قراءة
عرض

بسم الله الرحمن الرحيم

Bleeding in oral surgery and their management
A number of procedure performed in dentistry may cause bleeding. Under normal circumstances, these procedures can be performed with little risk to the patient.
However, the patient whose ability to control bleeding has been altered by drug or disease may be in grave danger unless the dentist identifies the problem before performing any dental procedure.

Bleeding disorders are conditions that alter the ability of blood vessels, platelets & coagulation factor to maintain homeostasis.
Bleeding disorders; divided into:
Inherited bleeding disorders: which are genetically transmitted.
Acquired bleeding disorders: occur secondary to diseases affecting vascular wall integrity, platelets, coagulation factors, drugs, radiation or chemotherapy for cancer.

The etiology of bleeding disorders:

Alteration in vascular walls.
Reduction in the platelets no., defective platelets or platelets dysfunction.
Deficiency in one or more of the coagulation factors.
Administration of anti coagulant drugs.
Inability to destroy free plasmin that result in abnormal clinical bleeding.

The phases of homeostasis for controlling of bleeding are:

Vascular phase: vasoconstriction of arteries & veins in area of injury. Begins immediately after injury.
Platelet phase: the platelet & vessel wall will become sticky, there is mechanical plug formation & stabilization of this plug will seals off openings of cut vessels. It begins seconds after injury.
Coagulation phase:
Blood lost into surrounding area coagulates through extrinsic & common pathway.
Blood in vessel in area of injury coagulates through intrinsic & common pathway.

The phases of homeostasis for controlling of bleeding are:

Fibronylitic phase: the fibrin lysing system is needed to prevent the intravascular coagulation & dissolve the clot once it had serves its function in homeostasis. This system involves plasminogin which converted in the liver to plasmin, also there is various plasminogin activator & plasmin inhibitors.

Classification of bleeding disorders:

Vascular disorders.

Platelets defects.

Coagulation disorders.

Fibrinolytic disorders.

Vascular disorders:

Abnormal vessel walls can result in excessive bleeding, which usually takes the form of bleeding into the skin (resulting in petechiae or bruising) or mucous membrane bleeding (which produces nose bleeds or gastrointestinal blood loss).
Vascular disorders:
Hereditary.
Acquired.

Vascular disorders:

Hereditary:Hereditary hemorrhagic telangiectasia (HHT).Ehlers – Danlos syndrome, osteogenesis imperfecta, pseudoxanthoma elastica and marfan syndrome.Acquired:Scurvy (vitamin C deficiency). Henoch–Schِnlein purpura. Corticosteroid-induced purpura. Senile purpura. Purpura associated with infection. Hyper gamma-globulinemic purpura.

Hereditary hemorrhagic telangiectasia (HHT).

It is inherited in an autosomal dominant manner and a genetic cause has been identified.
HHT is characterized by structural abnormalities of blood vessels and hereditary and acquired disorder of the connective tissues resulting in telangiectases; which are:
thin-walled, dilated, convoluted venules connecting directly to dilated arterioles that bleed easily.
The lesion are associated with epistaxis &other bleeding complication.

Hereditary hemorrhagic telangiectasia (HHT).

The bleeding may be mild or sufficiently serious to require multiple blood transfusions.
Arteriovenous malformations (AVMs) comprising direct connections between a branch of an artery and a vein are seen in a minority of patients with HHT; these may be found in the lung (causing cyanosis or polycythaemia) and in the brain (causing stroke or leading to brain abscess).
Diagnosis:
The family history.
The presence of telangiectases in the mouth or at endoscopy.
N.B:Some patients may lack these symptoms.

Hereditary hemorrhagic telangiectasia (HHT).

Management:
Local measures to control bleeding.
Correction of anemia by iron replacement.
Patients may require regular transfusion.
Surgery and embolization have been used for the treatment of pulmonary and cerebral AVMs, with varying success.
Genetic counseling should be offered.

Ehlers – Danlos syndrome, Osteogenesis imperfecta, Pseudoxanthoma elastica and Marfan syndrome. Which are a disorders of collagen with a variable inheritance pattern.
There is abnormal type III collagen which lead to vessel wall weakness.
Typically, patients have hyper flexible joints and elastic skin, and bleed abnormally following injury.
Management:
Treated by the local measures to control the bleeding.

Scurvy (vitamin C deficiency)

Causes an acquired abnormality of collagen leading to bleeding gums, and perifollicular and sub-periosteal hemorrhage.
Treatment:
Through adm. of vitamin C (250mg/day) which produces a rapid improvement.

Henoch–Schِnlein purpura is an immune-complex mediated hyper-sensitivity reaction leading to vasculitis.
It occurs most commonly in children after acute infection.
Patients present with purpura (typically affecting the buttocks and extensor surface of the legs), joint and abdominal pains, and haematuria. Renal failure may develop.
The condition is usually self-limiting.

