CHAPTER 170
HEMOSTATIC DRUGS
Angela Borchers, DVM, DACVIM, DACVECC
KEY POINTS
• Coagulopathies may arise from defects in primary hemostasis,
secondary hemostasis, or the fibrinolytic system or may be of
multifactorial origin.
• In situations in which transfusional therapy is not effective, is not
available, or should be avoided altogether, the administration of
hemostatic drugs may be considered.
• Several hemostatic agents are currently being used as blood-
saving agents in the bleeding human and veterinary patient.
However, they cannot replace good medical therapy and surgical
technique.
Coagulopathies may arise from defects in primary hemostasis, sec-
ondary hemostasis, or the fibrinolytic system, or maybe of multifac-
torial origin. Although specific defects in primary or secondary
hemostasis are often treated with blood products to replenish defi-
ciencies, patients with multiple coagulation abnormalities, severe
single coagulation defects, hyperfibrinolysis, or unclassified coagu-
lopathies may not respond adequately to blood product administra-
tion. In these cases, administration of nontransfusional hemostatic
drugs may be considered as alternative treatment.
Clinical disorders in small animals that may benefit from non-
transfusional hemostatic drugs include von Willebrand disease
(vWD), hemophilia A and B, and other hereditary coagulation factor
deficiencies; hereditary thrombopathies such as Glanzmann’s throm-
boasthenia; acquired thrombopathies; and enhanced hyperfibrino-
lytic states after surgery or trauma.
Briefly, according to our current understanding, the hemostatic
system involves a delicate balance between procoagulation pathways,
anticoagulant pathways, and fibrinolysis.
Primary hemostasis initiates the formation of a platelet plug in
response to injury to a blood vessel. This process is mediated by von
Willebrand factor (vWF), which triggers the adhesion and activation
of platelets in response to exposed subendothelium and the forma-
tion of the primary platelet plug. Secondary hemostasis leads to
thrombin generation, which mediates the production of a fibrin fiber
meshwork that stabilizes the platelet plug. This process is initiated
by the exposure of perivascular tissue factor (TF) to factor VII in
blood, which leads to the activation of both the extrinsic and intrinsic
coagulation pathways, cumulating in thrombin production (see
Chapter 104).
Anticoagulant pathways include antithrombin-mediated factor
inactivation, protein C activation via the thrombin-thrombomodulin
complex, and TF pathway inhibitor (TFPI).
Fibrinolysis is initiated as tissue plasminogen activator and/or
urokinase, which cleave plasminogen into plasmin, are released
from the endothelium following injury, ischemia, or exposure to
thrombin. Plasmin degrades fibrin into soluble fibrin degradation
products.1-5
ANTIFIBRINOLYTIC DRUGS
The antifibrinolytic agents most commonly used in human and vet-
erinary medicine are the synthetic lysine analogs ε-aminocaproic
acid (6-aminohexanoic acid; EACA) and tranexamic acid (trans-4-
aminomethyl cyclohexane carboxylic acid; TXA).2,6-11
Aprotinin was previously used widely in human medicine for
both its antifibrinolytic and its antiinflammatory properties. The
drug was removed from the world markets in May 2008 due to
patient safety concerns, including sudden death, thrombotic compli-
cations, kidney failure, and myocardial infarction.8,12
Plasminogen acts as a fibrinolytic substance by binding to fibrin
at a lysine-binding site. Plasminogen is then converted into plasmin,
its activated form, which breaks down fibrin into fibrin degradation
products. Both, EACA and TXA reversibly block the lysine-binding
site on plasminogen, which is essential for binding to fibrin. This step
consequently blocks the activation of plasminogen on the surface of
fibrinogen and thereby prevents the breakdown of fibrin, although
plasmin generation does occur.6-8
Indications
In human medicine antifibrinolytic drug therapy has been used
extensively for the treatment of intraoperative hemorrhage, particu-
larly in cardiac surgery, liver transplantation, spinal surgery, and
orthopedic surgery. Other indications include gastrointestinal bleed-
ing, urinary tract and uterine hemorrhage (both the urinary tract
and the endometrium are rich in plasminogen activators),2,6 and
hyperfibrinolytic states, often seen after traumatic events with hypo-
perfusion or extensive tissue injury.3,4 A recent comprehensive
Cochrane review reported a significant reduction in blood loss and
need for blood transfusions after the use of in EACA in patients
undergoing major surgery.13 A similar finding was reported for TXA
in a meta-analysis of bleeding surgical patients.14 Antifibrinolytic
drugs have also been used to reduce hemorrhage associated with
thrombocytopenia.15
Contraindications
Use of antifibrinolytic drugs may be contraindicated in patients with
prothrombotic disease processes because there is a concern of pro-
moting thrombus formation. In veterinary medicine these include
patients with disseminated intravascular coagulation, aortic throm-
boembolism, immune-mediated hemolytic anemia, and hyperadre-
nocorticism.5 A few case reports have described diffuse thrombotic
events and pulmonary embolism in association with antifibrinolytic
drug therapy, but a recent comprehensive Cochrane review did not
find any supporting evidence for an increased incidence of throm-
botic events with the use of EACA or TXA.2,6,13 Use of antifibrinolytic
drugs for treatment of upper urinary tract hemorrhage should be
avoided because urinary tract obstruction can occur with thrombus
formation.
