CLINICAL
Understanding disseminated
References
Adam, S.K., Osborne, S. (1997) Critical
Care Nursing Science and Practice.
Oxford: Oxford Medical Publications.
Baird, M.S. (1997) Disseminated
Intravascular Coagulation. In: Hicks
Keen, J., Swearingen, P.L. (eds) Mosbys
Critical Care Nursing Consultant.
London: Mosby.
Furlong, M.A., Furlong, B.R. (2001)
Disseminated Intravascular
Coagulation. Available at: www.
emedicine.com/emerg/
topic150.htm
To have your reflection published, see p31
38
advanced
intravascular coagulation
Author Robyn Backhouse, BSc, DipHE, RGN, is staff
nurse, cardiac intensive care unit, Leeds General
Infirmary.
Abstract Backhouse, R. (2004) Understanding dis-
seminated intravascular coagulation. Nursing Times;
100: 36, 3839.
Disseminated intravascular coagulation is associated
with a high mortality rate, with patient outcomes
largely dependent upon swift recognition and appropri-
ate management of events. This article provides a basic
overview of the condition, and its pathophysiology,
diagnosis, treatment and nursing management, so that
effective intervention may be implemented, maximis-
ing the chances of patient recovery.
Disseminated intravascular coagulation (DIC) is a haema
tological disorder characterised by inappropriate, accel
erated, systemic activation of the clotting cascade,
simultaneously causing thrombosis and haemor
rhage (Levi, 2004). The condition is associated with a
high rate of morbidity and mortality, but as it is always
secondary to a primary disorder, which may itself be
associated with a high mortality and morbidity rate, the
exact figures are difficult to gauge (Levi, 2004).
The condition is often seen in intensive care units in its
acute form as a complication of septic shock and shock
states, as well as septicaemia, transfusion reactions and
obstetric complications (Levi, 2004; Spence, 2003).
The two primary problems caused by DIC are:
Decreased tissue perfusion due to thrombi, anaemia
and hypotension leading to organ ischaemia and necro
sis (Adam and Osborne, 1997);
Haemorrhage, both externally and internally into all
body cavities, due to accelerated and inappropriate con
sumption of clotting factors (Thelan et al, 1998).
Pathophysiology and diagnosis
DIC develops when the bodys 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 (micro
thrombi 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 cor
rected or removed. If it is not corrected, clotting continues
throughout the body, leading to multi-organ ischaemia,
infarction and eventual failure.
Red blood cells become damaged trying to pass
through blocked capillary beds, causing excess haemoly
sis. The continued clot formation uses up the bodys sup
ply of platelets, fibrinogen and other clotting factors,
upsetting the balance between coagulation of circulating
blood and prevention of haemorrhage.
An intense lysis (breakdown) of clots is also caused by
the accelerated thrombosis formation through activation
of plasminogen that converts to plasmin then destroys
the clot. This leads to the production of fibrin degradation
products, which are powerful anticoagulants.
Depletion of clotting products along with the release of
these anticoagulants leads to the uncontrolled haemor
rhage (Levi, 2004) (Fig 1).
DIC is diagnosed primarily on clinical signs and patient
history, with confirmation provided by laboratory findings
(Table 1, p40). No single test will confirm DIC (Levi,
2004;), but Table 1 includes a guide to the expected
values one might expect to see.
Medical management
The primary aims of medical management in DIC are to
(Levi, 2004):
Treat the underlying cause;
Provide supportive management of complications;
Support organ function;
Stop abnormal coagulation and control bleeding.
Hypotension, hypoxaemia, and acidosis must be cor
rected, and infection must be prevented and aggressively
Learning objectives
 e able to describe the pathophysiological
B
process of disseminated intravascular
coagulation (DIC)
 ecome aware of the medical management
B
of a patient with DIC and its rationale
List the signs and symptoms of DIC
 nderstand the basic nursing management,
U
assessment and monitoring of patients with
DIC and the rationale behind each action
SPL
NT 7 September 2004 Vol 100 No 36 www.nursingtimes.net

