EVALUATION OF HEMOSTATIC RISK IN THE SURGICAL

PATIENT

Preoperative Evaluation of Hemostasis

Several hematologic disorders may have an impact on the outcome of surgery.
The more common clinical situations faced by the surgeon are pre-existing
anemia and oral anticoagulation therapy. Assessment of bleeding risk should
also be considered in patients with liver or renal dysfunction. When feasible,
diagnostic evaluation of the patient with previously unrecognized anemia
should be carried out before surgery, because certain types of anemia
(particularly sickle cell disease and immune hemolytic anemias) may have
implications for perioperative management. Hemoglobin levels below 7 or 8
g/dL appear to be associated with significantly more perioperative
complications than higher levels.94 Determination of the need for preoperative
transfusion in an individual patient must consider factors other than the
absolute hemoglobin level, including the presence of cardiopulmonary disease,
the type of surgery, and the likelihood of surgical blood loss. Many patients
have anemia postoperatively secondary to blood loss and hemodilution and do
not necessarily require transfusion.
The most important component of the bleeding risk assessment is a directed
bleeding history. A detailed patient history can provide meaningful clues to the
presence of a bleeding tendency, such as easy bruising or a family history of
bleeding problems. Patients who are reliable historians and who reveal no
suggestion of abnormal bleeding on directed bleeding history and physical
examination are at very low risk for having an occult bleeding disorder.
Laboratory tests of hemostatic parameters in patients with low risk of bleeding
are not required. When the directed bleeding history is unreliable or
incomplete or when abnormal bleeding is suggested, a formal evaluation of
hemostasis should be performed before surgery
including measurement of the PT, the aPTT, and the platelet count.

Evaluation of Excessive Intraoperative or Postoperative

Bleeding
Excessive bleeding during or after a surgical procedure may be the result of
ineffective hemostasis, blood transfusion, undetected hemostatic defect,
consumptive coagulopathy, and/or fibrinolysis. Excessive bleeding from the
operative field unassociated with bleeding from other sites usually suggests
inadequate mechanical hemostasis.
Massive blood transfusion is a well-known cause of thrombocytopenia.
Bleeding after massive transfusion can occur due to hypothermia, dilutional
coagulopathy, platelet dysfunction, fibrinolysis, or hypofibrinogenemia.
Another cause of hemostatic failure related to the administration of blood is
hemolytic transfusion reaction. The first sign of a transfusion reaction may be
diffuse bleeding. The pathogenesis of this bleeding is thought to be related to
the release of ADP from hemolyzed red blood cells, resulting in diffuse platelet
aggregation, after which the platelet clumps are removed out of the
circulation.
Transfusion purpura occurs when the donor platelets are of the uncommon
Pl(A1) group. This is an uncommon cause of thrombocytopenia and associated
bleeding after transfusion. The platelets sensitize the recipient, who makes
antibody to the foreign platelet antigen. The foreign platelet antigen does not
completely disappear from the recipient circulation but attaches to the
recipient's own platelets. The antibody then destroys the recipient's own
platelets. The resultant
thrombocytopenia and bleeding may continue for several weeks. This
uncommon cause of thrombocytopenia should be considered if bleeding
follows transfusion by 5 or 6 days. Platelet transfusions are of little help in the
management of this syndrome, because the new donor platelets usually are
subject to the binding of antigen and damage from the antibody.
Corticosteroids may be of some help in reducing the bleeding tendency.
Posttransfusion purpura is self-limited, and the passage of several weeks
inevitably leads to subsidence of the problem.
DIC is characterized by systemic activation of the blood coagulation system,
which results in the generation and deposition of fibrin, leading to
microvascular thrombi in various organs and contributing to the development
of multiorgan failure. Consumption and subsequent exhaustion of coagulation
proteins and platelets due to the ongoing activation of the coagulation system
may induce severe bleeding complications.
Lastly, severe hemorrhagic disorders due to thrombocytopenia have occurred
as a result of gram-negative sepsis. The pathogenesis of endotoxin-induced
thrombocytopenia has been suggested to be related to lability of factor V,
which appears necessary for this interaction. Defibrination and hemostatic
failure also may occur with meningococcemia, Clostridium perfringens sepsis,
and staphylococcal sepsis. Hemolysis appears to be one mechanism in sepsis
leading to defibrination.