893
894 PART XX • PHARMACOLOGY

Table 170-1 Suggested Drug Dosages for Commonly Used Hemostatic Drugs
Drug Dosage Special Considerations

ε-aminocaproic acid 50-100 mg/kg IV loading dose (over 1 hr) followed Dilute in 0.9% saline, LRS, or D5W to
by 15 mg/kg/hr CRI or q8h until bleeding is 20-25 mg/ml
controlled5,*
15-40 mg/kg IV bolus followed by 500-1000 mg PO
q8h10
Tranexamic acid 10-15 mg/kg SC, IM, or slow IV followed by 1 mg/ 10 mg/kg q12-24h in renal disease
kg/hr CRI for 5-8 hr5,*
Desmopressin Intranasal product: 1-3 mcg/kg SC5 Give slowly IV
Parenteral product: 0.3-1 mcg/kg SC, IV Tachyphylaxis after repeat administration
(slow)5,28-30,35,38 Dilute: 10 ml (<10 kg BW) or 50 ml (>10 kg BW)
Parenteral product: 0.3 mcg/kg IV, SC q12-24h41* 0.9% saline for IV administration
Protamine 1 mg for every 1 mg (100 U) heparin slowly IV May cause severe anaphylaxis, hypotension, and
Decrease dose by 50% for every 30 min elapsed pulmonary hypertension
since heparin administration5,45,*
Conjugated estrogens 0.6 mg/kg IV q24h for 4-5 days47,* Doses of 1-2 mg/kg may cause myelotoxicity
50 mg PO q24h for 7 days46,*
0.02 mg/kg PO q24h for 5-7 days, then every 2-4
days60†
Recombinant factor VIIa 90 mcg/kg bolus q2h until hemostasis is achieved49*
Yunnan Paiyao Dogs: Capsules can also be opened and sprinkled on
<15 kg—1 capsule PO q12h wound
15-30 kg—2 capsules PO q12h
>30 kg—2 capsules PO q8h61‡
Cats: 1/2 capsule PO q12h61‡
CRI, Constant rate infusion; D5W, 5% dextrose in water, IM, intramuscularly; IV, intravenously; LRS, lactated Ringer’s solution; PO, per os; SC, subcutaneous.
*Dosage extrapolated from human literature.
†
Dosage extrapolated from veterinary literature for the treatment of urinary incontinence.
‡
Dosage based on anecdotal evidence.

Use of Antifibrinolytic Drugs in Cats
Little information is available to date on the use of antifibrinolytic
drugs in cats. The few reports of the use of antifibrinolytic drugs in
cats in experimental studies report adverse effects, including seizures
and myocardial injury.16,17 It is important to note, however, that the
dosing of antifibrinolytic drugs in these studies may not mimic clini-
cal use, and it is difficult to determine if the adverse effects were due
to the inhibition of fibrinolysis or were a direct effect of the drug
itself. For this reason, the author recommends caution in the use of
these drugs in feline patients until more information regarding safety
is available.
ε-Aminocaproic acid
EACA competitively inhibits plasminogen activation and at higher
doses may also directly inhibit plasmin. The elimination half-life of
EACA is 1 to 2 hours in adult human patients. The majority of the
drug is eliminated unchanged by renal excretion (65%); about 30%
to 35% undergoes hepatic metabolism to adipic acid, which is also
excreted in the urine.6-11,18
Reported adverse effects in human patients are dose dependent
and include hypotension, which is usually associated with rapid
intravenous administration, as well as nausea, vomiting, diarrhea,
generalized weakness, myonecrosis with myoglobinuria, and
rhabdomyolysis.
