BLEEDING IN OTHER DISORDERS

2.4.2 RENAL FAILURE

Uraemia causes reversible bleeding disorder related to platelet
dysfunction.
There is as a result reduced platlet aggregation and adhesion.
There is also a reduction in platlets factor II and prolonged bleeding time.

The intravenous adminstration of desmopressin 0.3 ug/kg helps to
stop bleeding.
Cryoprecptitate also help to control the bleeding disorders.
Conjugated estrogens also of use in uremia bleeding disorders.

A vast number of etiologic agents have been identified here and
must be kept in mind when a patient presents with a bleeding
tendency.

**Acquired Disorders
Vitamin K deficiency
The causes of vitamin K deficiency are many.
Dietary intake may be poor, or the intake may be adequate but malabsorbed.
Vitamin K is a fat soluble vitamin, so any factor that causes decreased fat emulsification by bile salts can lead to malabsorption (e.g. biliary obstruction, decreased bile salt formation cholestasis, biliary fistula).

Antibiotic causes include oral antibiotics that can kill vitamin K producing bacteria in the gut, or cephalosporin antibiotics containing the N methylthiotetrazole side chain (e.g. cefoperazone, cefotaxime, cefamandole, moxalactam).

Other etiologies include parenteral alimentation without vitamin K supplementation, renal insufficiency, and hepatic dysfunction.

Vitamin K is a necessary cofactor in the y-carboxylation of glutamate residues of factors II, VII, IX and X as well as protein C and protein S. As these factors are referred to as the vatimin K-dependent factors. Without vitamin K, these coagulants cannot bind calcium properly and thus are not active.

Treatment
Vitamin K may be given orally or parenterally to correct coagulopathy form deficiency or to reverse the effects of warfarin.

Anticoagulant Drugs

Drugs that affect hemostasis are abundant and their numbers increase each year. More detailed information on hemoactive durgs can be found later in this chapter.
I Thrombocytopenia
Thrombocytopenia is generally defined as a platelet count less than 100,000/mm3 .

Bleeding is more common after surgery or injury in cases with counts from 50,000 to 100,000 mm3

Spontaneous bleeding usually does occurs with count below 20,000 and is common with count below 10,000.
The etiology of thromboeytopenia may be
- Decreased production of platelets
- Increased use, consumption or sequestration of platelets;
- Dilution

Decreased production may occur with various oncologic disorders or after chemotherapy. Consumption of platelets may occur in sepsis, disseminated intravascular coagulation (DIC), or thrombotic thrombocytopenic purpura, and sequestration can occur in the spleen.

Dilutional thrombocytopenia is possible after massive transfusion.

Many drugs can cause thrombocytopenia through an immune mechanism, antibodies are formed to platelet glycoproteins. These drugs are quinidine, sulfa drugs histamine antagonists oral hypoglycemies, gold salts, rifarnpin, and heparin.

The most common of these is heparin.
Chronic alcohol consumption may lead to alcohol induced thrombocytopenia.

Clinical
Clinical manifestations of thrombocytopenia include cutaneous petechiae or purpura, cucosal bleeding, easy bruising, and excessive bleeding after surgery or injury.

Treatment
Management involves correcting or reversing the underlying cause if found. Transfusion of platelet concentrates is indicated for active bleeding associated with thrombocytopenia, and to keep platelet counts above 10,000 to 20,000/ mm3.

If an invasive procedure or surgery is necessary in a thrombocytopenic patient, transfusion is most beneficial in providing hemostasis when given just before or during the procedure.

Multiple platelet transfusions often lead to formation of alloantibodies, thus decreasing the efficacy of repeated administration. Platelet transfusion is not indicated for empiric or prophylactic treatment during massive transfusion or resuscitation, unless there is clinical evidence of microvascular bleeding, or a prolonged bleeding time.**
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