TESTS OF HEMOSTASIS AND BLOOD COAGULATION (TABLE

3-3)

The most important assessment of hemostasis is a careful history and physical

examination. Only the history can indicate whether the patient has a hemorrhagic
diathesis. These should include
*queries to determine whether there was untoward bleeding during a major
surgical procedure, or
*if there was any bleeding after a minor operation such as tonsillectomy,
circumcision, or dental extraction, or
*if spontaneous bleeding was ever experienced. If there is any suggestion of a
bleeding diathesis,
 *the age of onset and family history is helpful to determine whether a hereditary
or acquired defect should be investigated.
*Questions should uncover a history of exposure to toxic agents, oral
anticoagulants, and drugs that might interfere with hemostasis. Aspirin and
ibuprofen are two of the more common medications in this category.
*A history of a recent regimen of broad-spectrum antibiotics should alert the
physician to the possibility of a deficiency of vitamin K-dependent clotting
factors.
*Patients with malignant disease may have a variety of abnormalities, such as
compensated intravascular coagulation and increased circulating fibrin
complexes.
*Complex hemostatic disorders may accompany liver and renal failure.

Platelet Count
Because thrombocytopenia is the most common abnormality of hemostasis in the
surgical patient, determination of the level of circulating platelets is a critical
screening test. Spontaneous bleeding only rarely can be related to
thrombocytopenia with platelet counts greater than 40,000/mm3. Platelet counts
of 60,000 to 70,000/mm3usually are sufficient to provide adequate hemostasis
after trauma or surgical procedures if other hemostatic factors are normal.

Inspection of the blood smear has the additional advantage of permitting the
examiner to identify other pathologic features that may have meaning in the care
of the patient. The presence of nucleated red blood cells or abnormal white cells
can provide information important to the diagnosis. The presence of giant
platelets or large fragments of megakaryocyte cytoplasm will alert the examiner
to possible pathologic platelet function.

Bleeding Time
Bleeding time provides an assessment of both the interaction between platelets
and a damaged blood vessel and the formation of the platelet plug. Bleeding time
may be abnormal in patients with
thrombocytopenia,
qualitative platelet disorders,
von Willebrand's disease, and
also in some patients with factor V deficiency or
hypofibrinogenemia.
Aspirin ingested within 1 week will affect the results. The tests can be performed
by a variety of techniques that do not have the same normal times or the same
degree of accuracy.
The Duke method of measuring bleeding time, should not exceed 3½ min.
The modified Ivy method has an upper limit of normal of 7 min.

Other Tests of Platelet Function

Platelet aggregation can be assessed with a variety of induction agents to uncover
specific abnormalities. The results may be affected by venipuncture, blood pH,
temperature, duration of storage, and the equipment itself. The degree of
abnormality detected by the test is not correlated with the extent of untoward
bleeding. Aspirin is the most common cause of platelet aggregation abnormality.
Failure of platelets to aggregate with the addition of arachidonic acid indicates an
aspirin effect. The failure of platelets to aggregate with ADP, epinephrine, and
collagen is characteristic of Glanzmann's thrombasthenia. Abnormal platelet
aggregation with ristocetin occurs in von Willebrand's disease and in Bernard-
Soulier syndrome.

The ability of the platelets to liberate platelet factor 3 (phospholipid), essential in

tiny amounts at several stages of the blood-clotting process (see Fig. 3-3), also
can be measured. Impairment of platelet factor 3 release has been reported in
conditions described as thrombocytopathia. This defect can represent a primary
disease entity, but similar impairment has been described as a secondary
phenomenon in uremia and liver disease. The inability of the platelet to make
platelet factor 3 available for the clotting process may be a part of a more
fundamental surface membrane abnormality. The ability of ADP, epinephrine,
collagen, and arachidonic acid to liberate serotonin, b-thromboglobulin, or
platelet factor 4 can be measured.

