[Analysis of thirteen cases with secondary coagulation disorder caused by raticide exposure].
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To summarize the clinical characteristics of secondary coagulation disorders caused by exposure to poison (raticide) in children and to investigate the diagnosis and corresponding treatment.The process of diagnosis, clinical characteristics, response to treatment and the prognosis were analyzed.The main clinical manifestation was mucosal bleeding (66.6%), including epistaxis, gingival bleeding, hematomas and so on. All these children were previously well and had no history of bleeding. Activated partial thromboplastin time (APTT) and prothrombin time (PT) were prolonged, factor II was undetectable and the levels of factors VII, IX, and X were lower. The fibrinogen was normal. A raticide was detected in blood and urine of 13 children although 12 of the patients had no definite history of raticide ingestion. Prothrombin complex, fresh frozen plasma and vitamin K(1) were effective in these cases. However, 2 - 3 weeks later, 6 patients presented with recurrent bleeding.For children with secondary coagulation disorders of unknown cause, intoxication of raticide should be considered. The administration of blood coagulation factors and vitamin K(1) are effective in early treatment, and the treatment period should be more than 2 months. The PT and APTT should be followed up. Vitamin K(1) should be stopped when PT and APTT are normal.Keywords:
Prothrombin time
Fresh frozen plasma
Coagulation testing
Factor IX
Vitamin K deficiency
Coagulation Disorder
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The presence of lupus anticoagulant is associated with an elevated risk of venous and arterial thrombosis, and recurrent miscarriages as well. For some cases, this disease can present with bleeding as a consequence of lupus anticoagulant hypoprothrombinemia (LAHPS). LAHPS is a rare disease and it is reported to be most frequent in young females with/without systemic lupus erythematosus or in healthy children who are suffering with a viral infection. In such cases, steroid therapy is usually effective in normalizing the biological abnormalities and controlling the bleeding problems.A 34-year-old previously healthy man was admitted to our department because of his prolonged coagulation times; these abnormalities were discovered before performing orthopedic surgery. The prothrombin time (PT) was 15.2 sec, and the activated partial thromboplastin time (APTT) was 37.7 sec. A 1:1 dilution of patient plasma with normal plasma nearly corrected the PT, but this failed to correct the APTT. Evaluation of the clotting factors revealed decreased levels of factors II, V, VIII, IX and XI. The presence of LA was demonstrated by the dRVVT test, and the patient was diagnosed with LAHPS. He was successfully treated with corticosteroid before performing the orthopedic surgery.
Hypoprothrombinemia
Lupus anticoagulant
Prothrombin time
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The first case report describes an extremely prolonged activated partial thromboplastin time (APTT) in a patient with no history of increased bleeding tendency. Heparin use was excluded. The APTT mixing study combined with the medical history suggests a deficiency in one of the non-essential coagulation factors. This was confirmed by factor XII activity of <1%. The second case report describes a prolonged APTT in a patient with no history of increased bleeding tendency. The negative bleeding tendency in combination with a failure of the mixing study to correct the coagulation assay results suggests a factor inhibitor, most probably lupus anticoagulant. Indeed, the lupus anticoagulant was positive and the anti-cardiolipin antibody titre was also positive. Aberrations in the process of haemostasis can be efficiently screened using a platelet count, an APTT, a PT and a thorough physical examination combined with a thorough medical history taking. Common causes of prolonged PT and/or APTT are the use of oral anticoagulants or heparin, vitamin K deficiency and liver disease. Other causes include coagulation factor deficiencies, coagulation factor inhibitors and diffuse intravascular coagulation.
