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DISSEMINATED INTRAVASCULAR COAGULATION

INTRODUCTION
Disseminated intravascular coagulation is a serious bleeding and thrombotic disorder. It
results from abnormally initiated and accelerated clotting. Subsequent decreases in clotting
factors and platelets ensue, which may lead to uncontrollable haemorrhage. The term
disseminated intravascular coagulation can be misleading because its suggests that blood is
clotting. However, the paradox of this condition is characterized by the profuse bleeding that
results from the depletion of platelets and clotting factors. Disseminated intravascular is
always caused by an underlying disease or condition. The underlying problem must be
treated for the disseminated to be resolve.

DEFINITION
Disseminated intravascular coagulation is a condition in which blood clots form throughout
the body's small blood vessels, reducing or blocking blood flow, which can damage organs.

According to international

TYPES
The two types of DIC are acute and chronic.

Acute DIC begins with clotting in the small blood vessels and quickly leads to serious
bleeding.

Chronic DIC causes blood clotting, but it usually doesn't lead to bleeding.

INCIDENCE
RELATED ANATOMY AND PHYSIOLOGY

Blood is a fluid of connective tissue .It circulate continuously around the body, allowing
constant communication between tissues distant from each other .Its transport

 Oxygen from the lungs to the tissues , and carbon dioxide from the tissues to the
lungs for excretion
 Nutrients from the alimentary tract to the tissues , and cell wastes to the excretory
organs , principally the kidneys
 Hormones secreted by endocrine glands to their target glands and tissues
 Clotting factors that coagulate blood ,minimising bleeding from ruptured blood
vessels

Blood is composed of clear , straw –coloured , watery fluid called plasma in


which several different types of blood cells are suspended .Plasma normally
constitutes 55% of the volume of blood .The remaining 45% is counted for by
the cellular fraction . Bloods makes up about 7% of body weight (about 5,6%
litres in a 70kg man )
a)Plasma : plasma is a clear ,slightly yellow liquid , containing a large number of organic and
inorganic substances dissolved in water .Plasma contains approximately 91% of water and
9% of solid .Of the solid ,about 7% are the plasma protein which consist of serum albumin
,serum globulin ,and fibrogen .Normal plasma volume is about 5% of total body weight
(3500ml)

b) Erythrocytes: Red blood cells are biconcave discs ,they have no nucleus and their
diameter is about 7 micrometers .The main function is in gas transport , mainly of oxygen but
they also carry some carbondioxide .Their characteristics shape is suited to their purpose ,the
biconcavity increases their surface area for gas exchange , and the thinness of the central
portion allows fast entry and the exist of gases. The cells are flexible so they can squeeze
through narrow capillaries , and contain no intracellular organelles , leaving more room for
haemoglobin , the large pigmented protein responsible for gas transport .Erythrocytes are
produced in red bone marrow ,which is present in the ends of long bones and in flat and
irregular bones .Their lifespan in the circulation is about 120 days .The process of
development of stem cells takes about 7days and is called erythropoiesis.The normal 4.5 to
5.5millions in males and 4 to 5 in females

c)Leukocytes (White blood cells): These cells have an important function in defence and
immunity .Leukocytes are the largest blood cells but they count for only about 1% of the
blood volume .They contain nuclei and some have granules in their cytoplasm .The two main
types
 Granulocytes (polymorphonuclear leukocytes)- Neutrophils ,
Eosinophils and basophils
 Agranulocytes – monocytes and lymphocytes

Rising of white cell numbers in the blood stream usually indicate a physiological problem ,
e.g infection ,trauma,or malignancy

 Granulocytes ( polymorphonuclear leukocytes)-During their formation


,granulopoiesis ,they follow a common line of development through myeloblast to
myelocyte before differentiating into three types