Prothrombin Time
This test measures the speed of the events described earlier as the extrinsic
pathway of blood coagulation. A tissue source of procoagulant (thromboplastin),
a lipoprotein, is added with calcium to an aliquot of citrated plasma and the
clotting time determined. The laboratory should establish a normal dilution curve
and normal values daily. The PT will be prolonged in the presence of even
minute amounts of heparin. The presence of heparin, by its antithrombin action,
will artificially prolong the clotting time of the mixture so that it appears that the
prothrombin complex is low. Accordingly, an accurate prothrombin
determination cannot be carried out in a patient receiving anticoagulation
treatment with heparin until the heparin has disappeared from the plasma. This
should be at least 5 h after the last intravenous dose. The amount of heparin used
to maintain patency of an intravenous line is usually insufficient to alter the PT.
The use of tissue procoagulants in the test eliminates the roles of factors VIII, IX,
XI, XII, and platelets. Properly done, the test will detect deficiencies of factors II,
V, VII, X, and fibrinogen. The one-stage PT is the preferred method of
controlling anticoagulation with the coumarin and indanedione drugs.

Partial Thromboplastin Time

The PTT is a screening test for the intrinsic clotting pathway. The in vitro
clotting system now is sensitive to factors VIII, IX, XI, and XII, as well as the
factors normally detected by the one-stage PT. The range of normal with this test
varies with the product used. The patient's plasma must be compared with a
normal control sample.

The PTT, when used in conjunction with the one-stage PT, can help to place a
clotting defect in the first or second stage of the clotting process. If the PTT is
prolonged and the one-stage PT is normal, factors VIII, IX, XI, or XII may be
deficient. If the PTT is normal and the one-stage PT is prolonged, a single or
multiple deficiency of factors II, V, VII, or X or of fibrinogen may be present.
The PTT is also abnormal in the presence of circulating anticoagulants or during
heparin administration. It may be prolonged when heparin is used to maintain the
patency of an intravenous line. The sensitivity of the test is such that only
extremely mild cases of factor VIII or IX deficiency may be missed.

Thrombin Time
This test is of value in detecting qualitative abnormalities in fibrinogen and in
detecting circulating anticoagulants and inhibitors of fibrin polymerization. The
clotting time of the patient's plasma is measured after the addition of a standard
amount of thrombin to a fixed volume of plasma. Control samples of normal
plasma must be run in parallel. Failure of the clot to form, in the absence of
circulating inhibitors such as heparin or the fibrinolytic degradation products of
fibrin and fibrinogen, is consistent with severe diminution of fibrinogen, usually
well below 100 mg/dL. It is also prolonged when fibrinolysis is taking place.

Other Tests of Coagulation

The fibrinogen level can be determined by clotting-time measurements or

gravimetrically. Specific assays of coagulation factors are performed by
measuring the clotting time of plasma from patients congenitally lacking in one
of these factors and noting the effect of the addition of each factor. Relatively
simple tests permit identification of circulating anticoagulants. The simplest of
these are based on the retardation of clotting of normal recalcified plasma by
varying mixtures of the test plasma. The sensitivity of such tests usually can be
increased by incubating the test plasma with the normal plasma for 30 min at
body temperature before recalcification. Detection of factor XIII deficiency
requires a special test.

Tests of Fibrinolysis
Fibrin degradation products (FDP) can be measured by immunologic methods.
Normally, dissolution of a recently formed blood clot will not occur for 48 h or
more. When fibrinolysis is a significant factor in hemostatic failure, dissolution
of the whole blood clot is observed in 2 h or less. The test has the disadvantage of
being time-consuming in a circumstance where time may be of the essence. In
addition, a false impression of increased fibrinolytic activity may be gained from
clots formed in patients with high hematocrit levels or in thrombocytopenia, in
which red cells may fall away from the clot. The euglobulin clot lysis time and
dilute whole-blood or plasma-clot-lysis time are more sensitive indices and
permit more rapid evaluation of fibrinolysis.

The thromboelastogram is a graphic representation of clotting. The record

obtained provides information about the clotting time, the speed of fibrin
polymerization, and the clot's strength and tendency toward dissolution.

