Activated coagulation times of whole blood in normal dogs and dogs with coagulopathies

The activated coagulation time (ACT) of whole blood was determined at 37C and at room temperature for 42 normal dogs and eight dogs with naturally–occurring or experimentally–induced coagulation defects.
Normal ACT values ranged from 64 to 95 seconds at 37C, and 83 to 129 seconds at room temperature. In abnormal dogs, ACT was increased on 14 of 17 occasions that a prolonged activated partial thromboplastin time (APTT) was recorded: the ACT failed to detect an abnormality on three occasions the APTT was slightly increased. ACT determination at 37C correlated better with APTT than did ACT testing at room temperature.
The ACT test is simple, inexpensive and convenient. It is a useful screening test for intrinsic coagulation defects in the dog. It is suggested that the test be performed at 37C: at this temperature an ACT of 95 seconds or more in a dog warrants further investigation.     

Haemothorax associated with Angiostrongylus vasorum infection in a dog

Angiostrongylosis was diagnosed in a dog presenting with haemothorax on the basis of detection of Angiostrongylus vasorum first-stage larvae both in the pleural effusion and in faeces. A one-year-old, male, mixed-breed dog was presented with fever, depression and persistent cough of one month's duration. Clinical examination revealed temperature of 39.5 degrees C, loud bronchovesicular sounds on thoracic auscultation and attenuated cardiac sounds. Thoracic radiographs showed a moderate bilateral pleural effusion and a diffuse interstitial pulmonary pattern, with an alveolar pattern in one lobe. Routine haematology revealed anaemia and leucocytosis with eosinophilia, basophilia and thrombocytopenia. Coagulation assays showed a consumptive coagulopathy resembling disseminated intravascular coagulation. The relationship between haemothorax and the presence of A vasorum larvae in the pleural effusion is discussed. The dog was successfully treated with fenbendazole until negative for larvae on faecal examination. This case report indicates that A vasorum infection should be considered as a possible aetiological cause of haemothorax in dogs.     

Extradural haematoma secondary to brown snake (Pseudonaja species) envenomation

A 4-year-old Siberian Husky dog was treated with brown snake antivenom by his regular veterinarian after a witnessed episode of brown snake envenomation. The dog was discharged 5 hours post presentation despite an ongoing coagulopathy. The dog was presented to the emergency centre 2 hours later because the owner believed the dog to be in pain. Initial examination revealed an ambulatory but neurologically normal patient with thoracolumbar pain and laboratory evidence of a coagulopathy. Despite correction of the coagulopathy, the signs progressed to bilateral hind limb paresis after approximately 3 hours of hospitalisation, and continued to deteriorate over the next 56 hours to loss of deep pain perception in the right hind limb. Computed tomography imaging identified the presence of an extradural haematoma which was subsequently removed via a hemilaminectomy. Surgical decompression was successful in treating the spinal compression and the dog recovered with minimal complications. To our knowledge this is the first report of extradural haematoma secondary to coagulopathy induced by brown snake envenomation.     

Changes in blood coagulation parameters of red deer (Cervus elaphus) experimentally infected with malignant catarrhal fever

Changes in blood coagulation parameters were followed in four red deer (Cervus elaphus) experimentally infected with malignant catarrhal fever (MCF) of deer. Blood platelet counts, activated partial thromboplastin time (APTT), one-stage prothrombin time (OSPT), activated clotting time (ACT), plasma anti-thrombin III (ATIII) activity, fibrinogen degradation production (FDP) and fibrinogen levels were measured. Inoculated deer became pyrexic after 17 or 19 days. Thereafter they developed watery diarrhoea which rapidly became haemorrhagic. The course of the clinical disease ranged from four to six days before the animals were killed or died. All inoculated deer developed abnormalities in laboratory parameters of blood coagulation. These varied within and between animals, but the coagulation profiles of all four animals remained abnormal until death. Post-mortem findings included extensive systemic petechiation, severe haemorrhage in the alimentary canal and vasculitis with disseminated thrombosis. Abnormal coagulation parameters included extension of APTT and OSPT, increased FDP, decreased ATIII and platelet counts and increased fibrinogen levels. The increases in fibrinogen were compatible with the acute phase response. The other coagulation abnormalities and haemorrhage and thrombosis were indicative of disseminated intravascular coagulation (DIC) with consumption coagulopathy, ACT remained normal in all deer although final clot quality was considered poor.     