 Neutrophils – these small , fast , and active scavengers protect the body against
bacterial invasion and remove dead cell and debris from damaged tissues.
Neutrophils live on average 6-9 hours in the blood stream
 Eosinophils – Eosinophils , although capable of phagocytosis, are less active in
this than neutrophils , their specialised role appears in the elimination of parasite ,
such as worms which are too big to be phagocytosed .They are equipped with
certain toxic chemicals ,stored in their granules which they release when the
eosinophil binds to an infecting organism .
 Basophils – Basophils which are closely associated with allergic reactions
,contain cytoplasmic granules packed with heparin (an anticoagulant) , histamine
(an inflammatory agent) and others substances that promote inflammation
.Usually the stimulus that causes basophils to release the content of their
granules is an allergen .
 Agranulocytes - The monocytes and lymphocytes make up 25 to 50% 0f the total
leukocyte count .They have a large nucleus and no cytoplasmic granules.
 Monocytes – These are the largest number of white blood cells .Some circulate
in the blood and are actively motile and phagocytic while others migrate into
tissue s where they develop into macrophages .Both types of cell produce
interleukin 1, which
 Act on the hypothylamus , causing the rise in the body temperature
associated with microbial infections
 Stimulates the production of some globulins by the liver
 Enhance the production of activated T-lymphocytes

 Lymphocytes – Lymphocytes are smaller than monocytes and have large nuclei
.They circulate in the blood and are present in great numbers in lymphatic tissue
such as lymph nodes and the spleen .Lymphocytes develop from pluripotent
stem cells in red bone marrow and from precursors in lymphoid tissue , then
travel in the blood to lymphoid tissue elsewhere in the body where they are
activated ,i.e they become immunocompetent which means they are able to
respond to antigens .
d)Platelets ( thrombocytes) – platelets are small , spherical ,non-nucleated mass of
protoplasm with a diameter of 2-4µm and derived from the cytoplasm of megakaryocytes in
red bone marrow .They contain a variety of substances that promote blood cloting ,which
causes haemostasis .Platelets donot have DNA and RNA .Therefore , there can be no protein
synthesis inside the platelet. The life span of platelets is between 8 to 11 days , after that they
destroyed in spleen .Normal platelets count is 1.5 to 2 lakh .

Blood cells are synthesised in red bone marrow .Some lymphocytes , additionally are
produced in lymphoid tissue .In the bone marrow , all blood cells originate from pluripotent
stem cells and go through several development stages before entering the blood .Different
types of blood cell follow separate line of development .The process of blood cell formation
is called haemopoiesis

FUNCTION OF BLOOD
 Transport of respiratory gases
 Excretory function
 Nutritional function
 Acid base balance
 Transport of hormones
 Protection of Defense
 Temperature regulation
 Water balance
 Osmotic pressure

CAUSES

Some diseases and conditions can disrupt the body's normal blood clotting process and lead
to disseminated intravascular coagulation (DIC). These diseases and conditions include:

 Sepsis (an infection in the bloodstream)


 Surgery and trauma
 Cancer
 Serious complications of pregnancy and childbirth
PATHOPHYSIOLOGY
Underlying disorder

Systematic activation of coagulation

Enhanced fibrin formation consumption of platelets and clotting factors

Micro vascular thrombosis Bleeding

Organ failure

CLINICAL MANIFESTATION

Signs and symptoms of disseminated intravascular coagulation (DIC) depend on its cause and
whether the condition is acute or chronic.

A) Acute DIC develops quickly (over hours or days) and is very serious. Chronic DIC
develops more slowly (over weeks or months). It lasts longer and usually isn't
recognized as quickly as acute DIC.

With acute DIC, blood clotting in the blood vessels usually occurs first, followed by
bleeding. However, bleeding may be the first obvious sign. Serious bleeding can occur very
quickly after developing acute DIC.

1) Internal Bleeding

Internal bleeding can occur in your body's organs, such as the kidneys, intestines, and brain.
This bleeding can be life threatening. Signs and symptoms of internal bleeding include:
 Blood in your urine from bleeding in your kidneys or bladder.
 Blood in your stools from bleeding in your intestines or stomach. Blood in your stools
can appear red or as a dark, tarry color. (Taking iron supplements also can cause dark, tarry
stools.)
 Headaches, double vision, seizures.

2) External Bleeding

External bleeding can occur underneath or from the skin, such as at the site of cuts or an
intravenous (IV) needle. External bleeding also can occur from the mucosa. (The mucosa is
the tissue that lines some organs and body cavities, such as your nose and mouth.)

External bleeding may cause purpura or petechiae. Purpura are purple, brown, and red
bruises. This bruising may happen easily and often. Petechiae are small red or purple dots on
your skin.

Other signs of external bleeding include:

 Prolonged bleeding, even from minor cuts.


 Bleeding or oozing from your gums or nose, especially nosebleeds or bleeding from
brushing your teeth.
 Heavy or extended menstrual bleeding in women.