EVALUATION OF THE SURGICAL PATIENT AS A HEMOSTATIC

RISK

Preoperative Evaluation of Hemostasis

The patient's history provides meaningful clues to the presence of a bleeding
tendency. It is reasonable to use a questionnaire on which the patient indicates:
 prolonged bleeding or swelling after biting the lip or tongue,
 bruises without apparent injury,
 prolonged bleeding after dental extraction,
 excessive menstrual bleeding,
 bleeding problems associated with major and minor operations,
 medical problems receiving a physician's attention within the past 5 years,
 medications including aspirin or remedies for headache taken within the
past 10 days, and
 a relative with a bleeding problem.
Four levels of concern have been proposed on the basis of the history and
surgical procedure being considered. At Level I, the history is negative and the
procedure contemplated is relatively minor, e.g., breast biopsy or hernia repair:
no screening tests are recommended. At Level II, the history is negative,
screening tests may have been performed in the past, and a major operation is
planned, but the procedure usually is not attended by significant bleeding: a
platelet count and blood smear and PTT are recommended to detect any
thrombocytopenia, circulating anticoagulant, or intravascular coagulation. Level
III pertains to the patient whose history is suggestive of defective hemostasis and
also to the patient who is to undergo an operative procedure in which hemostasis
may be impaired, e.g., operating using pump oxygenation or cell savers, or
procedures in which a large, raw surface is anticipated. Level III also pertains to
situations in which minimal postoperative bleeding could be injurious, such as
intracranial operations. At this level, a platelet count and bleeding time test
should be performed to assess platelet function; a PT and PTT should be used to
assess coagulation, and the fibrin clot should be incubated to screen for abnormal
fibrinolysis. Level IV pertains to patients who present with a history highly
suggestive of a hemostatic defect. A hematologist should be consulted, and, in
addition to the tests prescribed for Level III patients, the bleeding time test should
be repeated 4 h after the ingestion of 600 mg of aspirin, provided that the
operation is scheduled to take place 10 or more days after this study. In the case
of an emergency procedure, platelet aggregation tests using ADP, collagen,
epinephrine, and ristocetin should be performed, and a TT is indicated to detect
any dysfibrinogenemia or a circulating, weak, heparin-like anticoagulant. Patients
with liver disease, renal failure, obstructive jaundice, and the possibility of
disseminated malignant disease should have a platelet count, PT, and PTT
performed preoperatively. In uremic patients the most common deficit is a
qualitative platelet abnormality. This is best detected by the bleeding time test.

Evaluation of Excessive Intraoperative or Postoperative Bleeding

Excessive bleeding during or shortly after a surgical procedure may be due to one
or more of the following factors:
(1) ineffective local hemostasis,
(2) complications of blood transfusion,
(3) a previously undetected hemostatic defect,
(4) consumptive coagulopathy, and/or
(5) fibrinolysis.
Excessive bleeding from the field of the procedure, unassociated with bleeding
from other sites, e.g., central venous pressure line, intravenous line, or
tracheostomy, usually suggests inadequate mechanical hemostasis rather than a
defect in the biologic process. An exception to this rule applies to operations on
the prostate, pancreas, and liver because operative trauma may stimulate local
plasminogen activation and lead to increased fibrinolysis on the raw surface. In
these circumstances 24 to 48 h interruption of plasminogen activation by the
administration of EACA may prove effective.

Although one may be reasonably certain on clinical grounds that surgical

bleeding is related to local problems, laboratory investigation must be
confirmatory. Prompt examination should be made of the blood smear to
determine the number of platelets, and an actual platelet count should be done if
the smear is equivocal. A PTT, a one-stage PT, and a TT all can be determined
within minutes. Correct interpretation of the results should confirm the clinical
impression or identify the problem.

As pointed out previously, massive blood transfusion is a well-documented cause

of thrombocytopenia. Although most patients who receive 10 units or more of
banked blood within a period of 24 h will be measurably thrombocytopenic, this
is usually not associated with hemostatic failure. Therefore, prophylactic
administration of platelets is not indicated, but if there is evidence of diffuse
bleeding, 8 to 10 packs of fresh platelet concentrates should be given empirically,
because no clear association has been documented between the platelet count,
bleeding time, and the occurrence of profuse bleeding.

Another cause of hemostatic failure related to the administration of blood is a

hemolytic transfusion reaction. The first hint of a transfusion reaction in an
anesthetized patient may be diffuse bleeding in an operative field that had
previously been dry. The pathogenesis of this bleeding is thought to be related to
the release of ADP from hemolysed red cells, resulting in diffuse platelet
aggregation, after which the platelet clumps are swept out of the circulation.
Release of procoagulants may result in progression of the clotting mechanism
and intravascular defibrination. In addition, the fibrinolytic mechanism may be
triggered.