Limited data are available on the use of EACA in veterinary medi-
cine. In two separate studies, postoperative administration of EACA
significantly decreased the prevalence of postoperative bleeding in
greyhounds undergoing gonadectomy or limb amputation due to
appendicular bone tumors. Neither study reported clinical adverse
effects or thrombotic events.9,10
EACA can be administered intravenously or orally. The dosages
used in veterinary patients are largely extrapolated from human
medicine (Table 170-1). Reported dosages in dogs are in the range of
15 to 40 mg/kg intravenously over 30 minutes (rapid administration
can cause hypotension and vomiting) and/or 500 to 1000 mg orally
per greyhound dog q8h for 5 days, beginning the night of surgery.9,10
In human medicine EACA is given as a loading dose in an amount
on the order of 50 to 100 mg/kg over the first hour, followed by a
constant rate infusion of 15 mg/kg/hr thereafter.19
Tranexamic Acid
TXA is also a competitive inhibitor of plasminogen activation and at
high concentrations is a noncompetitive inhibitor of plasmin. Addi-
tionally, TXA competitively inhibits the activation of trypsinogen by
enterokinases and noncompetitively inhibits trypsin and thrombin,
hence prolonging activated thrombin time at high doses. TXA is
about 6 to 10 times more potent in vitro than EACA, with higher and
more sustained antifibrinolytic activity,7,20 and was shown to increase
thrombus formation in animal models in a dose-dependent manner.21
Similar to EACA, TXA is predominantly excreted unchanged via the
kidneys (95%). TXA has a terminal half-life of 2 to 3 hours.
Clinical indications are comparable to those for EACA, and a
recent randomized multicenter human trial (Clinical Randomisation
of an Antifibrinolytic in Significant Haemorrhage 2 [CRASH-2])
found that TXA safely reduced mortality in trauma patients with or
at risk of significant bleeding if given early (within 3 hours). TXA
given after 3 hours seemed to increase the risk of death due to
bleeding.22,23
Adverse effects are similar to those reported for EACA in human
patients and include hypotension after rapid administration and

clinical signs associated with the gastrointestinal tract (nausea, vom-
iting, diarrhea, abdominal cramps). Concerns regarding thrombo-
embolic complications were not supported by a recent Cochrane
review,8 but care should be taken in patients with renal disease.24
Convulsive seizures have been reported postoperatively after high
doses of TXA were given during cardiac surgery. A potential mecha-
nism for seizures is the structural similarity of TXA with
γ-aminobutyric acid.7
Limited data are available on the use of TXA in veterinary medi-
cine. An abstract presentation of a retrospective study evaluating 68
dogs with bleeding disorders severe enough to necessitate blood
transfusions reported no apparent difference in the total number of
blood products used in the group given TXA compared with a
control group. TXA was administered intravenously at a mean dose
of 8 mg/kg; adverse effects reported were vomiting in two dogs.25 The
human dose used in the CRASH trials was a loading dose of 1 g
(~15 mg/kg for a 70-kg person) over 10 minutes followed by 1 g
infused over the following 8 hours (~1.8 mg/kg/hr for a 70-kg
person).22 See Table 170-1 for more details regarding dosing.
Topical Antifibrinolytic Therapy
There is a growing interest in human medicine in the efficacy of
topical EACA and TXA in major surgical procedures associated with
significant blood loss.26 In addition, antifibrinolytic mouthwashes
can be beneficial in controlling bleeding associated with dental pro-
cedures in patients who have hemophilia or are taking anticoagulant
medications.27
DESMOPRESSIN
Desmopressin acetate (1-desamino-8-d-arginine vasopressin, or
DDAVP) is a synthetic vasopressin analog. DDAVP is pharmacologi-
cally altered from vasopressin by substitution of D-arginine for
L-arginine, which virtually eliminates the vasopressor activity (via V1
receptors) and significantly enhances antidiuretic activity and the
stimulation of endothelial release of factor VIII and vWF (via V2
receptors).6,18,28 The terminal half-life of DDAVP after intravenous
administration is 2.5 to 4.4 hours.6 The bioavailability of orally
administered DDAVP is not reliable because DDAVP is destroyed in
the gastrointestinal tract; hence, oral administration of DDAVP is not
recommended in the acutely bleeding patient. Plasma concentrations
of factor VIII and vWF approximately double to quadruple 30 to 60
minutes after intravenous administration and 60 to 90 minutes after
subcutaneous or intranasal administration.2 For this reason, patients
with hemophilia A (congenital deficiency of factor VIII) or type I
vWD (low circulating amount of vWF) who are bleeding spontane-
ously or are scheduled to have surgery benefit from the administra-
tion of DDAVP, often in conjunction with blood products.