Radiotherapy-induced tumor lysis syndrome in a dog with thymoma

A 13-year-old, female, mixed-breed dog with a huge cranial mediastinal mass underwent radiotherapy (RT). On the following day, the dog presented with lethargy and anorexia. Hematological examination revealed elevated levels of blood urea nitrogen, creatinine, inorganic phosphorus, potassium, lactate dehydrogenase, creatine phosphokinase and aspartate aminotransferase, decreased calcium level, and metabolic acidosis. Urine output markedly decreased. The patient recovered with fluid therapy and diuretic therapy; however, died suddenly from an unknown cause 11 days after RT completion. Histopathological examination after necropsy showed thymoma in the cranial mediastinum and extensive tubular necrosis of both kidneys which may be due to RT-induced tumor lysis syndrome (TLS). This report suggests that the risk of TLS should be evaluated in dogs with thymoma who undergo RT.     

The Evaluation of Coagulation Profiles in Calves with Suspected Septic Shock

The purpose of the study reported here was to evaluate the haemostatic function in calves with suspected septic shock and to reflect the occurrence of disseminated intravascular coagulation (DIC). Twenty-six calves suspected of having septic shock (experimental group) and 10 clinically healthy calves (control group) were used. On admission, the experimental group of calves had been ill for an average of 2 days. Therapy was applied to the experimental group of calves. The packed cell volume (PCV), haemoglobin (Hb), white blood cell (WBC), red blood cell (RBC) and platelet (PLT) counts were determined. Blood smears for toxic neutrophil and schistocyte intensity were evaluated. For the coagulation profile, plasma activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), fibrinogen and fibrin/fibrinogen degradation products (FDPs) values were determined. Toxic neutrophils in blood smears were observed in 12 calves of the experimental group. APTT was prolonged in the experimental group compared with the control group (p < 0.05). Fibrinogen concentration was found to be higher in the experimental group than in the control group (p < 0.001). Total leukocyte counts were higher in the experimental group compared with the control group (p < 0.01). Platelet counts in the experimental group were lower than the control group (p < 0.001). However, when the individual values of coagulation profiles of each calf were evaluated, 8 calves had at least three abnormal coagulation profiles (APTT >72 s, PT >34.5 s, TT >33.7 s, FDPs >5 microg/ml, PLT < or = 150 x 10(3)/mm(3)) and abnormal erythrocyte morphology (schistocytes > or = 1). The most common abnormal tests in the coagulation profile were APTT and PT (7 cases), FDPs (6 cases), thrombocytopenia (4 cases), and schistocytes in blood smears (8 cases) in these 8 calves. The results of this study indicate that DIC might be a significant risk factor for mortality in calves with suspected septic shock.     

Thromboelastographic profile for a dog with hypocoagulable and hyperfibrinolytic phase of disseminated intravascular coagulopathy