Transfusion purpura is an uncommon cause of thrombocytopenia and associated

bleeding after transfusion. When this occurs the donor platelets are of the
uncommon PlA1 group. These platelets sensitize the recipient, who makes
antibody to the foreign platelet antigen. The foreign platelet antigen does not
completely disappear from the recipient circulation but seems to attach to the
recipient's own platelets. The antibody, which attains a sufficient titer within 6 or
7 days after the sensitizing transfusion, then destroys the recipient's own platelets.
The resultant thrombocytopenia and bleeding may continue for several weeks.
This uncommon cause of thrombocytopenia should be considered if bleeding
follows transfusion by 5 or 6 days. Platelet transfusions are of little help in the
management of this syndrome, since the new donor platelets usually are subject
to the binding of antigen and damage from the antibody. Corticosteroids may be
of some help in reducing the bleeding tendency. Posttransfusion purpura is self-
limited, and the passage of several weeks inevitably leads to subsidence of the
problem.

DIC and disseminated fibrinolysis occur intraoperatively or postoperatively when

control mechanisms fail to restrain the hemostatic process to the area of tissue
damage. Either process can cause diffuse bleeding and can be caused by trauma,
incompatible transfused blood, sepsis, necrotic tissue, fat emboli, retained
products of conception, toxemia of pregnancy, large aneurysms, and liver
diseases. It is important to distinguish between the two processes or the dominant
element causing intraoperative or postoperative bleeding. No single test can
confirm or exclude the diagnosis or distinguish between the two disorders. The
combination of thrombocytopenia, defined by smear or platelet count, positive
plasma protamine test for fibrin monomers, a low fibrinogen level, and an
elevated level of FDP provides strong indications for DIC. The euglobulin lysis
time provides a method of detecting diffuse fibrinolysis.

Diffuse intraoperative and postoperative bleeding is a complication of biliary

tract surgery in cirrhotic patients. This has been related to portal hypertension and
coagulopathy associated with chronic liver disease. The tests used to distinguish
DIC from fibrinolysis pertain. The therapeutic approach includes the intravenous
administration of vasopressin to effect a temporary reduction in portal
hypertension, and EACA to correct the increased fibrinolysis.
An operation performed in a patient with sepsis sometimes is attended by
continued bleeding. Severe hemorrhagic disorders due to thrombocytopenia have
occurred as a result of gram-negative sepsis. The pathogenesis of endotoxin-
induced thrombocytopenia has been studied in detail, and it has been suggested
that a labile factor, possibly factor V, is necessary for this interaction.
Defibrination and hemostatic failure also may occur with meningococcemia,
Clostridium perfringens sepsis, and staphylococcal sepsis. Hemolysis appears to
be one mechanism in sepsis leading to defibrination. Evaluation of these patients
includes platelet count, PT, PTT, and TT.

LOCAL HEMOSTASIS
Surgical bleeding, even when alarmingly excessive, is usually caused by
ineffective local hemostasis. The goal of local hemostasis is to prevent the flow
of blood from incised or transected blood vessels. This may be accomplished by
interrupting the flow of blood to the involved area or by direct closure of the
blood vessel wall defect. The techniques may be classified as mechanical,
thermal, or chemical.

Mechanical Procedures
The oldest mechanical method of effecting closure of a bleeding point or
preventing blood from entering the area of disruption is digital pressure. When
pressure is applied to an artery proximal to an area of bleeding, profuse bleeding
is reduced, permitting more definitive action. A classic example is the Pringle
maneuver of occluding the hepatic artery in the hepatoduodenal ligament as a
method of controlling bleeding from a transected cystic artery or from the surface
of the liver. Direct digital pressure over a bleeding site, such as a lateral rent in
the inferior vena cava, is also effective. The finger has the advantage of being the
least traumatic vascular hemostat. All clamps, including the so-called atraumatic
vascular clamps, do result in damage to the intimal wall of the blood vessel. The
most obvious disadvantage of digital pressure is that it cannot be used
permanently.