Lupus anticoagulant
Coagulation testing
Prothrombin time
Medical History
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Factor XII (FXII), also known as Hageman factor, is a coagulation protein that is necessary for the functioning of the intrinsic coagulation cascade and fibrin formation. When deficient, it results in a significant prolongation of activated partial thromboplastin time (aPTT), mimicking a bleeding disorder. However, it does not result in clinical bleeding tendency. We report a case of an elderly male who was found to have prolonged aPTT, discovered during preoperative evaluation for operative repair of hip fracture. Although laboratory investigation was suggestive of bleeding tendency, he was diagnosed with factor XII deficiency and had no bleeding complications intra-operatively or in the post-operative period.
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Factor XI
Prothrombin time
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Sir, There are several causes of isolated elevated activated partial thromboplastin time (APTT), some of which are known to cause increased bleeding.This case report demonstrates not all causes of elevated APTT cause increased bleeding during acute burns surgery.A 2-year-old Indian girl was admitted to the burns unit the same day following a slip into freshly boiled water from which she sustained 6 % TBSA mixed partial/full-thickness scald of her left thigh and buttock.No immediate first aid was administered.There was no relevant past medical or family history.During her stay, she developed tonsillitis.Blood results showed the following: haemoglobin 12.8 g/L (normal 11.0-13.8),white blood count 7.4×10 9 /L (6-17) and C-reactive protein 229 mg/L (0-9).Intravenous benzylpenicillin and flucloxacillin and benzydamide hydrochloride 0.15 % mouthwash were administered.Later, pruritic petechial spots developed on her face and limbs.Following paediatric review, coagulation screen and varicella zoster virus serology were performed.APTT was raised at 87 s.Prothrombin time (PT) and fibrinogen levels were normal.After the haematologist advised blood cultures, meningococcal/pneumococcal PCR; viral screens and clotting factor 8, 9, 11 and 12 assays were tested and shown to be normal.Her APTT was 185 s when repeated using the SynthASil reagent, which has greater sensitivity to contact factor deficiencies.APTT synthetic phospholipid (SP), a reagent sensitive to lupus anticoagulant, was mildly elevated at 55.8 (normal value 25-38).Dilute Russell's viper venom time (DRVVT), a test used for the detection of lupus anticoagulant and antiphospholipid antibody including
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An algorithmic approach, termed the prolonged clot time profile (PROCT), consisting of initial screening with prothrombin time (PT) and activated partial thromboplastin time (aPTT), reflexive mixing studies if indicated, and follow-up assays depending on initial testing results, offers an efficient approach to delineate the etiology of a prolonged PT/aPTT. Herein, we present the outcomes of the PROCT in the outpatient setting.In this retrospective study, we reviewed medical records of consecutive outpatients who had prolonged PT and/or aPTT noted in the routine coagulation laboratory and who had PROCT ordered in our institutional Special Coagulation Laboratory between 2010 and 2017.One hundred and six patients, median age 55 years (IQR 30-67), met our study criteria. Twenty-nine patients had normal PT/aPTT, while 77 had persistent abnormalities and underwent reflexive testing. A prolonged PT, aPTT, or PT and aPTT was noted in 27 (35%), 27 (35%), and 23 (30%) respectively. Forty-nine (64%) had an acquired condition, 17 (22%) had a congenital condition, 7 (9%) had unclear etiology, and 4 (5%) were the result of laboratory artifact. The most common known cause of an isolated prolonged PT in our study was vitamin K deficiency in 8 (10%), the most common cause of an isolated prolonged aPTT was lupus anticoagulant in 4 (5%), and the most common cause of prolonged PT and aPTT was liver disease in 11 (14%).Prolonged PT/aPTT have a wide range of causes, including artifactual prolongation or abnormalities in secondary hemostasis due to both inherited and acquired conditions.