B) Incase of chronic DIC Blood clotting also occurs, but it usually doesn't lead to bleeding.
Sometimes chronic DIC has no signs or symptoms

In DIC, blood clots form throughout the body's small blood vessels. These blood clots can
reduce or block blood flow through the blood vessels. This can cause the following signs and
symptoms:
 Chest pain and shortness of breath if blood clots form in the blood vessels in your
lungs and heart.
 Pain, redness, warmth, and swelling in the lower leg if blood clots form in the deep
veins of your leg.
 Headaches, speech changes, paralysis (an inability to move), dizziness, and trouble
speaking and understanding if blood clots form in the blood vessels in your brain. These signs
and symptoms may indicate a stroke.
 Heart attack and lung and kidney problems if blood clots lodge in your heart, lungs, or
kidneys.
 Cyanosis , gangrene
 ECG changes
 Abdominal pain and paralytic ileus
 Oliguria
 ARDS

DIAGNOSTIC TESTS

1)Complete Blood Count and Blood Smear

A complete blood count (CBC) measures the number of red blood cells, white blood cells,
and platelets in your blood. Platelets are blood cell fragments that help with blood clotting.
Abnormal platelet numbers may be a sign of a bleeding disorder or a thrombotic disorder. A
blood smear is a test that may reveal whether your red blood cells are damaged.

2)Tests for Clotting Factors and Clotting Time

The following tests examine the proteins active in the blood clotting process and how long it
takes them to form a blood clot.

 PT and PTT tests: These tests measure how long it takes blood clots to form.
 Serum fibrinogen: Fibrinogen is a protein that helps the blood clot. This test
measures how much fibrinogen is in your blood.
 Fibrin degradation: After blood clots dissolve, substances called fibrin degradation
products are left behind in the blood. This test measures the amount of these substances in the
blood.
3)A diagnostic algorithm has been proposed by the International Society of Thrombosis
and Haemostasis. This algorithm appears to be 91% sensitive and 97% specific for the
diagnosis of overt DIC. A score of 5 or higher is compatible with DIC and it is recommended
that the score is repeated daily, while a score below 5 is suggestive but not affirmative for
DIC and it is recommended that it is repeated only occasionally: [12][13] It has been
recommended that a scoring system be used in the diagnosis and management of DIC in
terms of improving outcome.[14]

 Presence of an underlying disorder known to be associated with DIC (no=0, yes=2)


 Global coagulation results
o Platelet count (>100k = 0, <100 = 1, <50 = 2)
o Fibrin degradation products such as D-Dimer (no increase = 0, moderate
increase = 2, strong increase = 3)
o Prolonged prothrombin time (<3 sec = 0, >3 sec = 1, >6 sec = 2)
o Fibrinogen level (> 1.0g/L = 0; < 1.0g/L = 1[15])

MANAGEMENT

A) Medical management

Treatment for disseminated intravascular coagulation (DIC) depends on its severity and
cause. The main goals of treating DIC are to control bleeding and clotting problems, treat the
underlying cause and also symptomatic treatment .

Acute Disseminated Intravascular Coagulation

People who have acute DIC may have severe bleeding that requires emergency treatment in a
hospital. Treatment may include blood transfusions, medicines, and oxygen therapy.

 A blood transfusion: Blood transfusions are done to replace blood loss due to an
injury, surgery, or illness. Blood product support with platelets, cryoprecipitate and
fresh frozen plasma

 Medicines e.g proton pump inhibitor, antiemetic, antibiotic

 Oxygen therapy

Chronic Disseminated Intravascular Coagulation

People who have chronic DIC are more likely to have blood clotting problems than bleeding.
Incase of chronic DIC, treatment include
 Anticoagulants with heparin or low molecular weight heparin.

 Anti thrombin III

 A recommended human activated C protein

A recombinant

 Antifibrinolytics

B) Nursing management

 Assessment
 History collection and physical examination
 Monitor vitals sign and saturation level
 Assess the contributing factors so an appropriate care plan can be initiated
 Check laboratory reports
 Monitor electrocardiogram

 Nursing diagnosis

1.Ineffective tissue perfusion related to diminished blood flow secondary to thrombosis


as evidence by cyanosis

Expected outcome: maintain optimal tissue perfusion

Intervention :

 To assess the general condition of the patient.