The hemostat also represents a temporary mechanical device to stem bleeding. In

smaller and noncritical vessels, the trauma and adjacent tissue necrosis associated
with the application of a hemostat are of little consequence. These minor
disadvantages are outweighed by the mechanical advantage that the instrument
offers to subsequent ligation. When bleeding occurs from a vessel that should be
preserved, relatively atraumatic hemostats should be employed to limit the extent
of intimal damage and subsequent thrombosis.
In general, a ligature replaces the hemostat as a permanent method of effecting
hemostasis in a single vessel. When a vessel is transected, a simple ligature
usually is sufficient. For large arteries with pulsation and longitudinal motion,
transfixion suture to prevent slipping is indicated. When the bleeding site is from
a lateral defect in the blood vessel wall, suture ligatures are required. The
adventitia and media constitute the major holding forces within the walls of large
vessels, and therefore multiple fine sutures are preferable to fewer larger sutures.

Historically, Aulus Cornelius Celsus devised the use of ligatures in the first
century a.d. Because of the strong influence of Galen, who was inclined to
cautery, this method did not gain popularity. Paré, in 1552, rediscovered the
principle of ligature. In 1800 Physick used absorbable sutures of buckskin and
parchment. In 1858 Simpson introduced the wire suture, and in 1881 Lister
employed chromic catgut. Halsted, in the early 1900s, emphasized the
importance of incorporating as little tissue as possible in the suture and indicated
the advantages of silk. In 1911 Cushing reported on the use of silver clips to
effect hemostasis in delicate vessels in critical areas. A wide variety of staples
made of different metals, relatively inert in tissue, have been used.

All sutures represent foreign material, and their selection is based on the
characteristics of the material and the state of the wound. Nonabsorbable sutures,
such as silk, polyethylene, and wire, evoke less tissue reaction than absorbable
materials, such as catgut, polyglycolic acid (Dexon), and polyglactin (Vicryl).
The latter are preferable, however, in the face of overt infection. The presence of
nonabsorbable material in an infected wound can lead to extrusion or sinus tract
formation. Wire is the least reactive of the nonabsorbable sutures but the most
difficult to handle. Monofilament wire and coated sutures have an advantage over
multifilament sutures in the presence of infection. The latter tend to fragment and
permit sinus formation.

Diffuse bleeding from multiple transected vessels may be controlled by

mechanical techniques that employ pressure directly over the bleeding area,
pressure at a distance, or generalized pressure. These techniques are based on the
premise that as pressure and flow are decreased in the area of vascular disruption,
a clot will develop. As a standard procedure of military surgeons in the
seventeenth century, pressure at a distance was effected by application of
tourniquets and other pressure devices at pressure points proximal to bleeding
sites. Now it is generally believed that direct pressure is preferable and is not
attended by the danger of tissue necrosis associated with prolonged use of
tourniquets. Gravitational suits have been used to create generalized pressure and
temporarily decrease bleeding from ruptured major intraabdominal vessels.

Direct pressure applied by means of packs affords the best method of controlling
diffuse bleeding from large areas. Rarely is it necessary to leave a pack at the
bleeding site and remove it at a second sitting. If this is done, several days should
elapse before removal, and the possibility of recurrent bleeding should be
anticipated. The question of whether hot wet packs or cold wet packs should be
applied has been investigated. Unless the heat is so great as to denature protein, it
may actually increase bleeding, whereas cold packs promote hemostasis by
inducing vascular spasm and increasing endothelial adhesiveness. Bleeding from
cut bone may be controlled by packing beeswax in the area. This material effects
pressure and is relatively non irritating to the body.

Thermal Agents
Galen's favoring of cautery influenced medicine for 1500 years, until the
teachings of Paré were appreciated. The use of cautery was revitalized in 1928,
when Cushing and Bovie applied this technique for effecting hemostasis of
delicate vessels in recessed areas, such as the brain. Heat achieves hemostasis by
denaturation of protein, which results in coagulation of large areas of tissue. With
actual cautery, heat is transmitted from the instrument by conduction directly to
the tissue; with electrocautery, heating occurs by induction from an alternating-
current source.

