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Understanding disseminated
intravascular coagulation
Author Robyn Backhouse, BSc, DipHE, RGN, is staff may result in pulmonary embolism, thrombophlebitis,
nurse, cardiac intensive care unit, Leeds General cerebrovascular accident and renal failure. Thrombosis
Infirmary. formation can continue until the causative factor is cor
Abstract Backhouse, R. (2004) Understanding dis- rected or removed. If it is not corrected, clotting continues
seminated intravascular coagulation. Nursing Times; throughout the body, leading to multi-organ ischaemia,
100: 36, 3839. infarction and eventual failure.
Disseminated intravascular coagulation is associated Red blood cells become damaged trying to pass
with a high mortality rate, with patient outcomes through blocked capillary beds, causing excess haemoly
largely dependent upon swift recognition and appropri- sis. The continued clot formation uses up the bodys sup
References ate management of events. This article provides a basic ply of platelets, fibrinogen and other clotting factors,
Adam, S.K., Osborne, S. (1997) Critical overview of the condition, and its pathophysiology, upsetting the balance between coagulation of circulating
Care Nursing Science and Practice. diagnosis, treatment and nursing management, so that blood and prevention of haemorrhage.
Oxford: Oxford Medical Publications. effective intervention may be implemented, maximis- An intense lysis (breakdown) of clots is also caused by
ing the chances of patient recovery. the accelerated thrombosis formation through activation
Baird, M.S. (1997) Disseminated of plasminogen that converts to plasmin then destroys
Intravascular Coagulation. In: Hicks
Disseminated intravascular coagulation (DIC) is a haema the clot. This leads to the production of fibrin degradation
Keen, J., Swearingen, P.L. (eds) Mosbys
tological disorder characterised by inappropriate, accel products, which are powerful anticoagulants.
Critical Care Nursing Consultant.
London: Mosby. erated, systemic activation of the clotting cascade, Depletion of clotting products along with the release of
simultaneously causing thrombosis and haemor these anticoagulants leads to the uncontrolled haemor
Furlong, M.A., Furlong, B.R. (2001) rhage (Levi, 2004). The condition is associated with a rhage (Levi, 2004) (Fig 1).
Disseminated Intravascular high rate of morbidity and mortality, but as it is always DIC is diagnosed primarily on clinical signs and patient
Coagulation. Available at: www. secondary to a primary disorder, which may itself be history, with confirmation provided by laboratory findings
emedicine.com/emerg/ associated with a high mortality and morbidity rate, the (Table 1, p40). No single test will confirm DIC (Levi,
topic150.htm exact figures are difficult to gauge (Levi, 2004). 2004;), but Table 1 includes a guide to the expected
The condition is often seen in intensive care units in its values one might expect to see.
acute form as a complication of septic shock and shock
states, as well as septicaemia, transfusion reactions and Medical management
obstetric complications (Levi, 2004; Spence, 2003). The primary aims of medical management in DIC are to
The two primary problems caused by DIC are: (Levi, 2004):
Decreased tissue perfusion due to thrombi, anaemia Treat the underlying cause;
and hypotension leading to organ ischaemia and necro Provide supportive management of complications;
sis (Adam and Osborne, 1997); Support organ function;
Haemorrhage, both externally and internally into all Stop abnormal coagulation and control bleeding.
body cavities, due to accelerated and inappropriate con Hypotension, hypoxaemia, and acidosis must be cor
sumption of clotting factors (Thelan et al, 1998). rected, and infection must be prevented and aggressively
these procedures must be performed gently to avoid Renal support such as filtration or dialysis may be
further trauma and haemorrhage. required if urine output drops and remains less than 0.5
Suctioning should be carried out with great care and at ml/kg/hour in an adult despite other interventions (Adam
the lowest possible pressure research has shown an and Osborne, 1997).
optimum range of 80150mmHg (Griggs, 1998) to avoid Regular testing for protein and blood in the urine is
further haemorrhage. To avoid hypoxia, suction should important. The kidneys are common sites for micro
last no longer than 1015 seconds (Griggs, 1998). emboli so urea, creatinine and electrolyte levels should
also be monitored. Acute renal failure is common due to
Monitoring renal function acute tubular necrosis (Adam and Osborne, 1997).
Fluid intake and output must be recorded accurately at Daily weights are often useful as an indicator of fluid
least every 24 hours, increasing to every 3060 minutes overload, although other signs such as generalised
if the patient is actively bleeding (Swearingen and Keen, oedema, periorbital and facial oedema, excessive frothy
2001). Oliguria resulting from hypoperfusion of the kid- saliva, rapid dyspnoea, moist rales and cough, or rapid
neys may occur due to hypovolaemia. It is therefore pulse (Hudak et al, 1998) may be more practical in inten
essential to maintain an adequate blood pressure. sive care units.