Bleeding, clotting,platelet disorder and it's management

BLEEDING,CLOTTING,PLATELET
DISORDERS AND ITS NURSING
MANAGEMENT
BSC (H) NURSING
R.A.K.C.O.N

 INTRODUCTION
 BLEEDING ,CLOTTING AND PLATELET DISORDERS
 HEMOPHILIA
 DISSEMINATED INTRAVASCULAR COAGULATION
 HYPOPROTHROMBINEMIA
 IDIOPATHIC THROMBOCYTOPENIC PURPURA
 Each disorder include:1. Definition
2. Etiology/ Pathophysiology
3 .Clinical manifestations
4.Risk factors
5. Assessment and diagnostic findings
6.Medical management
7.Complications
8. Nursing management
 Summary and conclusion
 Bibliography

INTRODUCTION
 A bleeding disorder is a condition that effects the way our blood
normally clots. The clothing process, also known as coagulation, changes
a blood from liquid to a solid. When you’re injured your blood normally
begins to clot to prevent a massive loss of blood. Sometimes certain
conditions prevent blood from clothing properly, which may result in
heavy or prolonged bleeding .

BLEEDING, CLOTHING & PLATLETS DISORDERS
Hemophilia
Disseminated
intravascular
coagulation
Hypoprothrombinemia
Thrombocytopenia

WHAT IS HAEMOPHILLIA?
 Hemophilia is a common hereditary coagulation blood disorder
due to deficiency or reduced activity of clotting factor VIII or
clotting factor IX. This disorder is a X- linked recessive disorder.
Hemophilia is a bleeding disorder that slows down the blood
clotting process.
 It is transmitted by females to men who are sufferers
 People who have hemophilia often have longer bleeding after
some sort of contact to injury. people who have severe
hemophilia start to have spontaneous bleeding in the joints and
muscles or all around their bodies. Hemophilia is more common
in males than females.

There are three main types of hemophilia:
A B C
It is the most common
type of hemophilia
(severe)
It is the second most
type of hemophilia
(moderate)
It is a mild form of
hemophilia
(mild)
It is also known as
factor VIII deficiency or
classic hemophilia
It was originally named
“Christmas disease”
Caused by factor IX
deficiency.
Deficiency of factor XI.

ETIOLOGY/PATHOPHYSIOLOGY
 CAUSES OF HEMOPHILIA
• Hemophilia has a sex- linked recessive inheritance
• In most case, hemophilia is caused by a mutation in
a gene that encodes for one of the clotting factors.
• Since the hemophilia gene is located on the X
chromosome, hemophilia usually occur in males
and female is the carrier of hemophilia.

 The two major forms of hemophilia which can occur in
mild to severe forms are hemophilia A (Classic
hemophilia, factor VIII deficiency) and hemophilia B(
Christmas disease, factor IX deficiency).
 The disorder termed “von Willebrand’s disease” is a
related disorder involving a congenitally acquired
deficiency of von Willebrand compilation proteins.
 Factor VIII is synthesised in the liver and circulates
complexed to von Willebrand’s protein(VWP).
 And one more hemophilia C ( factor IX deficiency)

 The inherent pattern of these hemophilia are as
follows:
• Hemophilia A :Recessive sex- linked (transmitted by
female carriers, displayed almost exclusively in
men)
• Hemophilia B :Recessive sex- linked (transmitted by
female carriers, displayed almost exclusively in
men)
• von Willebrand’s disease (VWP dysfunction)
autosomal dominant, seen in both sexes ,
recessive(in severe form of the disease)

CINICAL MANIFESTATIONS
 Clinical manifestations and complications related to
hemophilia include:
• slow, persistent, prolonged bleeding from minor trauma and
small cuts
• Delayed bleeding after minor injuries (the delay may be for
several hours or days)
• Uncontrollable hemorrhage after dental extraction or irritation
of gingiva with a hard bristle tooth brush
• Epistaxis, especially after the blow to the face
• GI bleeding from ulcers and gastritis