The objective of this study is to report the use of thromboelastography as a diagnostic tool for the hyperfibrinolytic phase of disseminated intravascular coagulopathy in a dog with metastatic haemangiosarcoma. We established a cytological (i.e. fine needle aspirate) and histopathological (i.e. excisional surgical biopsy) diagnosis of haemangiosarcoma in a 10-year-old male castrated Bichon Frise with multiple dark purple dermoepidermal nodules on the ventral abdomen and medial stifle areas, multiple small pulmonary nodules and a solitary liver mass. The dog was treated with chemotherapy (AC protocol). Forty-nine days after completion of four treatment cycles, the dog was presented for recheck. Complete blood count revealed anaemia and mild thrombocytopenia. Chemistry profile showed no significant abnormalities. Analysis of haemostasis consisted of prolonged clotting times (prothrombin time, activated partial thromboplastin time), mild hypofibrinogenaemia and increased D-dimers. A presumptive diagnosis of disseminated intravascular coagulopathy was made. A re-calcified thromboelastography was simultaneously done to confirm the coagulopathy. Thromboelastographic tracings correlated with the plasma-based test results showing hypocoagulability (prolonged clotting times and prolonged thromboelastography clot kinetics; weaker clot with decreased fibrinogen levels, platelet count and lower thromboelastography tracing amplitude) and hyperfibrinolysis (increased D-dimers and increased D-dimers and increased thromboelastography lysis parameters). Based on these results, the dog was considered to be in the hyperfibrinolytic phase of disseminated intravascular coagulopathy. Results of the conventional haemostasis tests supported those obtained on thromboelastography. Humane euthanasia was performed because of poor prognosis and progressive disease, making further follow-up unavailable. As demonstrated in this case report, thromboelastography was found to be a helpful diagnostic tool for the diagnosis and monitoring of the hyperfibrinolytic phases of disseminated intravascular coagulopathy.     

Carcinocythaemia (carcinoma cell leukaemia) in a dog: an acute leukaemia-like picture due to metastatic carcinoma

An eight-year-old entire female boxer was presented with a two-week history of anorexia and lethargy and two-day history of unilateral left epistaxis. Clinical findings and laboratory test results suggested disseminated intravascular coagulation. On blood smear evaluation, occasional large epithelioid-like unclassified cells were detected. Occasionally these cells were organised in small clusters. Bone marrow examination revealed a marked infiltration by a malignant population of the same epithelioid-like cells. The dog was euthanased because of the guarded prognosis. Following histology and immunohistochemistry, a widespread undifferentiated carcinoma of unknown primary origin was diagnosed. To the authors' knowledge, this is the first case of carcinoma cell leukaemia reported in a dog. Carcinoma cell leukaemia is a rare oncological condition previously described in humans, characterised by non-haematopoietic neoplastic cells in peripheral blood.     

Failure of Routine Coagulation Screening Tests to Detect Heterozygous State of Bovine Factor XI Deficiency

In a survey of coagulation, biochemical and hematological parameters in cattle homozygous (deficient), heterozygous (carrier) and non-affected (normal) for Factor XI deficiency, only the Activated Partial Thromboplastin Time (APTT) results correlated with plasma Factor XI activity levels. The APTT results and the thrombokinetics for the deficient animals were markedly different from the results of either the carrier or normal animals. However, the APTT assay was shown not to be sufficiently sensitive to differentiate between the normal and carrier state for the coagulation disorder. Not only was there no statistical difference between the mean APTT results for the normal and carrier animals, but the thrombokinetics for fibrin clot formation for the two groups were also similar.     

Bilateral hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog

Objective: To describe an unusual site of hemorrhage in a case of anticoagulant rodenticide toxicity. Case summary: A dog treated for Brodifacoum anticoagulant rodenticide intoxication was referred for treatment of thrombocytopenia and dysuria. Sonographic examination revealed a large blood clot within the urinary bladder, extending proximally along both ureters, and a bilateral hydronephrosis. In this dog, management of the vitamin K₁‐dependent coagulopathy was unusually complicated by uremia and thrombocytopenia. New information provided: This is the first reported case of hydronephrosis secondary to anticoagulant rodenticide intoxication in a dog.     

