Subclinical Coagulopathy Research Articles

Liver fibrosis indices associated with hematoma expansion in patients with intracranial hemorrhage

Liver fibrosis may cause subclinical coagulopathy and endothelial dysfunction, which link to hematoma expansion (HE) after intracerebral hemorrhage (ICH). We evaluated the association between liver fibrosis indices and HE in a Chinese population with primary ICH.

Toddler with repeated fall frequently visiting hospital presented with acute subdural hematoma on readmission with ultra-rapid evolution: surgical management strategy

Repetitive fall producing head injury in children may lead to development of intracranial hematoma. The course of evolution may be rapid in case of repeated fall due to induction of sub-clinical coagulopathy caused by repetitive cranial injury. The awareness of such possibility is highly desired among the pediatrician and neurosurgeon and emergency team and quick diagnosis and pertinent imaging study is of immense value and appropriate surgical management for prompt and expediting the evacuation of intracranial hematoma evacuation should be attempted to preserve good neurological outcome. Authors reports a case, who had rapid neurological worsening, managed surgically with good neurological outcome, further various surgical management options along with pertinent literature are briefly reviewed.

Impact of low coagulation factor XIII activity in patients with chronic subdural hematoma associated with cerebrospinal fluid hypovolemia: A retrospective study.

Background:Cerebrospinal fluid hypovolemia (CSFH) is sometimes associated with chronic subdural hematomas (CSHs). Affected patients often develop enlargement and recurrence of the CSH, even if appropriate treatments such as epidural blood patch (EBP) and/or burr-hole surgery for the CSH are performed. This situation may lead to subclinical coagulopathy, including low coagulation factor XIII (CFXIII) activity. We retrospectively analyzed whether CFXIII activity was involved in the development of CSHs and post-treatment exacerbation of CSHs in patients with CSFH.Methods:We diagnosed CSFH by radioisotope (RI), magnetic resonance imaging (MRI) and computed tomography (CT) findings, and CSH by CT and/or MRI findings. The plasma CFXIII activity was assessed on admission. All patients with CSFH initially received conservative treatments. When these treatments were ineffective, the patients underwent EBP and/or CSH surgery according to previously reported therapeutic strategies.Results:Among 206 patients with CSFH, 19 developed CSHs. Fourteen patients with a thin hematoma underwent EBP and three with a thick hematoma underwent CSH surgery immediately after EBP on the same day. We were unable to diagnose two patients with CSFH at the time of admission, and one of these two patients underwent repeated CSH surgery before obtaining the correct diagnosis. Seven patients (36.8%) developed CSH exacerbation after the treatment. The CFXIII activity was significantly lower in patients with than without a CSH (42.1% vs. 12.8%, respectively; P = 0.003). The CFXIII activity was significantly lower in patients with than without post-treatment CSH exacerbation (P = 0.046). All five patients with low CFXIII activity who developed CSH exacerbation received intravenous injection of CFXIII and had no recurrence of CSH after the additional treatment.Conclusion:In patients with CSFH, low CFXIII activity is one of the risk factors for both the development of a CSH and the post-treatment exacerbation CSH.