• Hematuria from GU trauma and splenic rupture resulting
from fall or abdominal trauma.
• Ecchymoses and subcutaneous hematomas( common)
• Neurologic signs, such as pain, anaesthesia and paralysis
which may develop from nerve compression caused by
hematoma formation
• Hemarthrosis (bleeding from joints) which may lead to joint
deformity severe enough o cause unresolvable crippling (
most commonly in knees elbows, shoulders, hips, and
ankles)

RISK FACTORS
 Common risk factors :
o Family history of hemophilia /bleeding
o Male sex
 Risk factors for acquired hemophilia:
o Pregnancy
o Infections( Hepatitis C, AIDS)
o Drugs(alpha- Interferon)
o Dermatological conditions ( Pemphigus, Psoriasis)

ASSESSMENT AND DIAGNOSTIC
FINDINGS
 Complete Blood Count (CBC) : This common test measures
the amount of hemoglobin, the size and the number of red blood
cells and number of different types of white blood cells and
platelets found in the blood. The CBC is normal in people with
hemophilia
 Activated partial thromboplastin time test (aPTT):This test
measures how long it takes for blood to clot. It measures the
clotting ability of factors VIII, IX,XI and XII. If any of these clotting
factors are too low, it takes longer than normal for the blood to
clot. The result of this test will show a longer clotting time among
people with hemoplilia A or B.

 Clotting factor test: also called factor assays, are
required to diagnose a bleeding disorder. This blood
test shows the type of hemophilia and the severity.
 Prothrombin time test (PT): this test also measures
the time it takes for blood to clot. It measures primarily
the clotting ability of factor I, II ,V, VII, X. if any of
these factors are too low, it takes longer than normal
for the blood to clot. The result of these test will be
normal among most people with hemophilia A and B.

MEDICAL MAMNAGEMENT
 Gene therapy: With the cloning of factor VIII and the
advances in molecular technologies, the possibility of cure of
hemophilia with gene therapy is conceived , ex- vivo gene
therapy, in which cells to be transplanted are genetically modified
to secrete factor VIII and then are transplanted into the recipient,
in vivo gene therapy in which vector is directly injected into the
patients and non-autologous gene therapy, in which cells
modified to secrete VIII are packaged in immuno- protected
devices and implanted into recipients.

 Anti– fibrinolytic medicines
o Antifibrinolytic medicine may be used with replacement therapy.
They’re usually given as pills and they help keep blood clots from
breaking down.
o These medicines most often are used before dental work or to
treat bleeding from the mouth or nose or mild intestinal bleeding.

COMPLICATION
 Pain
 Bleeding or life threatening hemorrhage
 Joint/ muscular damage eg. Synovitis
 Allergic reaction to infused product
 Anemia
 Chronic arthritis

PREVENTION
 Avoid IM injection
 Avoid contact sports
 Immobilize joint during acute bleeding
 Progressive exercise

NURSING MANAGEMENT
 ASSESSMENT
 SUBJECTIVE DATA: 1. Patient feels pain in moving his /her
limbs.
2. Patient suffers from profuse
bleeding
3. Patient feels vulnerable about
himself
 OBJECTIVE DATA: 1.Swelling in joints
2. limited movement of limbs
3.Bony changes in the joints when
the bleeding
has stopped.

 NURSING DIAGNOSIS 1
 Acute pain related to traumatic injury to the muscles
 NURSING INTERVENTIONS
 Immobilise joints and apply elastic bandages to the affected
joint if indicated.
 Elevate the affected part
 Apply a cold compress to active bleeding sites.
 Provide gentle passive ROM exercises

 Risk for bleeding related to decreased concentration of clotting
factors circulating in the blood [factor VIII or IX]
 Monitor hemoglobin and hematocrit levels
 Assess for inhibitor antibodies to factor VIII
 Anticipate the need for prophylactic treatment before high risk
situation such as invasive diagnosis or surgical procedure
 Provide replacement therapy of deficient clotting factors.

 Risks for injury related to decreased clotting factor(VIII or IX)
 Provide appropriate oral hygiene ( use of water irrigation
device, use of soft/ sponge tipped toothbrush)
 Avoid rectal temperature
 Use of padded bed rail sides.