Prekallikrein deficiency in a family of Belgian horses

A 7-year-old Belgian stallion hemorrhaged excessively after castration; the hemostatic mechanism was investigated. The horse had normal one-stage prothrombin time and markedly prolonged activated partial thromboplastin time (APTT). Results of intrinsic coagulation factor assays were all normal with the exception of prekallikrein activity, which was markedly reduced (less than 1% activity; value for control population, 63 to 150%). Two of this horse's full siblings, a brother and sister, had markedly prolonged APTT and low prekallikrein values (2.5% and less than 1%, respectively). The addition of plasma from a normal equine plasma pool corrected the prolonged APTT in the 3 Belgian sibling with low prekallikrein activity. Prekallikrein activity in 10 other closely related Belgian horses ranged between 12.5 and 64% (mean, 29.3%), compared with 63 to 150% (mean, 91%) in 10 mixed-breed horses. In the 3 Belgian siblings with low prekallikrein activity, the APTT approached normal after prolonged incubation (15 minutes) with the contact activator and in response to addition of an ellagic acid activator. The 3 Belgian siblings with low prekallikrein activity may be homozygous for prekallikrein deficiency, whereas the other close relatives may be heterozygous for the genetic defect.     

Mammary gland carcinoma in a dog with peripheral blood and bone marrow involvement associated with disseminated intravascular coagulation

A 7-year-old female Leonberger dog was referred to the National Veterinary School of Lyon Teaching Hospital with a 2-day history of anorexia and bleeding. A mammary mass had been removed 7 months earlier, but histologic examination was not performed. On physical examination, the dog was depressed and had pale mucous membranes and numerous petechiae and hematomas. Significant laboratory findings were moderate thrombocytopenia, prolonged prothrombin, activated partial thromboplastin, and thrombin times, hypofibrinogenemia, and increased concentration of fibrin(ogen) degradation products. A peripheral blood smear, buffy coat preparation, and bone marrow aspirate contained low numbers of large atypical cells that had moderate nuclear:cytoplasmic ratios, oval nuclei with multiple prominent nuclei, and basophilic cytoplasm with villous projections. A small nodule was found in the left inguinal mammary gland, and a fine-needle aspirate contained cells similar to those in blood and bone marrow. In samples of blood, bone marrow, and the mammary mass, the neoplastic cells were immunoreactive for cytokeratin. The diagnosis was mammary carcinoma with secondary disseminated intravascular coagulation (DIC) and disseminated tumor cells in bone marrow and circulating tumor cells in blood; this diagnosis was not confirmed by histopathologic examination. Owing to clinical deterioration and the poor prognosis, the dog was euthanized and a necropsy was not performed. This is the first report of a canine mammary carcinoma with circulating tumor cells and secondary DIC.     

Myocardial infarction secondary to a disseminated coagulopathy in a cow

A 3-year-old Holstein cow was presented with a history of high fever, jaundice and subsequent recumbency. The animal died 3 hours after arrival at our department; continuous electrocardiographic examination was performed during those last 3 hours. There were ventricular premature beats (VPBs) with high frequency and complex patterns (bigeminal, trigeminal, repetitive or early cycle VPBs) and paroxysms of ventricular tachycardia (VT). Serum CK-MB was markedly elevated. On histopathological examination, large areas of myocardial necrosis were found in the anterior aspects of the left ventricle. Large, partially organized thrombi occluded the intramural coronary arteries within and adjacent to the lesion. From the histopathological findings, it appeared that a disseminated coagulopathy caused the thromboembolism in the intramural coronary arteries, resulting in acute myocardial infarction (AMI). Various clinical findings, such as arrhythmias, were similar to those in man.     

Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation

BACKGROUND: Serious postoperative hemorrhage has been reported in dogs after closure of congenital portosystemic shunts (CPS). HYPOTHESIS: In dogs with portosystemic shunting, low coagulation factor activity is responsible for coagulopathy, which can cause complications after surgery. ANIMALS: Thirty-four dogs with CPS and 39 healthy dogs. METHODS: In a prospective study, coagulation times, platelet count, and the activity of 8 coagulation factors were measured in dogs before and after surgical shunt attenuation and in 31 healthy dogs. The effect of abdominal surgery on hemostasis was determined at ovariectomy in 8 healthy dogs. RESULTS: Dogs with CPS had lower platelet counts, lower activity of factors II, V, VII, and X, and increased factor VIII and activated partial thromboplastin time (APTT) compared to healthy dogs. After surgical attenuation, dogs with CPS had decreased platelet counts and activity of factors I, II, V, VII, IX, X, and XI and a prolonged prothrombin time (PT). Ovariectomy resulted in decreased activity of factors VII and X. Six weeks after surgery, portosystemic shunting persisted in 9 of 30 dogs, with no improvement of hemostatic values. CPS dogs without shunting had improved coagulation times and increased activity of factors II, V, VII, and X. CONCLUSIONS AND CLINICAL IMPORTANCE: Dogs with CPS have lower activity of clotting factors compared to healthy dogs, resulting in a prolonged APTT. Surgical attenuation of the shunt results in increased abnormalities in coagulation times and factors immediately after surgery. Hemostasis is normalized after complete recovery of shunting after attenuation, in contrast to dogs with persistent shunting.     

Fatal aortic oesophageal fistula following oesophageal foreign body removal in a dog

An eight-month-old male Pomeranian was presented with hypovolaemic shock 7 days after successful oesophageal foreign body removal. On presentation the dog was anaemic and no coagulation abnormalities were detected. A fluid-filled oesophagus was visible on thoracic radiography and frank blood was aspirated from the oesophagus following oro-oesophageal intubation. Fluid resuscitation and blood transfusions were administered but attempts at stabilisation were unsuccessful and the dog died. At post-mortem examination, a 2-mm aortic oesophageal fistula was identified on the ventral aspect of the aorta at the level of heart base that communicated with the overlying oesophagus. Aortic oesophageal fistula has been reported in human medicine and occurs secondary to a number of conditions including oesophageal foreign bodies. These prove fatal without rapid stabilisation and surgery.     

Peliosis hepatis and hemoperitoneum in a dog with diphacinone intoxication

Objective: To describe the clinical course of a dog presented with peliosis hepatis and hemoperitoneum in concert with anticoagulant rodenticide intoxication.
Case summary: A 7.75-year-old spayed female Shetland Sheepdog presented with clinical signs consistent with hypovolemia, hemoperitoneum, and a history of bright green stool 3 days before the onset of clinical signs. Initial packed cell volume/total solids were consistent with acute hemorrhage. A coagulation profile showed prolongation in activated clotting time and prolongation of both prothrombin and activated partial thromboplastin time, suggesting abnormal coagulation. Abdominal hemorrhage persisted in the face of normalization of the hemodynamic status and coagulation profile, and treatment with Vitamin K₁. Abdominal ultrasound revealed multiple patchy hypoechoic areas throughout the caudate liver lobe. An exploratory laparotomy was performed 24 hours after presentation and revealed the caudate liver lobe as the source of the hemorrhage. Histopathologic examination of a specimen of the liver was consistent with peliosis hepatis. Toxicologic testing identified diphacinone levels in the blood consistent with anticoagulant rodenticide intoxication. Postoperative recovery was uneventful, and within 48 hours the dog was discharged. The dog returned to full function and a hepatic ultrasound performed 15 months postoperatively showed no significant abnormalities.
New or unique information provided: Exposure to anticoagulant rodenticides may be associated with the development of peliosis hepatis in dogs.     