Box 1. Signs and symptoms of DIC
Bleeding from venepuncture sites or incisions,
around tubes and intravenous lines or from mucosal
surfaces/body orifices
Skin haemorrhagic patches, pallor, mottling,
haematoma, thrombophlebitis, necrosis due to
infarction, decreased capillary refill, or microthrombi
Cardiovascular hypotension, tachycardia, ST and
T-wave changes, and eventual circulatory collapse
Respiratory dyspnoea, tachypnoea, acidosis,
pleural friction rub, lowered oxygen saturations, and
arterial PO2 and signs of development of adult
respiratory distress syndrome
Renal oliguria, haematuria
Gastrointestinal malaena, blood in nasogastric
aspirate and emesis, abdominal pain and distension,
hyperactive or absent bowel sounds
Neurological headache, altered level of
consciousness, vertigo, lethargy, anxiety, irritability,
confusion, restlessness, focal deficits, seizures, coma,
weakness, paralysis
General cyanosis/infarction of digits and tip of nose,
muscle weakness, fatigue, pain, menorrhagia, fever
Furlong and Furlong, 2001; Swearingen and Keen, 2001;
Murray and White, 1999; Webb et al, 1999; Hudak et al,
1998; Adam and Osborne, 1997; Baird, 1997
treated. Supportive measures include artificial ventila
tion, 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).
Despite the fact that transfusion reactions and ABO
blood group incompatibilities may precipitate the onset
of DIC, replacement of depleted blood and clotting com
ponents remains one of the cornerstones of current
management (Galardy and Grabowski, 2003; Levi, 2003).
Daily and as required (PRN) clotting studies should be
undertaken and arterial lactate levels monitored to indi
cate the presence of lactic acidosis and the severity of
impaired perfusion (Hudak et al, 1998).
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 hepa
rin use. In those instances where it is used, fresh frozen
plasma may first be infused to replace depleted coagula
tion factors.
Signs and symptoms
Symptoms of DIC depend on the underlying cause and the
predominance of clotting versus bleeding (Levi, 2004).
Nurses should be aware of the signs listed in Box 1.
NT 7 September 2004 Vol 100 No 36 www.nursingtimes.net
Keywords Medicine Coagulopathy Shock
Nursing management References
It is important to take a thorough history, especially in Galardy, P. J., Grabowski, E. (2003).
relation to previous bleeding disorders and any medica Consumption Coagulopathy. Available
tions that induce bleeding (Murray and White, 1999). at: www.emedicine.com/ped/
The patient should be turned every two hours to pre topic473.htm
vent pressure ulcers and to minimise blood stasis and
pooling, as this may precipitate clotting and thrombus Griggs, A. (1998) Tracheostomy:
formation (Hudak et al, 1998). Skin should be thoroughly suctioning and humidification. Nursing
assessed at least two-hourly for pressure areas and any Standard; 13: 2, 4956.
signs of bleeding, such as petechiae (Woods et al, 2000).
Hudak, C.M. et al. (1998). Critical Care
A Waterlow or other appropriate scale should be used to
Nursing: A Holistic Approach.
identify potential problems (Hudak et al, 1998). Philadelphia, PA: Lippincott.
Pressure relieving mattresses reduce the amount of
manual handling required and the risk of skin trauma Kennedy, J.F. (1997) Enteral feeding for
(Adam and Osborne, 1997), while the use of glide sheets the critically ill patient. Nursing
reduces the risk of skin shearing. Standard; 11: 33, 3943.
Skin should be kept clean and moisturised, as dry
skin is more easily damaged (Skewes, 1996) and poor Levi, M. (2004). Current understanding
hygiene can lead to further infections. Safety devices of disseminated intravascular
coagulation. British Journal of
such as padded side rails should be used where neces
Haematology; 124: 567576.
sary and patients should be assisted out of bed where
appropriate (Hudak et al, 1998). McCance, K.L., Huether, S.E. (1998)
To further reduce the risk of skin damage, sticky tapes Pathophysiology: The Biologic Basis
should be avoided, and electric rather than blade razors for Disease in Adults and Children.
should be used (Woods, et al, 2000). Soft swabs and mild London: Mosby.
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).
Temperature should be monitored and recorded at
least four-hourly. It should not be measured rectally due
to risk of trauma (Swearingen and Keen, 2001). Excessive
pyrexia should be treated with appropriate medications.
Light bed clothing and avoidance of an overheated
environment are common sense measures. However use
of fans, cool compresses and tepid sponges is recom
mended due to the increased risk of triggering heat-
conserving-and-producing mechanisms in the patient
case study
George Brown is 64 years old and was admitted to your
unit following bowel surgery three days ago. Apart
from a mild pyrexia and slightly raised white cell count
he had made an apparently good recovery on the ward
but deteriorated suddenly overnight, with an increased
temperature, cool clammy skin, tachycardia, reduced
blood pressure, and cold hands and feet. He also has
numerous small bruises and petechiae on his body,
