Coagulopathy

Mary Beth Callan , in Canine and Feline Gastroenterology, 2013

Hemostatic Disorder Causing Gastrointestinal Bleeding

Primary hemostatic disorders are more than probable than coagulopathies to cause gastrointestinal bleeding. Severe thrombocytopenia (platelet count <30,000/µL) is the most common principal hemostatic disorder causing mucosal surface bleeding. Differential diagnoses for severe thrombocytopenia include idiopathic thrombocytopenic purpura (ITP), secondary immune-mediated thrombocytopenia (associated with drugs, neoplasia, or infectious diseases), bone marrow suppression, or various infectious diseases (especially tick-borne diseases). ITP is the almost common cause of severe thrombocytopenia in dogs but is rare in cats. vWD and thrombopathia are other primary hemostatic disorders that may cause gastrointestinal haemorrhage, either spontaneous or associated with underlying gastrointestinal disorders. Dogs and cats with hereditary thrombopathies may present with petechiae, ecchymoses, excessive bleeding following surgery or trauma, or bleeding from various mucosal surfaces including the gastrointestinal tract. Well-characterized canine hereditary thrombopathies include thrombasthenic thrombopathia (also referred to as Glanzmann thrombasthenia), an absence or deficiency of the platelet glycoprotein (GP) IIb/IIIa receptor for fibrinogen (documented in Otterhounds and Great Pyrenees 17 ), Basset Hound thrombopathia (a platelet point transduction defect resulting in abnormal cyclic adenosine monophosphate [cAMP] metabolism eighteen ), platelet δ-storage pool deficiency (caused past decreased dumbo granule ADP content, reported in the American Cocker Spaniel 19 ), and platelet procoagulant deficiency (also referred to as Scott syndrome, which is a result of abnormal membrane PS exposure and described in the High german Shepherd 20 ). A thrombopathia caused past a platelet δ-storage pool deficiency has also been documented in blueish fume Persian cats with Chediak-Higashi syndrome. 21 Acquired platelet function defects may occur following ingestion of nonsteroidal antiinflammatory drugs (NSAIDs) or in association with uremia, cholestatic hepatic disease, and dysproteinemias. In gastrointestinal bleeding following NSAID administration, the cause is more likely gastrointestinal ulceration than an acquired thrombopathia, although concurrent platelet dysfunction could exacerbate bleeding.

Coagulopathies are more oft associated with cavity haemorrhage than mucosal surface bleeding, merely secondary hemostatic defects should be considered in patients with gastrointestinal bleeding. Mild to moderate thrombocytopenia has been documented in dogs with anticoagulant rodenticide poisoning, but marked thrombocytopenia (<xxx,000/µL) has besides been reported. 22 Melena, hematochezia, and other surface bleeding (e.grand., epistaxis, hematuria, gingival haemorrhage) have been noted in dogs with anticoagulant rodenticide poisoning and normal platelet counts. 23 A hereditary vitamin K–dependent coagulopathy attributable to defective γ-glutamylcarboxylase has been reported in Devon Rex cats with spontaneous hemorrhage into the thoracic cavity, articulation, and urinary float. 24,25 Hereditary FVII deficiency is typically considered an asymptomatic defect or a crusade of minor bleeding, although severe bleeding has been reported, most often subsequently surgery or trauma. 26 Hematochezia has been noted in FVII-deficient Beagles without other signs of colonic inflammation. 26 Of the intrinsic coagulopathies, hemophilia A (FVIII deficiency) or hemophilia B (Fix deficiency) may be more likely than others to cause haemorrhage within the gastrointestinal tract; severe gastrointestinal hemorrhage, potentially in association with coccidiosis, has been reported in hemophilic puppies. 27

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Coagulopathies

Astrid Nielssen , in Canine Internal Medicine Secrets, 2007

Hemophilia

11.

What are hemophilias A and B?

