In ICU, sometimes we have to refer our critically ill patients for surgical tracheostomy. The majority of these patients is suffering from MODS which include acute kidney injury. Very often, the level of urea varies from day to day, and also related to the frequency of dialysis in ICU. This is where we have a problem, since quite often the ENT surgeons request for a single digit of urea level. Their concern is bleeding associated with renal failure. Many times the procedure is delayed due to this request. This is what I read from uptodate.com:
The association between renal failure and bleeding was recognized more than 200 years ago. Impaired platelet function is one of the main determinants of uremic bleeding.
Clinical and Lab manifestations
1. Bleeding may involve the skin, oral and nasal mucosa, gingiva, gastrointestinal, urinary tracts and respiratory system. Excessive bleeding may also occur in response to injury or invasive procedures.
2. Although an association between bleeding time prolongation and uremia has long been suggested, there are no good studies demonstrating an increase risk of either spontaneous bleeding or bleeding with a procedure that is associated with prolonged bleeding time among patients with chronic kidney disease.
3. Degree of azotemia (elevation of BUN or creatinine) does not correlate with bleeding risk.
4. Patients may display increased sensitivity to aspirin. The platelet count is usually normal. Generally levels of circulating coagulation factors are normal and there is no prolongation of the PT or APTT unless there is coexisting coagulopathy.
Pathogenesis - the cause of uremic bleeding is multifactorial.
Causes of platelet impairment include intrinsic platelet defects, abnormal platelet-endothelial interaction, uremic toxins and anemia.
1. The most important factor is platelet dysfunction which is due to decreased platelet aggregation and impaired platelet adhesiveness.Contributing factors extrinsic to platelets include the action of uremic toxins, anemia, increased NO production, von Willebrand factor abormalities, decreased platelet production and abnormal interaction between the platelet and the endothelium of the vessel wall.
2. Uremic toxins:
Consistent with this postulate is the observation that mixing uremic plasma with normal platelets impairs platelet function. However urea is not the major platelet toxin and there is no predictable correlation between the BUN and the bleeding time in patients with renal failure. The addition of urea, guanidinoacetic acid or creatinine to the plasma did not affect platelet function. High levels of guanidinosuccinic acid and methylguanidine have been suggested as potential contributors to uremic platelet dysfunction, likely through simulation of NO production.
3. Anemia
Is common in patients with CKD and is primarily due to decreased renal erythropoietin production. Correction of anemia with blood transfusions or erythopoietic stimulating agents often improves platelet dysfunction. It has been proposed that rheologic factors play an important role in the overall relationship between anemia and platelet function.
4. Nitric oxide
NO is an inhibitor of platelet aggregation that is produced by endothelial cells and platelets. Studies have shown that platelet NO synthesis is increased, may be due to elevated levels of guanidinosuccinic acid (uremic toxin).
Treatment:
No specific therapy is required in patients without bleeding even in the setting of severe azotemia. Correction of platelet dysfunction is warranted in patients who are actively bleeding or who are about to undergo a surgical procedure. It is important to identify any sources of bleeding.
A number of modalities to improve platelet function and reduce bleeding, which vary in their onset and duration of action.
1. Dialysis:
Hemodialysis can partially correct the bleeding in about two thirds of uremic patients. It should be done without systemic anticoagulation.
2. Desmopressin
It is the simplest and most rapidly acting of acute treatment for platelet dysfunction in uremic patient. dDAVP is effective in at least one-half of patients and appears to act by increasing the release of large factor VIII: von Willebrand factor multimers from endothelial cells. Other factors may include increases in platelet membrane glycoprotein expression. dDAVP can be given intravenously at a dose of 0.3 mcg/kg (in 50 ml of saline over 15 to 30 minutes if IV) or 3 mcg/kg if intranasally. The improvement in bleeding time begins within one hour and lasts 4 to 8 hours. Tachyphylaxis typically develops after the second dose, perhaps due to depletion of endothelial stores of the factor VIII: von Willebrand factor multimers. Reduced urine volume and hyponatremia may occur in patients who have urine output.
3. Correction of anemia
Raising the Hb to about 10g/dL or higher will reduce the bleeding time in many patients, occasionally to a normal level. This can be achieved by RC transfusions or via administration of recombinant erytrhopoietic stimulating agents (ESAs). The improvement in platelet function persists for as long as the Hb remains elevated. ESAs may also have a direct beneficial effect on platelet function.
4. Estrogen
Most chronic control of bleeding can be achieved in many uremic patients by the administration of conjugated estrogens. The long term use is limited by estrogen related side effects. The mechanism is not well understood but may be due to decreased generation of NO.
5. Cryoprecipitate
The infusion of cryoprecipitate (10 units intravenously every 12 - 24 hours) can shorten the bleeding time in many uremic patients. The improvement in BT begins within one hour and lasts 4-24 hours; it is presumably mediated by the presence in cryoprecipitate of a substance that enhances platelet aggregation, such as factor VIII: von Willibrand factor multimers. The potential risk of infectious complications of this modality limit its use to patients with life threatening bleeding who are resistant to treatment with dDAVP and blood transfusions.
In my opinion, the surgeons (esp ENT surgeon in my case) should understand about the multifactoral causes of platelet dysfunction in uremia. There is no correlation in between the value of BUN and the risk of bleeding. If the patient is on regular dialysis, have a good Hb and no evidence of spontaneous bleeding there are no reasons to postpone the tracheostomy. If intermittent HD is done, anticoagulation should be avoided especially after the procedure. I should do more PDT in my ICU to overcome this problem.
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