Disseminated histiocytic sarcoma with peripheral blood involvement in a Bernese Mountain dog

Abstract: A 6‐year‐old Bernese Mountain dog was presented with a history of lethargy and weight loss of 2 weeks duration. On physical examination the dog had pale mucous membranes and tachypnea. Ultrasound examination revealed hepatomegaly, splenomegaly, and mesenteric lymphadenomegaly. Results of a CBC included marked normocytic normochromic nonregenerative anemia, marked thrombocytopenia, and moderate leukocytosis with mild neutrophilia and a large population of unclassified round cells (6.2 × 10³/μL). The unclassified cells occasionally were bi‐ or multinucleated and had variably abundant pale basophilic cytoplasm that contained multiple irregular clear vacuoles and occasionally erythrocytes. Fine needle aspirate specimens of the mesenteric lymph nodes and spleen were composed of a population of round pleomorphic cells with the same features as the circulating cells. On flow cytometric analysis of peripheral blood, the unclassified cells expressed CD18, CD45, CD11c, CD1c, and CD14; immunocytochemical analysis of blood smears also indicated the cells were positive for CD1c, CD1a, and CD11c. The dog died a few hours after referral. The histologic interpretation of samples collected from spleen, liver, and lymph nodes was malignant neoplasia of histiocytic origin. Immunohistochemical staining yielded negative results for CD11d, a marker of red‐pulp macrophages, ruling out hemophagocytic histiocytic sarcoma. Based on clinical and pathologic findings, the final diagnosis was disseminated histiocytic sarcoma (DHS) with peripheral blood involvement. To our knowledge, DHS in a dog with evidence and immunophenotyping of neoplastic cells in peripheral blood has been reported only rarely.     

Diagnosis of canine claw disease – a prospective study of 24 dogs

The aetiology of claw disease in 24 dogs exhibiting only claw disease was investigated with cytologic examination of claw exudate, complete blood count (CBC), serum biochemistry panel, urinalysis, total thyroxine (tT4) concentration, antinuclear antibody (ANA) titre, bacterial culture and sensitivity testing, fungal culture, histopathology of claw biopsy samples and elimination diet. Abnormalities on the CBC, serum biochemistry panel and urinalysis were minor and nonspecific. Total T4 concentrations were within the normal laboratory reference range. Fungal cultures and ANA titres were negative in all dogs. A bacterial infection was present in approximately half of the dogs. On histological examination of claw tissue, a cell-poor or cell-rich interface onychitis was seen in all but one dog. Evidence for an adverse reaction to food was present in four dogs. One dog responded completely to antibiotic therapy. Interface onychitis seems to be a histological reaction pattern of the claw matrix in the dog with various possible underlying aetiologies. In dogs with claw disease as the only clinical sign, the recommended initial diagnostic evaluation includes cytologic examination, bacterial culture and sensitivity, claw biopsy and an elimination diet.     

Intestinal haemorrhage associated with colonic vascular ectasia (angiodysplasia) in a dog

An eight-year-old, sexually intact, male, 37 kg crossbred dog was referred for investigation of two acute episodes of intestinal bleeding and severe anaemia within a five-month period. There was no evidence of coagulopathy or underlying systemic disease. Technetium-labelled red blood cell scintigraphy suggested the colon as the site of bleeding. Colonoscopy identified a focal area of dilated and tortuous mucosal blood vessels. Histopathology of the resected colon revealed vascular ectasia (angiodysplasia). At nine months post-resection, the dog remained healthy and free of any overt intestinal haemorrhage.     

Presumptive Intramural Gastric Hemorrhage Secondary to Rodenticide Intoxication in a Dog

A dog being treated for demodicosis with ivermectin was presented for intermittent vomiting. The vomiting progressed to hematemesis and an underlying coagulopathy was diagnosed. The etiology of the coagulopathy was determined to be ingested brodifacoum. Ultrasound evaluation of the abdomen revealed thickened gastric wall that was suspected to be intramural hemorrhage. Most likely, the intramural hemorrhage and resulting thickening of the stomach wall led to the clinical signs and metabolic alkalosis. This case represents an typical presentation of hemorrhage secondary to rodenticide intoxication. (J Vet Emerg Crit Care 2001; 11(1):27–31, 2001).