Administration of DDAVP does not shorten the bleeding times
in patients with type II vWD (deficiency of high-molecular-weight
vWF multimers) or severe type III vWD (absence of vWF).2,5
DDAVP enhances platelet function in uremic thrombocytopathia
and other congenital defects of platelet function and also appears to
be effective in bleeding disorders caused by chronic liver disease, even
though these patients often have normal plasma concentrations of
vWF and factor VIII. Patients with prolonged bleeding times due to
antiplatelet drugs such as aspirin, ticlopidine, and clopidogrel may
also benefit from DDAVP administration. The mechanism of action
of DDAVP in human patients is not well understood and may be
associated with the induction of supranormal plasma concentrations
of vWF, greater concentrations of large multimers of vWF, or high
plasma concentrations of factor VIII.2
In Doberman Pinschers with type 1 vWD disease, DDAVP admin-
istration increased both the quantity of vWF and its functional
CHAPTER 170 • Hemostatic Drugs 895
activity, and there was also a proportional increase in vWF multimer
of all sizes in plasma; these results indicate that the primary effect of
DDAVP on hemostasis cannot be explained solely by a preferential
increase in large vWF multimers, as postulated in humans.29,30 In
addition, the quantitative increase in vWF appears much less pro-
nounced, with an approximately 25% to 70% increase above baseline;
in comparison, in humans increases of twofold to fivefold were
reported.30,31
The effect of DDAVP on factor VIII is dose dependent, and
increases ranged from 37% to 140% above baseline in dogs with
vWD and in healthy dogs, whereas German Shepherds with hemo-
philia A did not show substantial increases in plasma factor VIII
activity after DDAVP administration.32-34 Administration of DDAVP
improved hemostatic function in Doberman Pinschers with type 1
vWD.29,35
DDAVP is often used in human patients who undergo cardiac
surgery and other nonurgent elective surgical procedures that are
associated with relatively large blood losses, but the true benefit
is questionable in patients who do not have an underlying con-
genital bleeding disorder. A recent Cochrane review did not find
any convincing evidence that DDAVP reduces the need for blood
transfusions in patients who do not have congenital bleeding
disorders.36
Adverse effects of DDAVP administration include water retention
and hyponatremia due to its antidiuretic actions. Hypotension has
been reported after rapid intravenous administration in human
patients. The therapeutic effectiveness of DDAVP tends to vary, and
tachyphylaxis has been reported after repeat administration within
48 hours, probably because all available factor VIII and vWF has been
mobilized from the endothelium.6,18 Thrombotic events have been
reported in individual studies in human patients but did not reach
statistical significance in a multicenter review.36 DDAVP administra-
tion may induce transient thrombocytopenia due to excess platelet
aggregation in type II vWD.37 German Shorthaired and Wirehaired
Pointers are the only dog breeds reported to be affected with type II
vWD; hence, care should be taken when administering DDAVP to
these breeds of dogs.
In veterinary medicine, DDAVP has been used for the treatment
of diabetes insipidus and congenital bleeding disorders as well as
perioperatively in dogs undergoing removal of mammary gland
tumors to minimize spread of metastasis and survival of residual
cancer cells.38 DDAVP also proved to be effective in shortening bleed-
ing times in dogs with canine monocytic ehrlichiosis, aspirin-induced
platelet dysfunction, and chronic liver disease.39,40 DDAVP is available
for oral, parenteral, and nasal administration. For hemostatic pur-
poses the oral form is not recommended. Parenteral DDAVP is ideal
but its use maybe limited due to cost. The human dose for intrave-
nous desmopressin is 0.3 mcg/kg infused over 15 to 30 minutes.41 In
veterinary patients it is common to use the nasal product and inject
it subcutaneously at doses of 1 to 2 mcg/kg (see Table 170-1). The
dose can be repeated every 6 hours for three to four consecutive
doses, after which the therapy should be discontinued for 24 to 48
hours due to concerns of tachyphylaxis.