which were previously unreported, and there is blood
oozing from his abdominal wound, around his
peripheral line, and from a small cut on his face, which
happened two days ago while he was shaving. Routine
blood tests reveal a decreased platelet count, raised PT
This article has been double-blind
and APTT, and lowered Hb and haematocrit levels. A peer-reviewed.
provisional diagnosis of DIC secondary to septic shock is
For related articles on this subject
made, and further investigations are carried out. and links to relevant websites see www.
nursingtimes.net
39
 advanced
References
Murphy, P. (ed) (1999) Handbook of
Critical Care. Leeds: Science Press.
Murray, S.E., White, B.S. (1999) Critical
Care Assessment Handbook. London:
WB Saunders Company.
Schmaier, A.H. (2003) Disseminated
Intravascular Coagulation.
Available at: www.emedicine.com/
med/
topic577.htm
Skewes, S. (1996) Skin care rituals
that do more harm than good. AJN;
96: 10, 3335.
The American Journal of Nursing
40
such as vasoconstriction, shivering and goosebumps.
Intravenous access should be maintained at all times
for fluid replacement therapy, emergency infusion of
blood products and medications (Hudak et al, 1998).
Insertion of invasive lines can cause haemorrhage, but is
often preferable to numerous venepuncture stabs
(Swearingen and Keen, 2001).
If injections are necessary, the smallest gauge needle
should be used. Injection sites should be rotated, direct
pressure applied for 35 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 haemor
rhage (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).
If the patient is on inotropic support or other medica
tion, the nurse must be aware of the specific observations,
assessment, and care appropriate to each drug. Be aware
of administering drugs that may precipitate bleeding
(Woods et al, 2000) such as aspirin, warfarin and NSAIDs.
table 1. test values expected in
DICdiagnosis
Test Normal value Value in DIC
Prothrombin
time 1115 sec Prolonged
Activated partial
thromboplastin 3948 sec Prolonged
time as blood loss and pulmonary microemboli may result
Thrombin time 1013 sec Usually
prolonged
Fibrinogen level 200400mg Decreased
/100ml
Platelet count 150,000 Decreased
400,000/mm3
F ibrinogen <10g/ml Increased
degradation
products port in the form of supplemental oxygen may be necessary.
Plasminogen levels Decreased
D-dimer assay Increased
Antithrombin III Decreased
Adapted from: Hudak, C. et al, 1998
Cardiovascular
Continuous ECG monitoring is necessary to detect dys
rhythmias and ST and T-wave changes brought on by
decreased myocardial or pulmonary perfusion (Swear
ingen and Keen, 2001). A 12-lead ECG should be carried
out (Adam and Osborne, 1997) for reference, and repeated
if wave or rhythm changes are suspected.
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 hypoten
sion disproportionate to blood loss (Murphy, 1999).
Tissue perfusion and cardiac output can be assessed
through monitoring vital signs, haemodynamic parame
ters, mental status, urine output and cardiac rhythm
(Swearingen and Keen, 2001). Haemoglobin (Hb) should
be regularly monitored as haemorrhage may lead to
anaemia (Swearingen and Keen, 2001).
Pulmonary artery pressures and central venous pres
sures should be measured at least hourly as they reflect
a patients 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 con
sumption should be measured every 612 hours if a
pulmonary artery catheter is in place (Hudak et al, 1998).
Pedal and peripheral pulses, capillary refill, skin tem
perature and colour should be checked at least every two
hours to assess peripheral perfusion, as this can identify
the formation of microclots in the peripheral vascular
system (Swearingen and Keen, 2001).
Monitoring respiratory function
Respiratory function requires close continual monitoring
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 patients colour and evidence of cyanosis
or shortness of breath (Adam and Osborne, 1997).
Respiratory failure caused by pulmonary shunting, pul
monary haemorrhage, haemothorax, pulmonary embolus,
or acute respiratory distress syndrome (ARDS) can occur, as
oxygen demand and cellular uptake can be greatly altered
(Thelan et al, 1998).
To maintain adequate organ perfusion, respiratory sup
If this is insufficient to maintain acceptable arterial oxygen
levels, artificial ventilation may be required, although this
should be used with caution due to the increased risk of
haemorrhage (Adam and Osborne, 1997).
Chest physiotherapy may be required to maintain opti
mal 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
NT 7 September 2004 Vol 100 No 36 www.nursingtimes.net
 figure 1. pathophysiology of disseminated intravascular coagulation References
Swearingen, P.L., Keen, J.H. (eds)
(2001) Manual of Critical Care Nursing:
Nursing Interventions and
Tissue injury, Blood cell injury or
Collaborative Management.
releasing tissue platelet contact with
London: Mosby.
factor, tissue collagen in vessel
thromboplastin, endothelium
Thelan, L.A. et al (1998) Critical Care
or other procoagulants Nursing Diagnosis and Management.
London: Mosby.

