BLEEDING & TRANSFUSION

APPROACH TO THE PATIENT WITH MASSIVE

HEMORRHAGE
• To treat patients with massive hemorrhage  rapidly and simultaneously
accomplish three tasks:
• Identify the source or cause of bleeding
• Stop or limit the bleeding
• Restore the patient’s circulation
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Causes of bleeding:
• Conditions involving loss of vascular integrity  ex. bleeding from peptic ulcer; bleeding
from trauma patient with a severe liver laceration
• Conditions involving a derangement of the hemostatic process
• Massive hemorrhage begins with a loss of vascular integrity, but derangement
of hemostatic frequently develop as secondary problem and play a major
role in the exacerbation of hemorrhage
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Control of the source of bleeding
• The goals of operative conduct change from definitive management of all issues to
damage control
• Focus on life-threatening problems
• Restoration of vascular integrity; restoration of the circulation of the viscera and limbs
firstly
• Reestablishment of intestinal or wound closure (organs) latterly
• Sometimes the best option to control hemorrhage is not necessarily an open operation 
interventional radiologic and endovascular
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Restoration of the Blood Volume
• Initially, when massive hemorrhage can be addressed with operation  resuscitation with
blood products and other IV fluids only as adjunct
• Fluid resuscitation should not delay procedures to control hemorrhage
• The decision to transfuse should be based primarily on hemodynamic status rather than
on the hemoglobin or hematocrit level.  lab values do not reflect acute hemorrhage
• The goals of transfusion  increase intravascular volume  prevent development of
profound deficits in oxygen-carrying capacity.
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Restoration of the Blood Volume
• Stabilize High risk patients for recurrent bleeding (liver injury, GI bleeding) should
receive transfusion (target hematocrit 30%)
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Management of Coagulopathy
• Coagulopathy may promote massive hemorrhage, massive hemorrhage causes a coagulopathy.
• Coagulopathy occurs when there is massive hemorrhage in concert with injury to a large volume of tissue.
• Coagulopathy factors:
• Platelet dysfunction and diminished availability of platelets at the interface between the vascular endothelium
and luminal flow.
• Dysfunctional formation of thrombi in acidosis and hypothermia
• Accelerated thrombolysis
• Consumption of clotting factors.
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Management of Coagulopathy
• Increased recognition of coagulopathy  administration of plasma and platelets early in
the treatment of the patient with massive hemorrhage
• Massive transfusion protocol  1:1:1 transfusion  ratio stays balanced throughout the
resuscitation phase
APPROACH TO THE PATIENT WITH MASSIVE
HEMORRHAGE
• Management of Coagulopathy
• Increased recognition of coagulopathy  administration of plasma and platelets early in
the treatment of the patient with massive hemorrhage
• Massive transfusion protocol  1:1:1 transfusion  ratio stays balanced throughout the
resuscitation phase
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• It is still important to rule out the possibility of technical causes of bleeding,
surgeons should also be able to recognize coagulopathic bleeding and know
how to prevent it.
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Exclusion of technical causes of bleeding
• Technical problem (unligated vessel) Is more likely to be the cause of falling hematocrit
• In all cases of ongoing bleeding, the first consideration must always be to exclude a
surgically correctable cause
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Initial assessment of the Potential Coagulopathy
• First step  stable patient with potential coagulopathy  blood sample
• Obtain personal and family history of bleeding tendencies.
• Mucosal and superficial bleeding is suggestive of platelet and deep bleeding is
suggestive of a factor deficiency
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• Patient with normal INR and aPTT with ongoing bleeding may have impaired platelet
activity
• Inadequate platelet activity is frequently manifested as persistent oozing from wound
edges or as a low-volume bleeding
• Oozing in a patient who as an adequate platelet count and normal coagulation
parameters may be a signal of platelet dysfunction
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• In patients with platelet dysfunction caused by an inhibitor of platelet function, such as an
elevated blood urea nitrogen (BUN) level or aspirin, 1-desamino-8-D-arginine
vasopressin (desmopressin) is capable of significantly improving the plate- let dysfunction
• Less common causes of bleeding in patients with a normal INR and a normal aPTT include
factor XIII deficiency, hypofibrinogenemia or dysfibrinogenemia, and derangements in
the fibrinolytic pathwa
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• In the absence of a history of significant bleeding, patients with a normal INR and an
abnormal aPTT are likely to have a drug-induced coagulation defect.
• The agent most commonly responsible is unfractionated heparin.
• the administration of plasma (e.g., fresh frozen plasma [FFP]) will not correct the
anticoagulant effect of either unfractionated heparin or LMWHs
• FFP should be given to attempt to correct the aPTT
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• An increased INR in association with a normal aPTT is potentially a more ominous finding
in a patient with a coagulopathy.
• An elevated INR occurs with the administration of vitamin K antagonists (e.g., warfarin),
with variable effects on the aPTT. If the aPTT is normal, this usually demonstrates that
warfarin was only recently started (usually < 3 days of treatment) or has been
underdosed.
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• a coagulopathy is the result of a pure factor deficiency, and its degree is propor- tional
to the prolongation of the INR.
• Because warfarin acts by disrupting vitamin K metabolism, the coagulopathy may be
corrected by giving vitamin K
• If the patient is actively bleeding, vitamin K should still be given, but the primary
corrective measures should be to administer FFP
• FFP should be administered in an amount proportional to the patient’s size and the
relative increase in the INR
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• Cirrhosis is arguably the most serious of the causes of an elevated INR.
• It is a major problem not so much because of the coagulopathy itself but because of the
associated deficits in wound healing and immune function that result from dysfunction of
reticuloendothelial cells and hepatocytes.
• Generally, factor replacement should be instituted with FFP, but use of rVIIa is reasonable
in the setting of active hemor- rhage or any intracranial hemorrhage
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• Increases in both the INR and the aPTT may be the most problematic finding of all.
• the patient is likely to have multiple factor deficiencies; possible causes include
disseminated intravascular coagulation (DIC), severe hemodilution, and renal failure with
severe nephrotic syndrome.
APPROACH TO THE PATIENT WITH A
DERANGEMENT OF HEMOSTATIC
• Interpretation of Coagulation Parameters
• Hemodilution and nephrotic syndrome result in a coagulopathy that is attributable to
decreased concentration of coagulation proteins.
• Dilutional coagulopathy may occur when a patient who is given a large volume of
packed RBC units is not also given coagulation factors
• Treatment of dilutional coagulopathy should be directed at replacement of lost factors.
• FFP should be given first, followed by cryoprecipitate, calcium, and platelets.
• Transfusion should be continued until the coagulation parameters are corrected and the
bleeding stops.
APPROACH TO THE PATIENT WITH ANEMIA