PROTAMINE
Protamine is a strongly positively charged, alkaline, low-molecular-
weight, polycationic amine derived from the sperm of salmon.
Approximately 67% of the amino acid composition in protamine is
arginine, which contributes to its strong alkalinity. Protamine is rou-
tinely used in human medicine after cardiopulmonary bypass to
reverse the anticoagulant effects of heparin but is also indicated for
the treatment or prevention of bleeding due to administration of
either unfractionated or low-molecular-weight heparin.18,42
896 PART XX • PHARMACOLOGY
The positively charged, polycationic protamine combines with
the negatively charged, polyanionic heparin, forming a protamine-
heparin complex that is devoid of anticoagulant activity. Excess prot-
amine is required to neutralize heparin because protamine competes
with antithrombin III for binding with heparin.18,42
Adverse reactions due to protamine administration in people are
often divided into three categories: (1) systemic hypotension, which is
thought to be the result of histamine release by mast cells after rapid
administration of protamine and the involvement of the nitric oxide
pathway42,43; (2) anaphylactic reactions, including antibody-mediated
and antibody-antigen complex–mediated anaphylaxis, which is often
a problem after repeat administration of protamine in diabetic
patients who take protamine-containing insulin daily; and (3) severe
pulmonary hypertension, which is thought to be due to protamine-
heparin complex–induced complement activation and generation of
thromboxane A2 and release of endothelin-1.42,44
Other reported adverse effects include delayed, noncardiogenic
pulmonary edema and paradoxic bleeding due to thrombocytopenia,
thrombocytopathia, and altered thrombin activity after administra-
tion of high doses of protamine. The “heparin-rebound effect” is
thought to be due to protein-bound heparin that is incompletely
bound by protamine. After the protamine-heparin complexes are
cleared from the circulation, remaining protein-bound heparin dis-
sociates slowly and binds to antithrombin III to produce an antico-
agulant effect. Other causes may include liberation of excess heparin
from extravascular spaces or intravascular surfaces, or excess break-
down of protamine by protaminases. Both excess doses of protamine
and the heparin-rebound effect can lead to excess bleeding after
protamine administration, and the two conditions may be difficult
to distinguish from each other and could be misinterpreted as resid-
ual heparin anticoagulation.18,42
Little is known about the use of protamine in veterinary
medicine, but in experimental research it appears to be effective
in stopping bleeding in animals that received unfractionated or
low-molecular-weight heparin. Adverse effects such as pulmonary
hypertension, anaphylactoid reactions, and bleeding after protamine
administration have been experimentally induced in dogs.18,42-44
The protamine dose is based on the original heparin dose given;
each milligram of protamine neutralizes 100 U or more of unfrac-
tionated heparin.45 Given the short half-life of heparin, the dose of
protamine should be reduced in accordance with the time elapsed
since the original heparin administration. A general guideline is
to halve the protamine dose for every 30 minutes that has elapsed
(see Table 170-1).45 Protamine should be given by slow injection
over 10 minutes in an effort to avoid hypotension or anaphylactoid
reactions.
CONJUGATED ESTROGENS
Conjugated estrogens shorten prolonged bleeding times and stop
hemorrhage in patients with uremia. They can be given orally or
intravenously and have reportedly shortened the bleeding time by
50% for at least 2 weeks in uremic patients.6,46 The effect of conju-
gated estrogens on bleeding times is longer lasting (10 to 15 days)
than that of DDAVP (6 to 8 hours); hence, their use should be con-
sidered when prolonged hemostasis is desired. Accordingly, conju-
gated estrogens should be administered for at least 4 to 5 days before
an event such as elective surgery to prevent bleeding in patients with
renal disease.6,18,47
The mechanism of action of conjugated estrogens on bleeding
time is unknown, but there is evidence that they increase the levels
of vWF and factors VII and XII.5,6 However, administration of
recombinant erythropoietin has become a routine treatment in the
management of uremic patients with chronic renal disease because
it helps to increase the hematocrit, shortens bleeding times, and
improves platelet adhesion. Hence, it appears that administration of
conjugated estrogens is rarely required in this subset of patients, and
they should be reserved for patients with acute and subacute renal
failure and used in combination with DDAVP.48
There is limited information about the usefulness of conjugated
estrogens for perioperative hemostasis in human and veterinary
patients. A few small human studies reported beneficial effects, and
conjugated estrogens were well tolerated with negligible adverse
effects.5,6,18 See Table 170-1 for dosing information.