Webb, A.R. et al (eds) (2001) Oxford

Extrinsic pathway Intrinsic pathway Textbook of Critical Care. Oxford:
Oxford University Press.

Wood, C.J. (1998) Can nurses safely

assess the need for endotracheal
Common pathway
suction in short-term ventilated
patients, instead of using routine
techniques? Intensive and Critical Care
Nursing;
Coagulation with thrombosis (clot formation) in vessels of major organs 14: 170178.

Woods, S.L. et al (2000) Cardiac

Nursing. Philadelphia: Lippincott.

Lysis of clots activated

(plasminogen converts to plasmin)

Thrombosis continues until

cause is removed or corrected

Production of fibrin Consumption of

degradation products platelets, fibrinogen and
other clotting factors

If not corrected, organ ischaemia and

Haemorrhage infarction occurs

Adapted from Thelan, et al (1998)

these procedures must be performed gently to avoid
further trauma and haemorrhage.
Suctioning should be carried out with great care and at
the lowest possible pressure research has shown an
optimum range of 80150mmHg (Griggs, 1998) to avoid
further haemorrhage. To avoid hypoxia, suction should
last no longer than 1015 seconds (Griggs, 1998).
Monitoring renal function
Fluid intake and output must be recorded accurately at
least every 24 hours, increasing to every 3060 minutes
if the patient is actively bleeding (Swearingen and Keen,
2001). Oliguria resulting from hypoperfusion of the kid-
neys may occur due to hypovolaemia. It is therefore
essential to maintain an adequate blood pressure.
Renal support such as filtration or dialysis may be
required if urine output drops and remains less than 0.5
ml/kg/hour in an adult despite other interventions (Adam
and Osborne, 1997).
Regular testing for protein and blood in the urine is
important. The kidneys are common sites for micro
emboli so urea, creatinine and electrolyte levels should
also be monitored. Acute renal failure is common due to
acute tubular necrosis (Adam and Osborne, 1997).
Daily weights are often useful as an indicator of fluid
overload, although other signs such as generalised
oedema, periorbital and facial oedema, excessive frothy
saliva, rapid dyspnoea, moist rales and cough, or rapid
pulse (Hudak et al, 1998) may be more practical in inten
sive care units.

NT 7 September 2004 Vol 100 No 36 www.nursingtimes.net 41

 advanced
Monitoring neurological function
Full neurological assessment should be undertaken at
least two hourly to check for intracranial haemorrhage,
ischaemia and cerebral infarction (Baird, 1997).
Pupillary reaction should be recorded in sedated patients
(Swearingen and Keen, 2001). When assessing con
sciousness levels in patients who are unresponsive to
verbal stimuli, the use of painful stimuli such as pinching
or pressure should be avoided or minimised as it may
lead to further haemorrhage.
Restlessness, agitation, visual disturbances, headaches
and sensory or motor dysfunction can indicate a change
in consciousness levels, which may point to intracranial
haemorrhage or cerebral ischaemia (Hudak et al, 1998).
Gastrointestinal tract and nutrition
Assess for gastrointestinal bleeding by checking emesis,
nasogastric aspirate and stools for blood.
Stool softeners may be required to help maintain
bowel function. Rectal procedures should be avoided as
they may cause unnecessary trauma (Swearingen and
Keen, 2001).
If the patient is unable to take an oral diet, then an
artificial feeding programme should be started in consul
tation with the dietitian or nutritional support service
(Kennedy, 1997).
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 control
Infection is one of the most common causes of DIC
(McCance and Huether, 1998) and is often already pre
sent, requiring treatment with appropriate antibiotics.
Strict infection control measures and effective handwash
ing are essential to avoid infection (Thelan et al, 1998).
Regular monitoring for infection markers will be neces
sary, as will extreme care with all invasive equipment and
strict aseptic techniques for all wounds (Thelan et al,
1998).
Comfort and pain control
Pain not only brings suffering, but also causes physiolog
ical complications such as vasoconstriction and tachycar
dia (Hudak 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 embo
lus-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).
Joint pain is also due to the formation of thrombi
within the joint.
A pain scale should be used to assess the patients
42
guided reflection
Each week we publish a guided reflection
article to help you with your CPD. After reading
the article use the following points to help you
write your reflection:
 ive details of where you work and why this
G
article is important to your area of practice;
 xplain how you would describe DIC and how
E
it occurs to a patient and his/her family;
 iscuss how you would recognise the signs
D
and symptoms of DIC;
 escribe any new or important information
D
you have learnt about the nursing care of a
patient with DIC;
 rite about how you will follow up what you
W
have learnt.
comfort, and appropriate analgesia or sedation should
be provided. Measures such as distraction, imagery or
relaxation may also be of help (Hudak et al, 1998).
Psychological and social care
The nurse should ensure that rest and sleep are ade
quate, and that sufficient meaningful sensory stimula
tion, 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 possi
ble during the night so that normal diurnal patterns may
be maintained (Hudak et al, 1998).
It is the nurses 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).
Conclusion
The nurses role in caring for the patient with DIC is
broad and requires constant assessment and evaluation
of physical and mental status, interpretation of all avail
able data, planning, implementation and constant eval
uation of appropriate individualised holistic care, as well
as an understanding of the pathophysiology of the con
dition, 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 edu
cation and the encouragement to take an active role in
their own treatment and management decisions.
NT 7 September 2004 Vol 100 No 36 www.nursingtimes.net