WHAT IS DISSEMINATED
INTRAVASCULAR COAGULATION?
 Disseminated Intravascular Coagulation (DIC) is a rare but
serious condition that causes abnormal blood clotting throughout
the body’s blood vessels.
 It is caused by another disease or condition, such as an infection
or injury, that makes the body’s normal blood clotting prcess
become overactive.
 DIC may develop quickly over hours or days, or more slowly.

ETIOLOGY
 DIC is not a disease, it’s an abnormal response of the normal
clotting cascade stimulated by another disease process or
disorders. The diseases and disorders are known to predispose
the patient with DIC are as follows:
1. Acute DIC
• Shock hemorrhagic
• Septicemia
• Hemolytic process
a) Transfusion of mismatched blood
b) Acute hemolysis from infection or immunologic disorders

• Obstretric conditions
a) abruption placenta
b) Toxemia
c) Septic abortion
• Tissue damage
a) Extensive burns and trauma
b) Heat stroke
c) Severe head injury
d) Snake bites
e) Acute anoxia (after cardiac arrest)

2. Chronic DIC
 Liver disease
 SLE
 Localized malignancy

PATHOPHYSIOLOGY
 DIC occurs when monocytes and endothelial cells are activated
or injured by toxic substances elaborated in the course of certain
diseases. The response of monocytes and endothelial cells to
injury is to generate tissue factor on the cell surface, activatng
the coagulation cascade.
 In acute DIC, an explosive generation of thrombin depletes
clotting factors and platelets and activates the fibrinolytic system.
Bleeding into the subcutaneous tissues, skin, and mucous
membranes occur, along with occlusion of blood vessels caused
by fibrin in the micro-circulation.

 In chronic DIC, the process is the same, but it is less
explosive. Usually there is time for compensatory
responses to take place, which diminish the likelihood
of bleeding but gives rise to a hyper coaguable state.

PATHOPHYSIOLOGY – FLOW
CHART

CLINICAL MANIFESTATIONS
 Petechiae
 Ecchymoses
 Oral and rectal bleeding
 Prolonged bleeding from venipuncture
 Hypoxia
 Hypertension
 Tachycardia
 Dizziness, vomitting, nausea
 Severe bleeding during menstruation

RISK FACTORS
 Blood transfusion reaction
 Cancer, especially certain types of leukemia
 Inflammation of the pancreas (pancreatitis)
 Infection in the blood, especially by bacteria or fungus
 Liver disease
 Pregnancy complications (such as placenta that is left behind
after delivery)
 Recent surgery or anaesthesia
 Severe tissue injury ( as in burns and head injury)
 Large hemangioma (blood vessels that are not formed properly.

FINDINGS
 CBC (Complete Blood Count) : includes a platelet count
in DIC, platelets are often low.
 Blood smears : from individuals with DIC often show
decreased number of platelets and presence of large platelets
and fragmented red cells (schistocytes)
 D- Dimer : a test that detects a protein that results from clot
breakdown, it is often markedly elevated with DIC if normal than
DIC is unlikely

MEDICAL MANAGEMENT
 Replacement therapy:
 Coagulation factor deficiency require replacement with fresh
frozen plasma (FFP)
 Platelet transfusion should be used to maintain a platelet
count greater than 30000/ microlitre and 50000/microlitre.
 Fibrinogen is replaced with cryoprecipitate. One unit of
cryoprecipitate usually raises the fibrinogen level by 6-8
mg/dL, so that 15 units of cryoprecipitate will raise the level
from 50-150 mg/dL

 Heparin therapy: In some cases, heparin therapy is
contraindicated, but when DIC is producing serious clinical
consequences and the underlying cause is not rapidly reverible,
heparin may be necessary.
Dose: 500-750 unit/hour is necessary.