• Anemia is common among hospitalized surgical patients.

• Anemia results from at least three factors:
(1) blood loss related to the primary condition or to the operation,
(2) serial blood draws (totaling, on average, approximately 40 mL/day in the ICU),30 and
(3) diminished erythropoiesis related to the primary illness.
APPROACH TO THE PATIENT WITH ANEMIA

• randomized trials comparing a restrictive RBC transfusion protocol

(hemoglobin concentration maintained at 7.0 to 9.0 g/dL) vs (hemoglobin
maintained at 10.0 to 12.0 g/dL) for critically ill patients have not
demonstrated harm with the restrictive approach.
• In fact, as suggested by the Transfusion Requirements in Criti-cal Care (TRICC)
study, the restrictive approach may even improve survival for younger or less
severely ill patients
APPROACH TO THE PATIENT WITH ANEMIA

• The decision whether to transfuse should be based on the patient’s current and
predicted need for additional oxygen-carrying capacity
• First, it is important to determine whether significant hypovolemia or active
bleeding is present.
• In such patients, liberal transfusion is indicated as a means of increas- ing
intravascular volume and preventing the development of profound deficits in
oxygen-carrying capacity
APPROACH TO THE PATIENT WITH ANEMIA

• In a hemodynamically stable but critically ill patient without evidence of active

hemorrhage, it is appropriate to take a more restrictive approach and
administer transfusion only when the hemoglobin concentration is less than 7.0
g/dL (hematocrit 21%)
• Less acutely ill patients can even be followed for hemoglobin concentrations
below 7.0g/dL, especially if they are asymptomatic and at minimal risk for
hemorrhage. In the absence of transfusion, iron supplementation should be
considered, particularly for menstruating women.
APPROACH TO THE PATIENT WITH ANEMIA

Acute Coronary Artery Ischemic Syndromes

• Currently, there is no consensus regarding the most appro- priate transfusion
strategy for patients with acute coronary artery ischemic syndromes, such as
active myocardial infarc- tion and unstable angina
• a target hemoglobin of 10 g/dL is generally considered acceptable for
patients with acute coronary artery ischemic syndromes or significant coronary
artery disease.
APPROACH TO THE PATIENT WITH ANEMIA

Symptomatic Anemia
• An additional consideration in the decision to transfuse blood is the oxygen-carrying
capacity that is necessary to prevent patient fatigue or discomfort.
• Typical symptoms of anemia include lightheadedness, tachycardia, and tachypnea
either during activity or at rest.
• The key judgment to make in deciding whether to treat symptomatic anemia with
transfusion is whether the anemia is truly compromising the patient’s health or
recovery.
APPROACH TO THE PATIENT WITH ANEMIA

Observation of Anemia
• Reviews of patients suggest that a hemoglobin below 5 g/dL results in
substantial increases in mortality, especially in elderly persons and patients
with cardiovascular disease.
• When RBC transfusion is not possible a number of temporizing measures can
be used
APPROACH TO THE PATIENT WITH ANEMIA

Observation of Anemia
• First, steps should be taken to minimize additional iatrogenic blood loss. Laboratory tests should be
restricted to those that are most likely to benefit the patient and should be conducted with the
smallest amount of blood possible
• Second, any impediments to native erythropoiesis should be removed: iron should be supplemented
(orally if possible), and the administration of recombinant erythropoietin should be considered.
• Third, 100% oxygen should be administered because oxygen dissolved in plasma contributes a
significant proportion of oxygen delivery at very low hemoglobin levels.
• Fourth, in extreme cases, consideration should be given to decreasing oxygen demand