Hemophilias A and B are inherited coagulopathies resulting from deficiencies in functional factors Viii and Ix (Christmas gene), respectively. They are both 10-linked disorders, with clinical signs of disease identified in males and the rare homozygous female. The carrier heterozygous female person does not demonstrate signs of the disorder.

12.

What are the clinical signs of hemophilia A and B?

Both disorders effect in signs associated with disorders of secondary hemostasis. With hemophilia A, mildly afflicted animals with factor activity higher than 5% practise non tend to accept notable bleeding tendencies. Those with factor activity between 2% and 5% can demonstrate prolonged hemorrhage resulting from minor trauma. Those with factor activity less than 2% can have severe, spontaneous hemorrhage. With hemophilia B, severity of disease is associated with the size and activity of the fauna, with larger and more active dogs disposed to demonstrate the most astringent clinical signs.

13.

How are hemophilia A and B diagnosed?

The prothrombin time is within normal limits and the activated partial thromboplastin time is prolonged for both hemophilia A and B. The improver of normal fresh serum (which contains factor 9, but non cistron VIII) to the brute sample can correct the activated partial thromboplastin time of the animal with hemophilia B merely not A. Nevertheless, definitive diagnosis of hemophilia A or B requires specific factor assays.

fourteen.

How is hemophilia A treated?

Basic supportive care and abstention of trauma is essential for these dogs. Cryoprecipitate or fresh frozen plasma tin can be used to increase gene VIII levels and minimize bleeding. Cryoprecipitate contains 10 times more factor VIII per unit of measurement volume than plasma and is therefore a more than effective fashion to deliver this gene to the domestic dog without having to be concerned well-nigh book overload. Red blood prison cell transfusion, either with fresh whole blood or packed cells, may also be indicated in the markedly anemic dog. Clinical benefits with the use of deamino-d-arginine vasopressin (DDAVP) or fibrinolytic inhibitors in animals with hemophilia A have non yet been convincingly identified. Use of the homo factor 8 concentrate in these animals cannot exist recommended, given that as a foreign protein from another species, information technology is almost certain to elicit a profound neutralizing antibody response that could diminish the efficacy of any future therapies.

15.

How is hemophilia B treated?

Appropriate therapy for dogs with hemophilia B is similar to that for dogs with hemophilia A, with the exception that cryoprecipitate should not be used in these dogs because it does not contain pregnant concentrations of factor 9.

16.

How can these diseases exist prevented?

Unfortunately, coagulation studies cannot be used to try and identify females that are carriers for hemophilia A. With hemophilia B, however, about heterozygotes take factor 9 activeness levels in a range that falls above that of the affected animals and beneath that of unaffected individuals, thereby making this a reasonable screening test to identify most carriers. Dna assay is now also available to screen for carriers of these disorders in selected breeds.

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Hematopoietic System Toxicology

K. Tanaka , D. Bolliger , in Comprehensive Toxicology (3rd Edition), 2018

Abstract

Acquired coagulation disorders are caused by qualitative or quantitative changes in vasculatures, platelets, or any of the soluble coagulation factors and inhibitors. Acquired coagulopathy tin be associated with either hemorrhagic or thrombotic tendency, and triggered by a variety of underlying disease processes including traumatic injury, surgical procedures, liver failure, autoimmune disease, chronic inflammation, and infections. The primary approaches to acquired coagulopathy are to care for underlying illness(southward), and to apply blood component transfusion, hemostatic, or antithrombotic therapy as indicated. In addition to conventional transfusion of plasma and platelets, therapeutic options for hemorrhage and thrombosis have widened in the recent years as plasma-derived and recombinant factor concentrates, and novel antithrombotic agents take been introduced in clinical practice. The pathomechanism and diagnosis of acquired coagulopathy are discussed, and electric current treatment options for the management of coagulopathy will exist reviewed in this article.