COMPLICATION
 Acute kidney injury
 Change in mental status
 Hepatic dysfunction
 Caardiac tamponade
 Hemothorax
 Intracerebral hematoma
 Stroke

NURSING MANAGEMENT
 ASSESSMENT
 Subjective Data :Patient feels chest pain
Shortness of breath (SOB)
Pain in affected limb
Headache
Dizziness
Double vision
 Objective Data: Erythema
Warmth of affected area
Swelling
Melena
Petechiae
Uncontrolled bleeding

 Impaired gas exchange related to oxygen carrying capacity of
blood, possibly evidenced by abdominal arterial blood
gases(ABG)
 Assess the clients breath sounds. Assess for signs od bloody
sputum
 Monitor oxygen saturation and assess arterial blood
gases(ABG)
 Perform chest physiotherapy

 Ineffective tissue perfusion, related to blood circulation
obstruction , possibly evidenced by abddominal blood profile
and capillary refill greater than 3 seconds.
 Assess client’s level of consciousness
 Assess arterial blood gases (ABG)
 Monitor platelet count

 Risk for bleeding , related to side effects of drugs taken,
possibly evidenced by abnormal blood profile.
 Assess the heart rate and blood pressure of the patient.
 Observe for signs of external bleeding from the
gastrointestinal and genitourinary tract
 Monitor hemoglobin and hematocrit levels.

WHAT IS
HYPOPROTHROMBINEMIA?
 Defined as prothrombin deficiency in the blood usually due to
vitamin K deficiency or liver disease (especially obstructive
jaundice) and resulting in delayed clotting of blood or
spontaneous bleeding (as from the nose or into the skin, also
called prothrombinopenia.

ETIOLOGY
 Genetic defect
 May be acquired as a result of another disease process
 Adverse effects of medication
 Exclusively breast-fed infants are acquiring lower vitamin K as
compared to formula-fed infants.
 Vitamin K deficiency
 Severe liver disease
 Disseminated intravascular coagulation (DIC)
 Warfarin overdose
Hypoprothrombinemia can be the result of:

PATHOPHYSIOLOGY
 Hypoprothrombinemia, disease characterised by a deficiency of
the blood clotting substance prothrombin, resulting in a tendency
of prolonged bleeding
 It is usually associated with a lack of vitamin K which is
necessary for the synthesis of prothrombin in the liver cells
 In adults, this condition occurs most commonly in cases of
obstructive jaundice in which the flow of bile to the bowel is
interrupted ; bile is necessary for the intestinal abortion of vitamin
K
 In the newborn, a lack of prothrombin leads too a condition
known as Hemorrhagic disease of the newborn,characterised by
spontaneous internal and external hemorrhage although this
abnormal bleeding tends to run a short, self- limited course,it can
sometimes have fatal outcomes.

CLINICAL MANIFESTATIONS
 Ecchymosis after minimal trauma
 Epistaxis
 Post operative hemorrhage from the incisions
 Hematuria
 Gastrointestinal tract bleeding
 Prolonged bleeding from a venipuncture
The major manifestations of hypoprothrombinemia are:

FINDINGS
 Factor assay – To observe the performance of specified
factors (11) to identify missing/poorly performing factors. These
lab tests are typically performed first in order to determine the
status of factor.
 Prothrombin blood test- To determine if patient has
deficiency or low levels of factor 11
 Vitamin K test - Performed to evaluate bleeding of unknown
causes, nosebleeds and identified bruising. However, the exam
is rarely used as a prothrombin blood test in performed
beforehand.

MEDICAL MANAGEMENT
 Treatment is carried to control haemorrhages, treating underlying
causes and taking preventive steps before performing invasive
surgeries.
 Hypoprothrombinemia can be treated with periodic infusions of
purified prothrombin complexes.
 A known treatment for hypoprothombinemia is Menadoxime.
 4-Amino-2-methyl-1-naphthol (vitamin K5) is another treatment
for hypoprothrombinemia.