Corticosteroid-induced purpura

It may occur in patients receiving long-term corticosteroid therapy, and in Cushing’s syndrome. Senile purpura
It is common and results from atrophy of the tissues that support cutaneous blood vessels.

Purpura associated with infection

Bacteria, viruses and rickettsia may cause purpura by direct vascular damage or as a result of immune-complex formation.
Overwhelming infection (particularly meningococcal septicemia) is often associated with purpura, thrombo-cytopenia and disseminated intravascular coagulation.
Hyper gamma-globulinemic purpura.
It is ch.ch. by polyclonal hyper gamma globulinemia associated with recurrent attack of purpura.
This occur due to deposition of the Cryoglobulins in the dermal vessels. So, the vessels become fragile and purpura will result.

Platelet disorders

Disorders of platelet number: The normal platelet count is 150,000–450,000 /mm3, regardless of age. There is some racial variation. The severity of the haemostatic defect is directly related to platelet count. Thrombocytopenia: Is defined as a platelet count less than 150,000/mm3. With normal platelet function, thrombocytopenia is rarely the cause of bleeding unless the count is less than 50,000/mm3. Thrombocytopenia should always be confirmed by examination of a peripheral smear.
It can be caused by decreased platelet production, increased destruction, sequestration, or a combination of these causes.

Platelet disorders

Disorders of platelet function:Congenital: The patients with congenital platelet function defects often present with mucocutaneous bleeding, and menorrhagia may be a significant problem in women.Bernard–Soulier syndrome: It is an autosomal recessive condition in which platelets lack glycoprotein (Gp) Ib, a receptor for von Willebrand factor; this results in defective adhesion to blood vessels. The platelet count is low and the platelets are abnormally large.

Platelet disorders

Glanzmann’s thrombasthenia: It is inherited in an autosomal recessive manner. Platelets lack GpIIb/IIIa, leading to defective aggregation. Patients usually present as infants with bleeding episodes. Platelet count and size are normal.Storage pool disorders: These are abnormalities of platelet-dense granules containing storage adenine nucleotides. The platelet count is normal.Grey platelet syndrome: The granules containing platelet-specific factors are abnormal.

Platelet disorders

Defects of platelet metabolism:
It is a rare disease, they include abnormalities of cyclo-oxygenase and thromboxane synthetase.
Von Willebrand's Disease (VWD):
Von Willebrand's Disease (vWD) is the most common inherited bleeding disorder in humans occurring in approximately 1% of the population.
Unlike hemophilia which is a sex-linked trait.
VWD may be discovered at any age and in either sex.

Platelet disorders

While hemophilia is usually associated with bleeding into joints and muscles, VWD is more commonly associated with easy bruising, recurrent nose bleeds, prolonged postoperative or post traumatic bleeding, excessive bleeding from the gums or mouth and menorrhagia. VWD is a complex hemostatic defect with multiple variations.
Diagnosis:
Diagnosis may require correlation of clinical observations with laboratory testing and family studies especially in mild forms of the disease.

Platelet disorders

The disease process is mediated by a qualitative or quantitative deficiency of a large glycoprotein called Von Willebrand Factor (VWF).
VWF is synthesized in the endothelial cells where it is stored in the Weibel-Palade bodies and in Megakaryocytes where it is stored in the granules of platelets.
The mature VWF subunit is assembled into multimers which are required for biological function.
VWF functions in homeostasis by permitting adhesion of platelets to exposed endothelium and by forming a non-covalent complex with Factor VIII, thus stabilizing and protecting it from rapid removal from the circulation.

Platelet disorders

The disease may be classified into three main types:
Type 1: partial quantitative deficiency of VWF (autosomal dominant, 70% of cases).
Type 2: qualitative deficiency of VWF (autosomal dominant / recessive, 25%).
Type 3: almost complete absence of VWF (autosomal recessive, 5%).

Platelet disorders

Disorders of platelet function:
Acquired:
Antiplatelet agents:
This will include aspirin, which irreversibly acetylates platelet cyclo-oxygenase, thereby impairing thromboxane A2 production; this may contribute to the haemorrhage caused by aspirin in the gastrointestinal tract. Low doses of aspirin, however, may help to prevent thrombosis.
The effect of aspirin lasts 1 week, until acetylated platelets have been lost from the circulation by natural wastage.
Other antiplatelet agents are dipyridamole (which has a complex mechanism of action including inhibition of phosphodiesterase), prostacyclin and analogues, ticlopidine, clopidogrel and GpIIb/IIIa inhibitors.

Platelet disorders

Defects of platelet aggregation:
Are seen in uraemic patients and can be improved by dialysis, Haemostatic improvement can also be achieved by desmopressin (DDAVP) or cryoprecipitate.
Hypergammaglobulinaemia:
It can interfere with platelet function. Plasma exchange may be helpful.
In cardiopulmonary bypass:
The flow through the bypass circuit causes trauma to platelets, leading to thrombo-cytopenia, platelet function abnormalities.
Platelet transfusions are often given to control excessive operative bleeding. Bleeding in these patients is often compounded because they have received aspirin preoperatively.
Aprotinin (an antiproteolytic agent) has been shown to reduce surgical bleeding by inhibiting fibrinolysis, but does not affect platelet function.