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Liver

In Canine and Feline Gastroenterology, 2013

Coagulopathy

Coagulopathy is a complexity of both acute and chronic liver disease in dogs and cats. A recent study reported ane or more coagulation abnormalities (prolongation of coagulation times, changes in platelet counts, d-dimers, fibrinogen, or poly peptide C) in 24 (57%) of 42 dogs afflicted with liver disease. 18 Coagulation abnormalities are too common in cats with liver affliction and one study plant abnormalities in 18 (82%) of 22 cats with liver disease. 19

Multiple mechanisms of coagulopathy are possible in liver disease patients. In ALF cases such every bit xylitol toxicity in dogs, twenty HL in cats, 21 and cirrhosis in dogs, xviii loss of normal hepatocyte function results in severe coagulation gene deficiency. Vitamin G deficiency has as well been implicated in coagulopathy especially in cats in which cholestasis impedes bile common salt secretion, emulsification, and micellarization of fat and fat-soluble vitamins and fat-soluble vitamin absorption. 21 Concurrent inflammatory bowel disease and pancreatitis exacerbate this condition in many cats with cholangitis. 21 Finally, platelet abnormalities (cytopenia and cytopathy) may contribute to coagulopathy in dogs with liver disease. xviii,22

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Alveolar Hemorrhage and Rare Infiltrative Diseases

Harold R. Collard MD , ... Marvin I. Schwarz Dr. , in Murray and Nadel's Textbook of Respiratory Medicine (6th Edition), 2016

Coagulation Disorders

Coagulation disorders associated with DAH include disseminated intravascular coagulation, 103 idiopathic thrombocytopenic purpura, 104 thrombotic thrombocytopenic purpura, 105 acquired vitamin K deficiency, 106 and anti­phospholipid antibiotic syndrome. 107 Uniquely among coagulation disorders, primary antiphospholipid antibody syndrome–associated DAH is oft associated with capillaritis (eFig. 67-five). 108

All anticoagulant medications have been associated with DAH, including warfarin (Coumadin) and its derivatives, 109-111 thrombolytics, 112,113 agents targeting the platelet glycoprotein IIb/IIIa, 114-116 and clopidogrel. 117 In almost iatrogenically anticoagulated patients, correction of the coagulation defect resolves the DAH. It has been suggested that patients using coumarins with confirmed DAH are at take chances for the development of fibrosing interstitial pneumonitis. 118

DAH is common in patients with acute leukemia who take undergone induction chemotherapy and are thrombocytopenic (eFig. 67-6). 119-121 Although thrombocytopenia surely contributes to the DAH, these patients as well have evidence of DAD due to chemotherapy, oxygen toxicity, and infection that likely plays a central part.

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Avian Clinical Biochemistry

J.T. Lumeij , in Clinical Biochemistry of Domestic Animals (6th Edition), 2008

A Introduction

Hemostatic disorders in birds accept received less attention than those in mammals, but they can exist considered clinically relevant. Although the knowledge of avian bleeding disorders lags backside that of mammals, information technology was already in 1929 in chickens that the role of vitamin Grand in blood coagulation was discovered in (Dam, 1935). Currently avian hemostasis enquiry is still in its infancy, and the pathophysiology of many clinically intriguing bleeding disorders, such equally the conure bleeding syndrome, awaits farther clarification. Although blood coagulation in birds was addressed extensively in textbooks of avian physiology more than 30 years ago (east.1000., Sturkie and Grimminger, 1976), inclusion of divide chapters on avian coagulation in clinical textbooks was only initiated at the beginning of this century (Espada, 2000; Powers, 2000). A brief synopsis of avian coagulation volition be presented here, followed past diagnostic tests and a cursory description of some known coagulation disorders.