NURSING MANAGEMENT
 ASSESSMENT
 SUBJECTIVE DATA : Backache
dizziness
bleeding gums
joint pain in the knees
 OBJECTIVE DATA : Blood in vomit
Dark, smoky urine
Tachycardia
High blood pressure

 Potential for bleeding related to hypoprothrombinemia
 NURSING INTERVENTION
 Review laboratory results for coagulation such as platelet
count, prothrombin time (PT) activated partial thromboplastin
time (aPTT) ,fibrinogen, bleeding time, fibrin degradation
products, activated coagulation time(ACT)

 NURSING DIAGNSIS 2
 Potential for injury related to formation of venous thrombus
 to decrease the incidence of thrombus in the pelvic veins/
deep leg veins, exercises are done
 Adequate hydration is given to the patient
 Avoid the patient having venous constriction such as crossing
legs, wearing stockings or any garments that compress the leg
veins

 Potential for injury related to heparin therapy
 safely monitor the patient who is being anti- coagulated with
heparin
 Do regular assessment to determine platelets count
 Ensure that the patient receiving heparin is not taking other
medications that could potentiate or interfere with the intended
therapeutic action of heparin.

WHAT IS THROMBOCYTOPENIA?
 Defined as the subnormal amount of platelets in the circulating
blood
 Normal platelet count is 1.5 lakhs to 4.5 lakhs /microlitre.
Thrombocytopenia is defined as a platelet disorder having
platelet count less than 1.5 lakhs/ microlitre.
 Not usually clinically detected until the platelet count falls to
levels below 1 lakh/ microlitre. However, a recent fall in the
platelet count by 50% while still in the norml range, may herald
severe clinical problems and require active follow- ups .Eg: HIT.

ETIOLOGY
 Platelet disorders can be inherited but vast majority are acquired.
Acquired disorders occur because of decreased platelet
production, or increased platelet production and many
abnormalities occur following ingestions of some foods and
drugs.
1. Decreased platelet production
a. INHERITED
 Fanconi’s Syndrome (Pancytopenia)
 Hereditary Thrombocytopenia
b. ACQUIRED
 Viral infections
 Chronic alcoholism
 Exposure to ionising radiations
 Malignant hematologic disorder

ETIOLOGY
2. Increased platelet destruction
a) NON IMMUNE
 Pregnancy
 Infection
 Severe burns
b) IMMUNE
 Human immunodeficiency virus infection
 Drugs induced

ETIOLOGY
3. Drugs, spices and vitamins causing abnormalities in platelet
function
a) SUPPRESSION OF PLATELET PRODUCTION
 Thiazide diuretics, alcohol, estrogen and chemotherapeutic drugs
b) ABNORMAL PLATELET AGGREGATION
 Antibiotics : Penicillin, Cephalosporin
 Analgesics: Aspirin and Aspirin containing drugs
 Heparin
 Vitamins: Vitamin C and Vitamin E

PATHOPHYSIOLOGY
 The major signs of hrombocytopenia observable by physical
examination are petechiae, echymoses and purpura.
 Petechiae occur only in platelet disorders.
 Client may give a history of menorrhagia, epistaxis and gingival
bleeding.
 Client is also questioned about recent viral infections which may
produce a transient thrombocytopenia; drugs in current use and
extent of alcohol ingestion

CLINICAL MANIFESATIONS
 Thrombocytopenia is commonly manifested in:
 Petechiae :Appearance of small flat red or reddish brown
microphagia ( tiny spots), due to the leak of RBCs out of the
blood vessels and into the skin.
 Purpura : When petechiae are numerous,the resulting reddish
skin bruise- like patch on the skin.
 Ecchymosis : large purplish lesions caused by hemorrhage.

 Venipuncture : Prolonged bleeding commonly after this
procedure indicates thrombocytopenia
 Weakness
 Fainting, dizziness
 Tachycardia
 Abdominal pain
 Hypertension

RISKS FACTORS
 Alcohol drinkers
 Pregnant women
 Autoimmune disease
 Are exposed to certain medicines
 Cancer
 Aplastic anemia
 Have certain genetic conditions
 HIV/AIDS

FINDINGS
 Diagnostic studies include complete laboratory studies to
ascertain the status of all blood components.
 The most commonly used test for assessment of platelets are
 platelet count
 Peripheral blood smear
 Bleeding bone
 In addition, bone marrow examination is performed to determine
the presence of megakaryocyte ( precursors of platelets in the
bone marrow) and other abnormalities such as :
 Neoplastic invasion
 Aplastic anaemia
 Fibrosis

 Physical examination
 The doctor performs a physical examination to look into the signs
and symptoms of bleeding, such as bruises or spots on the skin.
 The abdomen is inspected to see the signs of an enlarged
spleen or liver.
 The patient will be checked for certain for certain signs of
infection, such as a fever.