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後天性血液凝固第Ⅷ因子障害（後天性血友病A）は，凝固第Ⅷ因子（FⅧ）に対する自己抗体（インヒビター）が後天的に出現し，重篤な出血症状を来し得る疾患である．年間発症率は0.25～1人/100万人と言われていたが，疾患概念が浸透したことで成人領域では診断例が増加している．一方，小児では0.045人/100万人と極めてまれな疾患であるが，成人と同様に重篤な出血を起こすため早期診断が重要である．今回，活性化部分トロンボプラスチン時間（APTT）クロスミキシングテストの結果から後天性血友病Aを疑い，早期診断が可能であった小児例を経験した．症例は12歳女児．出血性疾患の家族歴，出血症状の既往はない．誘因のない両側大腿痛を主訴に近医整形外科を受診し，MRIで筋肉内出血を認めた．その後，鼻出血も出現したため出血性疾患を疑われ産業医科大学小児科を受診した．血液検査ではAPTTのみ延長していた．APTT延長の原因精査のために施行したAPTTクロスミキシングテストでは，即時反応より遅延反応でより明確な凝固第Ⅷ因子に対する抗凝固因子（インヒビター）パターンを認めたため，初診時よりインヒビターの存在を強く疑い注意深く経過観察を行った．確定診断後から治療を開始した．筋肉内出血は止血治療を要さず安静のみで軽快し，後天性血友病Aはプレドニゾロン内服のみで寛解した．小児期（12歳）発症の後天性血友病Aは極めてまれであるが，重篤な出血も起こすため早期に診断することが重要であり，APTTクロスミキシングテストが診断に有用であった．
Prothrombin time
Coagulation testing
Bleeding time
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Hematology
Prothrombin time
PROTHROMBIN COMPLEX
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Introduction: Inborn factor X deficiency (FXD) is a very rare (1: 500,000) hereditary coagulation disorder, which is characterized by clinical mani- festations including hematoma, epistaxis, menorrhagia, ecchymosis, and central nervous system (CNS) or gastrointestinal (GI) bleeding (depending on the zygosity). In homozygote patients, the risk of spontaneous intracranial hemorrhage (ICH) is high. Objectives: The aim of this investigation was to study and long-term follow-up of the patients with FXD and ICH. In addition, we investigated their frequent bleeding symptoms throughout their life and the results were compared with results of other studies. Patients and Methods: This study investigated 2 cases with spontaneous intracranial hemorrhage in patients with severe congenital (factor X) FX deficiency including a 3-year-old boy and a 1-month-old female neonate. The world literature was explored through the PubMed Medline and Scopus using appropriate and pertinent key words. Results: The Patients referred to the hematology department due to the neurological complications such as vomiting, unconsciousness, prolonged nasal bleeding for recent 12 hours. They had no familial history of spontaneous CNS bleeding. The blood coagulation test analysis indicated a pro- longed activated partial thromboplastin time (APTT) and also revealed a prolonged prothrombin time (PT) and the low levels of coagulation factor X implicating severe congenital FX deficiency. They followed up by our hematologists to prevent intracranial hemorrhage. Discussions: As one ICH patient whose PT and aPTT suggest a coagulation disorder secondary to vitamin K deficiency or coagulation factor deficiency, unresponsiveness to vitamin K therapy should be useful to take FX deficiency into consideration.
Kowsar
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Objective To investigate the clinical characteristics of poisoning caused by long-acting anticoagulant rodenticide and its therapeutic methods.Methods Retrospective analysis was performed on the data of clinical manifestations,routine examinations,diagnoses and treatments of 12 patients with clear histories of anticoagulant rodenticide poisoning.Results The presentations of hemorrhage of the patients were many and various,the bleeding symptoms were serious.Laboratory examinations showed basically normal platelet count,prolonged plasma prothrombin time (PT) and activated partial prothrombin time PT (AT).There were significant differences in PT,APTT and Hb of the patients before and after treatment (P0.01).Conclusion The histories are usually delitescent in patients with coagulation disorder caused by anticoagulant rodenticide poisoning.So it is easily misdiagnosed,and the coagulation function disorder is due to acquired reduction of vitamin K-dependent blood coagulation factors.
Prothrombin time
Coagulation Disorder
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