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Preoperative Pitfalls

Aimee M. Crago MD, PhD , Stephen R.T. Evans Medico , in Surgical Pitfalls, 2009

• Prevention

Coagulation disorders can be elucidated on history by inquiring about previous episodes of unusual haemorrhage. Recurrent GI bleeding, epistaxis, hematuria, menorrhagia, or hemarthroses advise a bleeding disorder. History of ESRD is associated with platelet dysfunction, and stigmata of ESLD are worrying for coagulopathy and thrombocytopenia. Collagen vascular diseases including lupus and Ehlers-Danlos are risks for intraoperative bleeding. Poor diet is associated with vitamin Grand deficiency and deficits in clotting factors. Organomegaly warrants further work-up to rule out liver or hematologic disorders. 58 In the absence of any of the previously cited take chances factors, no prove has been found to indicate that further piece of work-upward is necessary earlier elective surgery to exclude bleeding disorders. In fact, in a population of low-risk patients, the partial thromboplastin time (PTT) was found to have no predictive value as related to postoperative hemorrhage. 59 Preoperative grooming with known coagulation defects are described in Table 4-7. 60

Patients on oral anticoagulation or antiplatelet regimens require special care. Recovery of adequate platelet function requires at least 2 to iv days after stopping aspirin. Similar results affect direction of patients on clopidogrel and ticlopidine, irreversible inhibitors of platelet function. Complete recovery of platelet function takes seven days, and patients should be instructed to cease taking antiplatelet agents 5 to 7 days before constituent surgery. If the risk of acute thrombus is high as in patients with recently placed coronary artery stents, elective surgery should be postponed. Emergent surgery can be performed on patients taking aspirin or novel antiplatelet drugs because postoperative bleeding gamble is by and large express to wound hematoma. More severe bleeding risk is present, however, when patients are on both aspirin and clopidogrel considering these drugs deed synergistically and perioperative morbidity is peachy in this population. 61

Management of coumadin in the perioperative setting is based on the indication for which information technology is prescribed (Fig. 4-6). The complications of thromboembolic events require perioperative bridging with unfractionated heparin or low-molecular-weight heparin in patients with mechanical centre valves. Recent venous embolic illness (inside 1 mo) similarly indicates the need for perioperative heparin derivatives. 62–64

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Emergency and Critical Care of Small Mammals

Marla Lichtenberger DVM, Diplomate ACVECC , Angela K. Lennox DVM, Diplomate ABVP (Avian) , in Ferrets, Rabbits, and Rodents (Tertiary Edition), 2012

Utilise of Prothrombin and Partial Thromboplastin Times

Coagulopathy is not commonly reported in small mammals, although the number of cases of warfarin poisoning in ferrets may be similar to that seen in dogs and cats (ASPCA, personal communication). The use of coagulation parameters in small-animal critical care medicine is very important; nearly coagulopathies in such patients occur with liver disease, toxicity, and disseminated intravascular coagulation. Unpublished data (Grand. Lichtenberger and Z. Schwartz) for normal ferrets comparing reference laboratory values (Antech Diagnostics, Irvine, CA) for prothrombin time (PT) and partial thromboplastin time (PTT) and values derived from the in-business firm SCA2000 (Synbiotics Corporation, Kansas City, MO) gave results of 12 ± 1.5 seconds from the reference laboratory and 20 ± i seconds for the SCA2000 device. PTT from the reference laboratory was 18 ± 2 seconds and for the SCA2000 was 52 ± 19 seconds. In that location was a good correlation betwixt the PT results from the two different testing methods merely non for the PTT. To the authors' knowledge, no studies have been done in ferrets to determine normal activated clotting times (ACT). The ACT of ferrets may be like to the PTT measurements in this report.