MEDICAL MANAGEMENT
 The primary treatment modalities for immunothrombocytopenia
purpura (ITP) are corticosteroid therapy and splenectomy.
 Steroids appear to decrease both antibody production and
phagocytosis of the antibody coated platelets.
 Splenectomy removes the principal organs involved in the
destruction of the antibody coated platelets.
 Blood or platelet transfusion : if the body platelets level becomes
too low, the lost blood can be replaced by transfusions of
packed red blood cells or platelets.

COMPLICATIONS
 Adverse effects of treatment
 Anemia
 Excessive or uncontrolled bleeding
 Gastrointestinal bleeding
 Intracerebral hemorrhage (bleeding in the brain)
 Severe nosebleeds

NURSINNG MANAGEMENT
 ASSESSMENT
 SUBJECTIVE DATA : Bleeding of gums
Inability to eat
Fatigue
Vomitting of blood
 OBJECTIVE DATA: Petechial rash
Spontaneous bleeding
Excessive post surgical bleeding

 NURSING DIAGNOSIS 1 :
 Risk for bleeding related to decreased platelet count
 NURSING INTERVENTIONS:
 Review laboratory results for coagulation status as appropriate
platelet count, prothrombin time, international normalized ratio (PT/
INR), activated partial thromboplastin time (aPTT), fibrinogen,
bleeding time, Vitamin K, activated coagulation time (ACT).
 Educate the at- risk patients and caregivers about precautionary
measures to prevent tissue trauma.

 risk for injury related to abnormal profile
 NURSING INTERVENTION:
 Thoroughly confirm patients to surroundings and teach how to call
for assistance.
 Obtain a physician’s order if restraints needed
 Eliminate or drop all possible hazards in the room such as razors,
medications and matches

 risk for infection related to suppression of the immune system by
steroids.
 NURSING INTERVENTIONS :
 Teach patients about general hygiene such as washing of hands
 Encourage fluid intake of 2,000- 3,000 ml of water each day, unless
contraindicated
 In case of infection, encourage patients to take antibiotics as
prescribed, instruct patient to take full course of antibiotics even if the
symptoms disappear.

RESEARCH
New research by the Georgia Institute of Technology
and Emory University published in the journal “ Biomaterials”
sheds new light on the mechanics and physics of blood clotting
through modeling the dynamics at play during a still poorly
understood phase of blood clotting called Clot Contraction.
The workhorses to stop bleeding are the platelets –
which are tiny cells of 2 micrometre in the blood and responsible
for the initial plug. The clot that forms is fibrin strands, which act
as glue scaffold that platelets attach to .
Blood clot contraction arises when these platelets
interact with the fibrin scaffold. To demonstrate the contraction,
researchers embedded a 3 mm mould with millions of platelets
and fibrin to recreate a simplified version of a blood clot.

SUMMARY
The nurse is often involved in the administration of blood and
blood products for treatment of these various disorders . Many of
these blood disorders are life threatening, others are easily
controlled with proper nutrition or regular medications.
Because blood and blood products transfusion are widely
used in the treatment of hematologic disorders. It is vital that we
understand the management and the proper techniques of
administration so that the patient will received safe and effective
care.

CONCLUSION
Today we all have discussed together about
the topic which is “BLEEDING, PLATELETS
AND CLOTHING DISORDERS AND ITS
NURSING MANAGEMENT”. In this we all got
to know about the types of the disorders, their
causes , signs and symptoms, their
assessment and diagnostic findings, their
medical and nursing management .

BIBLIOGRAPHY
 Blacks “medical surgical nursing” volume 2, 6th edition, page no.
2122-2127
 www.nih.gov
 www.mayoclinic,org
 www.nurselabs.com

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