torrential pouring from surgical wounds and major openings or ORIFICES in the body like the mouth, nose, rectum and vagina.
Due to sometimes often ignored clot blockage of major blood vessels of organs known as THROMBOSIS, some subtle signs like shortness of breath known as DYPSNOEA due to lung damage and stroke or brain attack, may not be noticed until they become full blown and terminal events. Kidney or RENAL failure is not uncommon in chronic DIC due to thrombosis of the blood supply to the kidneys.
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In its full blown, severe and irreversible form HYPERVOLAEMIC SHOCK is the hallmark and this is fatal. However there are less severe symptoms in chronic or long standing DIC. In such cases, there may no symptoms at all or just mild bleeding from the gums when a patient brushes his teeth. In that case the need for further investigation becomes urgent. It might just be a warning sign for an underlying malignancy like LUKAEMIA which is the malignancy of the white blood cells.
There is NO GOLD STANDARD for the Diagnosis of DIC in its chronic or less severe form. This is because it is a complex condition in its entire ramification and simply does not happen if there is NO underlying challenge. Notwithstanding; there should be a high index of suspicion whenever there is prolonged PROTHROBIN TIME, which simply is how long it takes for blood to clot. FIBRINOGEN is the protein that is converted to FIBRIN the building block of clots. A low level of fibrinogen in the blood is an indication that consumption is going on.
Fibrin resulting from breakdown of clots by PLASMIN can also be used to diagnose DIC in what is generally referred to as D-dimer test. A high level of this in the blood is highly suggestive of DIC. A full blood count is usually mandatory in all blood abnormalities. The number of red blood cells, white blood cells and their different types together with platelets must be estimated. The hallmark in this test is a drop in the number of platelets in the blood. Under microscopy, commonly it would be observed that the concave shape of the red cells is often distorted.
The treatment of DIC would involve firstly reversing the trigger or the underlying disease. In a situation where bleeding is not massive and blood clots pose a danger to the patient like trying to cause stroke or cerebrovascular disease, anticoagulants like HEPARIN may be used. This must be done under the supervision of an experienced hand or better still a HAEMATOLOGIST.
Blood loss may have to be replaced by freshly donated blood, fresh frozen PLASMA, which is the non-cellular component of blood, is popular but it also has its drawback. Its effect is temporary and could actually worsen the thrombotic phenomenon.This again may necessitate infusion of ANTITHROMBIN! Talk of balancing act in a dilemma.
The truth is that those who survive do so because of the AUTOREGULATORY mechanism of the body. Unfortunately more than 50% of those who have DIC will not make it. The outcome is that bad.
While preparing this piece, I saw an old pal who had this chronic ulcer on the left leg. It had started as an infection of the skin known as cellulitis. He had complained that anytime he bent down, his nose bled; a condition known as EPISTAXIS. My heart skipped a beat and we started running tests and doing all things possible to salvage the situation. The last time we met the bleeding had stopped and the wound was healing well. LUCKY FELLOW.