 To monitor vital signs
 To monitor neurological status
 Position client in a semi-Fowler’s to high-Fowler’s as tolerated.
 Provide oxygen therapy
 Monitor intake and output
 Provide IV fluid Ringer lactate
 Administer anticoagulant as prescribed.
2.Decreased cardiac output related to fluid volume deficit and hypotension as evidenced
by patient blood pressure

Expected outcome:

Intervention:

 Assess the contributing factors so an appropriate care plan can be initiated


 Check for any alterations in level of consciousness.
 Note skin color, temperature, and moisture
 Assess heart rate and blood pressure.
 Check for peripheral pulses, including capillary refill.
 Provide IV fluid
 Monitor laboratory report
 Monitor intake and output and also the colour of urine
 Administer blood product as prescribed
 Closely monitor fluid intake including IV lines. Maintain fluid restriction if ordered.
 Administer

3.Imbalanced nutrition less than body requirement related to nausea, vomiting

Expected outcome: Maintain nutritional status

Interventions:

 Weigh daily to monitor caloric status


 If NPO provide total parental nutrition as prescribed
 Administer IV fluids to promote hydration and nutrition when on oral restrictions
 Advance diet as tolerated.Small and frequent diet is recommended, which is high
calorie high protein
 Instruct patient to avoid spicy and caffeineted foods which are gastro irritants
 Monitor intake output chart

4. Activity intolerance related to generalised weakness, imbalance between oxygen


supply and demand as evidenced by decrease blood pressure as evidenced by fatigue
Expected outcome: maintain the daily activities of the patient

Intervention

- To assess the general condition of patient


- Monitor vitals sign before, during and after activity
- Assess psychological factors affecting the current situation
- Adjust activities to prevent over exertion
- Increase exercise or activity levels gradually and plan rest periods between
activities
- Provide rest to the patient
- Assist the patient in doing daily activities
- Provide passive exercise

PROGNOSIS

Prognosis varies depending on the underlying disorder, and the extent of the intravascular
thrombosis (clotting). The prognosis for those with DIC, regardless of cause, is often serious:
Between 20% and 50% of patients will die. [17] DIC with sepsis (infection) has a significantly
higher rate of death than DIC associated with trauma.

COMPLICATION
Complications of DIC include the following:
 Acute kidney injury
 Respiratory dysfunction
 Hepatic dysfunction
CONCLUSION

Disseminated intravascular coagulation is a condition in which blood clots form throughout


the body, blocking small blood vessels. Symptoms may include chest pain, shortness of
breath, leg pain, problems speaking, or problems moving parts of the body. As clotting
factors and platelets are used up, bleeding may occur. This may include blood in the urine,
blood in the stool, or bleeding into the skin. Complications may include organ failure
REFERENCES

1) Chintamani.Lewis’s Medical Surgical Nursing:assessment and management of


clinical problems.7edition.New Delhi: Published by Elseveir, a division of Reed
Elseveir India Private Limited;2011.715-718

1. Levi, M; Toh, C-H; et al. (2009). "Guidelines for the diagnosis and management of
disseminated intravascular coagulation". British Journal of Haematology. 145 (5): 24–
33. doi:10.1111/j.1365-2141.2009.07600.x. PMID 19222477.
2. ^ Taylor, F; Toh, C-h; et al. (2001). "Towards Definition, Clinical and Laboratory
Criteria, and a Scoring System for Disseminated Intravascular Coagulation".
Thrombosis and Haemostasis. 86 (5): 1327–30. PMID 11816725.
3. ^ Gando, S (2012). "The Utility of a Diagnostic Scoring System for Disseminated
Intravascular Coagulation". Critical Care Clinics. 28 (3): 378–88.
doi:10.1016/j.ccc.2012.04.004. PMID 22713612.
4. ^ "Guidelines for the diagnosis and management of disseminated intravascular
coagulation". British Journal of Haematology. 145 (1): 24–33. doi:10.1111/j.1365-
2141.2009.07600.x.
5. Franchini, M; Manzato, F; Salvagno GL; et al. (2007). "Potential role of recombinant
activated factor VII for the treatment of severe bleeding associated with disseminated
intravascular coagulation: a systematic review". Blood Coagul Fibrinolysis. 18 (7):
589–93. doi:10.1097/MBC.0b013e32822d2a3c. PMID 17890943.
6. Becker, Joseph U and Charles R Wira. Disseminated intravascular coagulation at
eMedicine, 10 September 2009

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