Myelo-proliferative disorders:

Are often associated with abnormal platelet function that may lead to a thrombotic or bleeding tendency.
Correction of the high platelet count often leads to an improvement in homeostasis.
Platelet disorders

Coagulation disorders

Coagulation disorders may be divided into:
Congenital:
Hemophilia A & B.
Disseminated intra vascular coagulation.
Acquired:
Anticoagulant drugs.
Vitamin K deficiency.
Massive blood transfusion.

Heamophilia A & B

Hemophilia A and B are the most common inherited disorders of coagulation, but are rare (1/10,000 population). Hemophilia A (deficiency of factor VIII:C) is about five times more common than hemophilia B (deficiency of factor IX). Both exhibit X-linked inheritance – all of the daughters of an individual with hemophilia are carriers of the disease and all of the sons are normal.

Heamophilia A & B

On average, one-half of the sons of a hemophilia carrier have the disease and one-half of the daughters are carriers.
Female carriers may have a sufficiently low factor level to appear as if they have mild hemophilia; this occurs because of extreme lonization.
In general, the severity of hemophilia in affected males is similar between generations, dependent on the resting level of factor VIII:C or IX .

Heamophilia A & B

Clinical features: At birth, patients with hemophilia are usually healthy, though bleeding from the cord and cephalo-haematoma may occur. The infant is usually asymptomatic until 6–12 months, when bruising becomes more obvious as activity and mobility increase. Bleeding from the mouth is common. During childhood severely affected patients, spontaneous bleeds may occur into the joints and muscles, including the psoas muscle.

Heamophilia A & B

Clinical features:
The frequency of spontaneous bleeding usually decreases in adults, but joints may already have been damaged. Intracranial hemorrhage is a life-threatening complication.
Spontaneous bleeds are common in mildly affected patients, but after injury bleeding continues until appropriate therapy is administered.

Disseminated intra vascular coagulation:

It is a systemic process that results in both thrombosis and hemorrhage. It is estimated to occur in 1% of hospitalized patients.
Patho- physiology:
DIC represents a massive activation of the coagulation cascade, that results in excessive production of thrombin, systemic intravascular fibrin deposition, and clotting factors and platelet consumption. The initiating factor is the release of tissue factor from a variety of causes:
Extensive endothelial injury.
The monocytes response to endotoxin exposure or to various cytokines.

Disseminated intra vascular coagulation:

Diagnosis:
The diagnosis of acute DIC relies on:
History.
Clinical setting (with particular attention to trauma, sepsis, malignancy, pregnancy, and miscarriages); moderate to severe thrombocytopenia.
Evidence of microangiopathic hemolysis on the peripheral smear.
Decreased in fibrinogen.

Anticoagulant drugs:

Warfarin and other oral anticoagulants interfere with the synthesis of vitamin K-dependent factors II, VII, IX and X, and proteins C and S.
Heparin is an inhibitor of serine proteases (particularly thrombin and factor Xa) and a co-factor for anti-thrombin, potentiating its action. Low molecular weight heparins have a greater effect on factor Xa inhibition than on thrombin. They cannot be monitored by APTT; an anti-factor Xa assay is required.
Newer anticoagulants include the heparinoids and hirudin (recombinant direct thrombin inhibitor). They are particularly useful in patients with heparin-induced thrombocytopenia.

Vitamin K deficiency

Vitamin K deficiency not caused by oral anticoagulants is usually a result of obstructive jaundice, malabsorption or dietary lack.
In infants, vitamin K deficiency leads to haemorrhagic disease of the newborn. The underlying cause should be treated, and vitamin K may be given orally or parenterally.

Massive blood transfusion:

Large volumes of transfused stored blood cause deficiency of labile haemostatic factors, particularly factors V and VIII, and platelets.

Fibrinolytic disorders

Primary fibrinogenolysis may develop if active plasmin generated in the circulation at a time when the clotting cascade is not in operation.
It occur in patient with liver disease, cancer of the lung or cancer of the prostate.
Severe bleeding result from depletion of fibrinogen (split by plasmin) & formation of the fibrin split products (with their anti coagulant property from the fibrinogen.




رفعت المحاضرة من قبل: صهيب عاصف الحيالي
المشاهدات: لقد قام 4 أعضاء و 30 زائراً بقراءة هذه المحاضرة






تسجيل دخول

أو
عبر الحساب الاعتيادي
الرجاء كتابة البريد الالكتروني بشكل صحيح
الرجاء كتابة كلمة المرور
لست عضواً في موقع محاضراتي؟
اضغط هنا للتسجيل