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VENOM

J. White , in Encyclopedia of Forensic and Legal Medicine, 2005

Coagulopathy

Coagulopathy with promotion of haemorrhage is a mutual theme among venomous animals, especially snakes (Table 5). The mechanisms of coagulopathy in snake venoms are varied, with numerous points of attack (Table 7). Several distinct components in the venom may human activity synergistically. In particular, the combination of toxins that disrupt the coagulation pathways and hemorrhagins that disrupt small blood vessels, as seen in some viper venoms, is a potent crusade of hemorrhage. Common clinical features include persistent oozing of blood from the bite site and venepuncture or cannulation sites (Effigy iv), bleeding gums, and extensive hemorrhage or bruising into the skin of the bitten limb (Figure 5). In improver to the local damage caused past hemorrhage and the effects of blood loss, several organs are at special risk. Intracranial hemorrhage is usually lethal in this setting and can occur either spontaneously or post-obit otherwise piddling head trauma, as may occur when a snakebite victim collapses (Figure 6). The kidneys may be damaged (Figure 7), resulting in astute renal failure or fifty-fifty bilateral renal cortical necrosis (particularly some South American lance head viper bites, Bothrops spp., and Australian taipans). Burmese Russell's viper, Daboia russelli, can crusade anterior pituitary hemorrhage and infarction, resulting in Sheehan's syndrome (Figure viii). Recent surgery can also consequence in specific hemorrhage, as the hyperfibrinolysis often associated with snakebite coagulopathy causes breakdown of healing wounds. While many serpent venom coagulopathic toxins cause activation of clotting in vitro, in vivo, with one exception, information technology is hypocoagulability that predominates. Often there is partial or consummate defibrination, resulting in fluid blood ante- and postmortem. However, in the early stages of envenoming for a few of these venoms, particularly Australian brown snakes, Pseudonaja spp., at that place may be a brief initial period where thrombosis occurs prior to fibrinolysis, resulting in occlusion of critical vessels. This is believed to exist the explanation for early cardiac collapse and death following bites by these snakes. Equally hyperfibrinolysis will quickly activate, such thrombi will have been consumed by autopsy.

Tabular array 7. Broad classification of types of action of ophidian coagulopathic and hemorrhagic toxins

Grade of toxin Specific activity
Procoagulants Factor V-activating
Cistron Ten-activating
Gene IX-activating
Prothrombin-activating
Fibrinogen-clotting
Anticoagulant Poly peptide C-activating
Factor Nine/X-activating poly peptide
Thrombin inhibitor
Phospholipase A2
Fibrinolytic Fibrin(ogen) degradation
Plasminogen activation
Vessel-wall interactive Hemorrhagins
Platelet activity Platelet aggregation inducers
Platelet assemblage inhibitors
Plasma protein activators SERPIN inhibitors

© Julian White. Reproduced with permission.

Effigy four. Persistent bleeding from an intravenous site due to taipan envenoming coagulopathy. © Julian White. Reproduced with permission.

Effigy 5. Extensive bruising of the bitten limb due to green pit viper envenoming coagulopathy. © Julian White. Reproduced with permission.

Effigy 6. Computed tomography head browse showing intracranial hemorrhage secondary to Brazilian lance head viper envenoming coagulopathy. © David Warrell. Reproduced with permission.

Figure vii. Autopsy kidney showing astute impairment due to Russell'south viper envenoming. © David Warrell. Reproduced with permission.

Figure viii. Anterior pituitary infarction due to Burmese Russell'south viper envenoming. © David Warrell. Reproduced with permission.

One species of serpent, the Martinique viper, Bothrops lanceolatus, has venom components that crusade widespread thrombosis, resulting in deep-vein thrombosis and pulmonary emboli, with occasionally lethal effects.

The South American hairy caterpillars of the genus Lonomia tin can inflict, through peel contact, coagulopathic envenoming causing severe, even lethal, coagulopathy and hemorrhage.

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Reproductive Medicine

Amparo Santamaría , María Cerdá Sabater , in Encyclopedia of Reproduction (2nd Edition), 2018

Abstract

Coagulation disorders are one of the causes of impaired woman fertility. The knowledge of reproductive physiology and hematology is required to manage haemorrhage disorders such every bit von Willebrand disease, immune thrombocytopenia or thrombotic disorders that may lead to thromboembolism diseases or thrombotic complications mainly related with placenta-mediated complications throughout a woman's reproductive life in club to mitigate them. Management of reproductive issues requires knowledge of both reproductive physiology and hematology. This chapter reviews the most of import and common nonmalignant and malignant hematological disorders related to female fertility, in order to constitute the best coagulation screening that physicians will face with caring for women in her reproductive age.

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