Study on Plasma D-Dimer for Early Diagnosis of Ischemic Stroke

Background: Plasma D-Dimer is a biomarker of thrombo-embolism and a sensitive indicator of subclinical coagulopathy. Its level begins to rise within the first 6 hours of onset of symptoms of acute ischemic stroke. The availability of a rapid diagnostic test like plasma D-Dimer in acute ischemic stroke would be a substantial adjunct to CT and MRI. The test for plasma D-Dimer is quick and easy to perform based on principle of latex agglutination. This study is taken to estimate Plasma D-Dimer level in ischemic stroke patients and to see its role in early diagnosis, and also to differentiate different types of acute ischemic stroke in Bangladeshi population.Methods: This case control study was conducted in Dhaka Medical College Hospital (DMCH) from July 2010 to June 2012. Plasma D-Dimer was estimated by latex agglutination method in DMCH laboratory. Fifty stroke patients (age, 58.36±14.8 years; sex-M/F: 34/16) and 50 age matched control (58.80±15.01 years; sex-M/F: 36/14) were enrolled. In ischemic stroke group all patients were presented from 4 hours to 3 days. CT scan of brain revealed both cortical and subcortical lesion (56%), subcortical lesion (34%) and cortical lesion (10%). The CT volume of the involved brain lesion was 19.95±4.92 cm3. The value of plasma D-Dimer were evaluated in both control and ischemic stroke patients, correlated with CT size of infract and different types of acute ischemic strokes.Results: Qualitative analysis of plasma D-Dimer reveals 76% positive and 24% negative in the ischemic stroke group. On the other hand, plasma D-Dimer value was only 6% positive and 94% negative in the control group. Qualitative analysis of plasma D-Dimer differs significantly (c2=50.64; p=0.001) between the two groups. The analysis also reveals 76% sensitivity and 94% specificity of the Plasma D-Dimer test. Quantitative measurement of plasma D-Dimer (p=0.001) was 804±120 hg/ml and 126±16 hg/ml in ischemic and control groups respectively. The plasma concentration of D-Dimer between the two groups was statistically highly significant (t=31.21; p=0.001). Mean plasma D-Dimer level was highest in embolic infarct (1700±964 hg/ml) followed by atherothrombotic (536±234 hg/ml) and lowest in lacunar (100±00 hg/ml) subtype.J Dhaka Medical College, Vol. 24, No.2, October, 2015, Page 117-125

An Additional Patient With 3q27.3 Microdeletion Syndrome

The 3q27.3 microdeletion syndrome has been recently delineated in 7 subjects from 5 families sharing a 1.4 Mb smallest region of overlap. This condition appears recognizable by the association of Marfanoid habitus, mild but distinctive facial dysmorphism, intellectual disability, psychosis, and mood disorder. Here, we describe an additional 17-year-old man with an ~7.7-Mb deletion encompassing the 3q27.3 microdeletion critical region, previously run undetected at standard karyotyping. The constellation of major clinical findings overlaps with those reported in the 7 previously published patients and thus confirms the existence of a strongly recognizable syndrome linked to imbalance of 3q27.3. The role of AHSG and, possibly, of other genes in determining the 3q27.3 microdeletion habitus is discussed by comparison of the deleted segments. The involvement of adjacent loci and genes, such as OPA1 and GP5, may contribute in this patient to novel satellite features, such as optic atrophy and subclinical coagulopathy.

Coagulopathy of the critically ill equine patient

To review the hemostasis literature relevant to development of coagulopathy in the critically ill equine patient. Original scientific and review articles. Inflammation plays a critical role in the activation and amplification of clot formation, as well as the impairment of physiologic anticoagulant mechanisms, and fibrinolysis. Earlier identification of coagulopathy in patients at risk and restoration of physiologic hemostasis may result in better outcome. Development of scoring systems based on information other than coagulation markers alone may better identify patients with subclinical coagulopathy. Critically ill equine patients commonly at risk for coagulopathy include those with severe gastrointestinal disease, septic foals, and adults subjected to severe systemic inflammatory response syndrome. Publications provide information regarding coagulation markers helpful for identification of hemostatic dysfunction in specific patient populations, as well as information regarding the influence of coagulopathy on outcome. Data regarding clinically relevant information on therapeutic intervention are lacking. The relationship between inflammation and endotoxemia and development of coagulopathy is better understood in both human patients and the critically ill equine patient. Prospective clinical trials evaluating clinically relevant and financially feasible approaches to treatment are still needed.

Comparison of plasma D-dimer and thrombus precursor protein in patients with operable breast cancer as a potential predictor of lymph node metastasis.

Fibrin formation and removal is continuous during the development of malignancy. Plasma D-dimer is indicative of ongoing fibrinolysis, and circulating soluble fibrin polymer [thrombus precursor protein (TpP)] represents thrombogenic activity. We evaluated the relationship between plasma D-dimer and TpP levels with tumor extent and examined the use of these markers as possible predictors of lymph node metastasis in breast cancer. Preoperative plasma levels of D-dimer and TpP were measured in these 120 patients (93 breast cancer, 27 benign breast disease) and 29 healthy controls. Plasma levels of D-dimer in patients with breast cancer were significantly higher than in healthy controls and in those with benign breast disease. Plasma D-dimer levels in patients with breast cancer were found to be significantly increased according to tumor stage. We also observed that plasma levels of D-dimer were higher in patients with lymph node metastasis than in patients without metastasis. In contrast, TpP levels were not significantly different by the tumor stages and lymph node metastasis. In conclusion, increased D-dimer levels in breast cancer may suggest that an ongoing fibrinolysis within breast cancer tissue occurs during tumor progression. Positive D-dimer levels might be useful for identifying metastatic lymph node in patients with operable breast cancer. However, plasma TpP was not found to be a sensitive marker for detecting tumor-associated subclinical coagulopathy.