When electrocautery is employed, the amplitude setting should be high enough to

produce prompt coagulation but not so high as to set up an arc between the tissue
and the cautery tip. This avoids burns outside the operative field and prevents the
exit of current through electrocardiographic leads or other monitoring devices. A
negative plate should be placed beneath the patient whenever cautery is
employed to avoid severe skin burns. The advantage of cautery is that it saves
time; its disadvantage is that more tissue is necrosed than with precise ligature.
Certain anesthetic agents cannot be used with electrocautery because of the
hazard of explosion.

A direct current can also result in electrical hemostasis. Since the protein
moieties and cellular elements of blood have a negative surface charge, they are
attracted to the positive pole, where a thrombus is formed. Direct currents in the
20- to 100-mA range have been applied to control diffuse bleeding from large
serous surfaces. Argon gas has been applied successfully to the control of
bleeding from superficial erosions.
At the other end of the thermal spectrum, cooling has been applied to control
bleeding, particularly from the mucosa of the esophagus and stomach.
Generalized hypothermia is of little avail, since in order to reduce the blood flow
to visceral organs, the systemic temperature must be brought down to the level of
35°C. At this point shivering and ventricular fibrillation may occur.
Thrombocytopenia may also be a consequence of generalized cooling. Direct
cooling with iced saline is effective and acts by increasing the local intravascular
hematocrit concentration and decreasing blood flow by vasoconstriction.

Extreme cooling, i.e., cryogenic surgery, has been applicable particularly in

gynecology and neurosurgery. Temperatures ranging between -20 to- 180°C are
used, and freezing occurs around the tip of the cannula within 5 s. At
temperatures of -20°C or below, the tissue, capillaries, small arterioles, and
venules undergo cryogenic necrosis. This is caused by dehydration and
denaturation of lipid molecules. The muscular walls of large arteries are an
exception. Although the major arteries and blood may be frozen solid, the blood
contained in these vessels does not clot. When thawing occurs, normal circulation
is resumed.

Chemical Agents
Chemical agents vary in their hemostatic action. Some are vasoconstrictive, while
others have coagulant properties. Still others are relatively inert but possess
hygroscopic properties which increase their bulk and aid in plugging disrupted
blood vessels.

Epinephrine, applied topically, induces vasoconstriction, but extensive

application can result in considerable absorption and systemic effects. The drug
generally is used on oozing sites in mucosal areas, e.g., during tonsillectomy.

Historically, skeletal muscle was one of the first materials with locally hemostatic
properties to be employed, its use having been introduced by Cushing in 1911.
Shortly thereafter, hemostatic fibrin was manufactured. The properties required
for local hemostatic materials include handling ease, rapid absorption, hemostatic
action independent of the general clotting mechanism, and they should be
nonirritating. The most widely used of the commercially available materials are
gelatin foam (Gelfoam), oxidized cellulose (Oxycel), oxidized regenerated
cellulose (Surgicel), and micronized collagen (Avitene). All these materials act,
in part, by transmitting pressure against the wound surface, and the interstices
provide a scaffold on which the clot can organize (Table 3-4).

Gelfoam is made from animal skin gelatin that has been denatured. In itself
Gelfoam has no intrinsic hemostatic action, but it can be used in combination
with topical thrombin, for which it serves as an absorbable carrier. Its main
hemostatic activity is related to the contact between blood and the large surface
area of the sponge and to the pressure exerted by the weight of the sponge and
absorbed blood. Before Gelfoam is applied, the sponge should be moistened in
saline or thrombin solution and all the air should be removed from the interstices.

Oxycel and Surgicel are altered cellulose materials capable of reacting

chemically with blood and producing a sticky mass that functions as an artificial
clot. These substances are relatively inert and are removed by liquefaction in 1 to
4 weeks. They should be dry when they are applied. Like Gelfoam, these
materials are nontoxic and relatively nonirritating but are somewhat detrimental
to wound healing and require phagocytosis to be removed. Surgicel has been
shown to have an antibacterial effect. Microcrystalline collagen has been shown
to be as effective as other materials as a topical hemostatic agent for large oozing
surfaces.

Fibrin glue is commercially available in Europe and Canada but not in the United
States, because of the potential of disease transmission when fibrinogen is
obtained from pooled plasma. Single-donor fibrinogen can be mixed with bovine
thrombin to make the sealant. The glue is particularly effective in controlling
surface bleeding from the liver and spleen.