RECOMBINANT FACTOR VIIa
Recombinant factor VIIa (rFVIIa) was developed for the treatment
of hemophilia A and B patients with antibodies against factor VIII
and IX, respectively. Factor VIIa is a vitamin K–dependent glycopro-
tein consisting of up to 406 amino acid residues that is originally
produced in baby hamster kidney cells and proteolytically converted
via chromographic purification into the active two-chain form of
rFVIIa.6,49
Even though hemophilia A and B are primarily deficiencies of
factor VIII and IX, respectively, the extrinsic pathway involving TF
and factor VII may also be impaired in hemophilia A patients.50 The
rFVIIa is believed to act in two ways: through the formation of a
TF–factor VIIa complex at the site of endothelial damage, which
initiates coagulation, production of thrombin, and clot formation;
and through a TF-independent mechanism in which rFVIIa at sup-
raphysiologic doses binds directly to the phospholipid membrane of
activated platelets, activating factor X and leading to a massive rise
in thrombin generation at the platelet surface.6 Hence, high doses of
rFVIIa (up to 10 times higher than physiologic concentrations of
factor VII) can compensate for a lack of factor VIII or IX in hemo-
philia A and B patients. This is called the bypass effect and may also
explain the effectiveness of rFVIIa in patients with platelet function
disorders.6,49
rFVIIa has been used successfully in human patients with bleed-
ing problems caused by hemophilia A and B, quantitative and quali-
tative platelet disorders, vWD, uremia, liver disease, trauma, and
surgical procedures, and it may also be administered to patients
without preexisting hemostatic defects.6 The half-life of rFVIIa is
short (2.7 hours), and it therefore needs to be administered fre-
quently (every 2 hours) or as a continuous infusion.
Adverse effects are rare, and reports of thromboembolic compli-
cations have been limited to a few case studies in human patients.51
In experimental dog models, rFVIIa administration resulted in a type
1 hypersensitivity reaction.50
rFVIIa has been used experimentally in dogs with hemophilia A
and B and vWD; it was effective in stopping nail cuticle bleeding in
dogs with hemophilia A and B but not in dogs with vWD.50 The
reported half-life in dogs was 2.8 hours, which is very similar to that
in humans. It is unclear if rFVIIa will find its way into veterinary
medicine. Clinical indications would be comparable to those in
human patients, but current cost and the occurrence of hypersensi-
tivity reactions in dog models may limit its future use.
YUNNAN PAIYAO
Yunnan Paiyao (or Yunnan Baiyao) is a Chinese herb mixture that is
commonly used to stop bleeding but is also employed for pain relief,
reduction of inflammation, and promotion of wound healing. The
herbal mixture was developed in the Yunnan province of China in
the early 1900s and was historically carried by foreign soldiers as a
hemostatic agent for trauma. The exact ingredients of this herbal
formula are kept secret, but the main active ingredient is thought to

be a pseudoginseng root called Panax notoginseng. Biochemical
analysis also revealed high concentrations of polysaccharides
(94% starch), calcium, and phosphorus.52-54
Yunnan Paiyao markedly shortened bleeding and clotting times
after experimental oral and topical administration in rabbits, rats,
and humans.53,55 Other mechanisms of action include dose-dependent
platelet activation.56 No adverse effects have been reported after oral
and topical administration, but in general, quality control and manu-
facturing regulations may be lacking for Chinese herbal products,
and there is concern about contamination with mycotoxins, heavy
metals, microbial agents, and pesticides.57 Yunnan Paiyao is currently
not approved by the U.S. Food and Drug Administration.
Yunnan Paiyao has been widely used in human and veterinary
medicine, but evidence supporting the clinical use of Yunnan Paiyao
is scarce. One randomized controlled trial evaluating the effect of
Yunnan Paiyao on the severity of exercise-induced pulmonary hem-
orrhage (EIPH) in horses showed no effect of the drug on EIPH
severity and other coagulation variables,58 but Yunnan Paiyao signifi-
cantly decreased blood loss in a group of human patients undergoing
maxillary surgery.59 See Table 170-1 for dosing information.
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