Low Prevalence of Coagulation and Fibrinolytic Activation in Patients with Primary Untreated Cancer

The prevalence of subclinical coagulation abnormalities greatly differs in the various studies due to selection of patients and differences in study design. We performed coagulation studies in 69 consecutive patients with primary untreated cancer of various origin. The control group consisted of 42 sex and age matched healthy volunteers. Plasma coagulation tests included thrombin-antithrombin-III-complex (TAT), plasmin-alpha 2-antiplasmin-complex (PAP) and tissue-plasminogen-activator-antigen (t-PA-ag). These tests were performed once, prior to any anti-cancer treatment. We evaluated if activation of the coagulation system (elevated TAT-complexes) and the fibrinolytic system (elevated PAP-complexes and t-PA-ag) correlated with the tumor-type or the extent of the tumor. To document clinical manifest haemorrhage or thromboembolic disease (TED) we performed a 6 months follow-up study. In 8 patients (12%) and in 3 control subjects (7%) an elevated TAT-complex level was observed (this difference is not significant). An increased plasma level of PAP-complex was seen in 8 patients (12%) versus none in the control group (p less than 0.05). In one patient both TAT and PAP-complex concentrations were elevated. Consequently, 15 of the 69 patients (22%) showed activation of the coagulation and/or fibrinolytic system. Fibrinolysis seems to be enhanced in a subset of cancer patients in contrast to blood coagulation. In 10 patients (14%) we found raised t-PA-ag levels. Three patients had both elevated levels of PAP-complex and t-PA-ag. These findings suggest that in a minority of patients increased PAP-complex levels may be a result of t-PA induced plasminogen activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemostatic Abnormalities in Malignancy, a Prospective Study of One Hundred Eight Patients: Part I. Coagulation Studies

A prospective study of hemostatic abnormalities in 108 cancer patients was undertken at an oncology clinic in a university teaching hospital. Tests included Quick prothrombin time, activated partial thromboplastin time, thrombin time, platelet count, modified Ivy bleeding time, fibrinogen, fibrin degradation products (FDP), euglobulin lysis time, protamine sulfate test, and factor V, VII, VIII and X assays. Ninety-eight per cent of the patients had one or more abnormal coagulation tests. The commonest abnormalities were elevated fibrin degradation products and prolonged thrombin time. Thrombocytosis occurred in 57% of patients, hyperfibrinogenemia in 46%, thrombocytopenia in 11%, and non had hypofibrinogenmia. It is suggested that platelet count, fibrinogen concentration, and serum FDP assay are the most useful tests in assessing the hemostatic abnormalities in cancer patients, although thrombin time, factor V assay, and bleeding time may also be helpful. The peripheral blood smears of 53 patients were reviewed, and only one showed microangiopathic hemolytic anemia. The data illustrate that subclinical coagulopathy is relatively frequent in patients with malignancy.

Subclinical coagulopathy following amnioinfusion with hypertonic saline

Previously reported blood coagulation changes in unselected cases undergoing hypertonic saline amnioinfusion for second-trimester abortion were reviewed and compared with the authors' experience in 22 cases. The majority of cases studied developed laboratory evidence of coagulopathy within hours following infusion although no cases developed bleeding problems. Nearly all studies demonstrated an early postinfusion appearance of fibrin monomer complexes along with depression of platelet count, fibrinogen, and Factor VIII. Fibrin and fibrinogen degradation products also appeared early, and two studies demonstrated a significant drop in plasminogen. Only the author's work demonstrated a significant shortening of euglobulin clot lysis time indicating possible systemic activation of fibrinolysis. All factors exhibited a tendency to return toward normal by 24 to 48 hours after infusion, sometimes even before abortion was completed. Plasma fibrinogen and activated partial thromboplastin times are recommended in evaluating heavy uterine hemorrhage following saline amnioinfusion.