Understanding disseminated intravascular coagulation. clinical nursing times

DIC develops when the body’s ‘normal’ clotting processes are activated systemically and uncontrollably. Coagulation is either extrinsic (caused by tissue injury, resulting in release of tissue factor, tissue thromboplastin, or other procoagulants), or intrinsic (pathway occurs as a result of blood cell injury or platelet contact with collagen in the damaged vessel endothelium – platelets adhere to the collagen surface, triggering clot formation).

Both lead to coagulation with thrombosis (microthrombi formation) in vessels and major organs, which may result in pulmonary embolism, thrombophlebitis, cerebrovascular accident and renal failure. Thrombosis formation can continue until the causative factor is corrected or removed. If it is not corrected, clotting continues throughout the body, leading to multi-organ ischaemia, infarction and eventual failure.


Hypotension, hypoxaemia, and acidosis must be corrected, and infection must be prevented and aggressively treated. Supportive measures include artificial ventilation, cardiac supportive therapy, volume replacement therapy, and renal and neurological support (Galardy and Grabowsky, 2003). Positive inotropic agents and colloid infusions may be given to support organ function and maintain tissue perfusion (Webb et al, 1999).

Heparin and antifibrinolytic agents may be given to reduce thrombosis by partly inhibiting coagulation activation. However, due to the resultant increased risk of further bleeding and the lack of evidence proving increased survival rates its use remains controversial (Levi, 2004; Schmaier, 2003). Adam and Osborne (1997) reported that in 95 per cent of patients with DIC who took part in their study, there was no indication for heparin use. In those instances where it is used, fresh frozen plasma may first be infused to replace depleted coagulation factors.

The patient should be turned every two hours to prevent pressure ulcers and to minimise blood stasis and pooling, as this may precipitate clotting and thrombus formation (Hudak et al, 1998). Skin should be thoroughly assessed at least two-hourly for pressure areas and any signs of bleeding, such as petechiae (Woods et al, 2000). A Waterlow or other appropriate scale should be used to identify potential problems (Hudak et al, 1998).

To further reduce the risk of skin damage, sticky tapes should be avoided, and electric rather than blade razors should be used (Woods, et al, 2000). Soft swabs and mild saline solution or water should be used for mouth care, as toothbrushes can damage mucous membranes and small capillaries and alcohol-based mouthwash can cause irritation (Swearingen and Keen, 2001).

If injections are necessary, the smallest gauge needle should be used. Injection sites should be rotated, direct pressure applied for 3-5 minutes (Swearingen and Keen, 2001) and a pressure dressing used. The site should be observed regularly for haemorrhage. If bleeding from cannulation sites continues, haemostatic dressings may be applied (Adam and Osborne, 1997).

An accurate fluid balance record is essential due to the risk of a volume deficit related to bleeding or haemorrhage (Swearingen and Keen, 2001). Wound dressings and linen can be weighed for accurate measurement of blood loss (Woods et al, 2000). Blood pressure should be monitored via an arterial line, as this is less traumatic than frequent cuff inflations, which can lead to further tissue trauma and haemorrhage (Woods et al, 2000).

Blood pressure, pulse and respiratory rate should be observed at least every 15 minutes to rapidly identify deterioration, and arterial pressure should be observed and kept above 90mmHg systolic to ensure adequate tissue perfusion (Swearingen and Keen, 2001). Fibrin degradation products have a myocardial depressant action and may therefore lead to exacerbated hypotension disproportionate to blood loss (Murphy, 1999).

Pulmonary artery pressures and central venous pressures should be measured at least hourly as they reflect a patient’s fluid status (Swearingen and Keen, 2001). Hypovolaemia should be rectified promptly to avoid organ damage. Cardiac output, cardiac index, systemic vascular resistance, oxygen delivery and oxygen consumption should be measured every 6-12 hours if a pulmonary artery catheter is in place (Hudak et al, 1998).

Respiratory function requires close continual monitoring as blood loss and pulmonary microemboli may result in reduced oxygenation (Swearingen and Keen, 2001). Pulse oximetry and arterial blood gases should also be monitored regularly, as should respiratory rate, rhythm and effort, the patient’s colour and evidence of cyanosis or shortness of breath (Adam and Osborne, 1997).

Chest physiotherapy may be required to maintain optimal lung function. This may involve regular turning and repositioning, deep breathing and coughing, percussion and vibration, and regular tracheal and oropharangeal suctioning as indicated by assessment (Wood, 1998). All these procedures must be performed gently to avoid further trauma and haemorrhage.

Enteral feeding via a nasogastric or orogastric tube is usually preferred over parenteral feeding as it helps to maintain mucosal integrity, reduces translocation of gut bacteria, increases blood flow to the gut, and reduces the incidence of septic complications (Thelan et al, 1998). Feeding tubes must be inserted with great care to avoid unnecessary trauma and further haemorrhage.

Infection is one of the most common causes of DIC (McCance and Huether, 1998) and is often already present, requiring treatment with appropriate antibiotics. Strict infection control measures and effective handwashing are essential to avoid infection (Thelan et al, 1998). Regular monitoring for infection markers will be necessary, as will extreme care with all invasive equipment and strict aseptic techniques for all wounds (Thelan et al, 1998).

Ischaemic pain can occur throughout the body and is caused by obstruction of the microvasculature. Severe abdominal pain is common and may be due to an embolus-induced small bowel infarction, ischaemia or necrosis of the gut, or from haemorrhaging into the retroperitoneal space, which can also cause tingling and numbness due to nerve compression (Hudak et al, 1998).

The nurse should ensure that rest and sleep are adequate, and that sufficient meaningful sensory stimulation, such as familiar voices, TV and music, is provided, thereby avoiding sensory overload or deprivation (Hudak et al, 1998). The patient should be allowed uninterrupted periods of no less than 90 minutes (an average sleep cycle), with as little disturbance as possible during the night so that normal diurnal patterns may be maintained (Hudak et al, 1998).

It is the nurse’s responsibility to provide reassurance and explanations to the patient and their loved ones on the disease process, diagnostic procedures and planned therapy (Hudak et al, 1998). A trusting, open, honest relationship with good communication will help to allay anxiety. Social services, clergy, interpreters and other community services should be consulted as appropriate for provision of specialist needs (Hudak et al, 1998).

The nurse’s role in caring for the patient with DIC is broad and requires constant assessment and evaluation of physical and mental status, interpretation of all available data, planning, implementation and constant evaluation of appropriate individualised holistic care, as well as an understanding of the pathophysiology of the condition, the signs and symptoms and the various forms of treatment available. The patient and their family will need much support and understanding, as well as education and the encouragement to take an active role in their own treatment and management decisions.