scholarly journals The concept of hemostasis disorders in severe leptospirosis

2021 ◽  
Vol 13 (3) ◽  
pp. 70-81
Author(s):  
D. L. Moisova ◽  
V. N. Gorodin
Keyword(s):  
Plasma Exchange ◽  
Thrombotic Microangiopathy ◽  
Fatal Outcome ◽  
Pulse Therapy ◽  
Fresh Frozen Plasma ◽  
Platelet Concentrate ◽  
Severe Thrombocytopenia ◽  
Therapy Regimen ◽  
Fresh Frozen ◽  
Severe Leptospirosis

The purpose of the research to create a concept for diagnostics and therapy of hemostasis disorders of patients with severe leptospirosis.Patients and Methods. The study included 474 patients with severe serologically confirmed leptospirosis with a favorable outcome of the disease and 31 patients with fatal outcome (total 505 people). Variant of coagulopathy was determined by using a set of special methods for studying hemostasis. The influence of platelet concentrate transfusion, plasma exchange and various tactics of glucocorticoid therapy on patient survival and correction of hemostasis disorders was evaluated. Survival analysis was made using Kaplan-Meyer method with a Cox proportional intensity model. Relative risk (RR) was calculated with a 95% confidence interval (CI).Results: the use of early diagnosis of coagulopathy variants and the use of a differentiated therapy regimen in the choice of the variant of hemostasis disorder led to a decrease of mortality from 16.45% to 11.5% and decrease in the consumption of platelet concentrate and fresh frozen plasma.Conclusion: patients with severe leptospirosis develop a multivariate hemostatic pathology: isolated thrombocytopenia (38%) with thrombotic microangiopathy (20,5%), disseminated intravascular coagulopathy (37,1%), uremic coagulopathy (4,9%), hepatic coagulopathy (3,4%). Plasma exchange in thrombotic microangiopathy is pathogenetically justified. Also, plasma exchange is pathogenetically justified in order to reduce plasma volume in DIC syndrome with consumption coagulopathy and hepatic coagulopathy. The use of GCS in isolated thrombocytopenia can be effective and safe in both “medium doses” and in the form of “pulse therapy” if the following conditions are met: acute renal injury (AKI) III stage according to AKIN and the absence of renal replacement therapy (RRT). The main indication for platelet concentrate transfusion in severe leptospirosis is extremely severe thrombocytopenia (grade 4) with active life-threatening bleeding at the time of transfusion.

scholarly journals Therapeutic Plasma Exchange for Thrombotic Microangiopathy

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 4939-4939
Author(s):  
Osman Ilhan ◽  
Erden Atilla ◽  
Pinar Ataca Atilla ◽  
Sinem Civriz Bozdag ◽  
Meltem Kurt Yuksel ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Thrombotic Microangiopathy ◽  
Conflicts Of Interest ◽  
Complete Response ◽  
Fresh Frozen Plasma ◽  
Therapeutic Plasma Exchange ◽  
Time Period ◽  
Fresh Frozen ◽  
Neurological Disturbance

Abstract Background: Thrombotic microangiopathy (TMA) is a syndrome characterized by thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, fever and renal dysfunction. Therapeutic Plasma Exchange (TPE) is a standart treatment approach for the patients. Our aim is to determine the clinical characteristics and outcome of patients with TMA treated with TPE in our center. Patients and Methods: We retrospectively evaluated 46 patients who have been diagnosed as TMA at Ankara University Department of Hematology between 2007 and 2015. Patients were treated with TPE (Frensenius Kabi AG, Homburg, Germany) until the normalization of laboratory parameters. The plasma exchanged was 1.5 times the predicted plasma volume with fresh frozen plasma for the first procedure, and usually 1.0 time the predicted volume thereafter until remission. Results: 22M/24F was included in the study with a median age of 55 (range, 18-8310 of 46 patients (22%) were consultated from intensive care units, 7/46 (15%) from emergency unit and 6/46 (13%) from nephrology unit. The most common presenting symptom was purpura in 52%, followed by neurological disturbance 48%, renal function abnormality in 43% and fever in 28% of patients. At diagnosis the median hemoglobin (g/dl), leucocyte count (10^9/L) and thrombocyte count (10^9/L) were as follows: 9.4, 11.4 and 58.6. Median time period of procedure was 99 minutes (range, 64-313). 5/46 (11%) patients had femoral catheters and central venous catheters were the access for the rest of patients. None of the patients had severe adverse events during procedures. 21 patients achieved complete response (46%) after 2-40 sessions and 2 of them were died during follow-up. Responders were diagnosed mostly with infectious related TMA. 21 patients (46%) who had progressive disease died within 30 days after diagnosis. 2 non-responder patients had diagnosis of TTP and treated with succesfully with Rituximab (Table 1). Conclusions: TPE is safe treatement modality in patients with TMA however there is still high mortality rate. Disclosures No relevant conflicts of interest to declare.

scholarly journals Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management

2021 ◽  
Vol 10 (3) ◽  
pp. 536
Author(s):  
Senthil Sukumar ◽  
Bernhard Lämmle ◽  
Spero R. Cataland
Keyword(s):  
Thrombotic Thrombocytopenic Purpura ◽  
Initial Therapy ◽  
Fresh Frozen Plasma ◽  
Organ Injury ◽  
Severe Thrombocytopenia ◽  
Front Line ◽  
Thrombocytopenic Purpura ◽  
Fresh Frozen ◽  
Biallelic Mutations ◽  
Line Setting

Thrombotic thrombocytopenic purpura (TTP) is a rare thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, severe thrombocytopenia, and ischemic end organ injury due to microvascular platelet-rich thrombi. TTP results from a severe deficiency of the specific von Willebrand factor (VWF)-cleaving protease, ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13). ADAMTS13 deficiency is most commonly acquired due to anti-ADAMTS13 autoantibodies. It can also be inherited in the congenital form as a result of biallelic mutations in the ADAMTS13 gene. In adults, the condition is most often immune-mediated (iTTP) whereas congenital TTP (cTTP) is often detected in childhood or during pregnancy. iTTP occurs more often in women and is potentially lethal without prompt recognition and treatment. Front-line therapy includes daily plasma exchange with fresh frozen plasma replacement and immunosuppression with corticosteroids. Immunosuppression targeting ADAMTS13 autoantibodies with the humanized anti-CD20 monoclonal antibody rituximab is frequently added to the initial therapy. If available, anti-VWF therapy with caplacizumab is also added to the front-line setting. While it is hypothesized that refractory TTP will be less common in the era of caplacizumab, in relapsed or refractory cases cyclosporine A, N-acetylcysteine, bortezomib, cyclophosphamide, vincristine, or splenectomy can be considered. Novel agents, such as recombinant ADAMTS13, are also currently under investigation and show promise for the treatment of TTP. Long-term follow-up after the acute episode is critical to monitor for relapse and to diagnose and manage chronic sequelae of this disease.

SP787SELECTIVE PLASMA EXCHANGE IN ABO-INCOMPATIBLE KIDNEY TRANSPLANTATION: EFFICACY OF PARTIAL SUBSTITUTION WITH FRESH FROZEN PLASMA

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Toshihide Naganuma ◽  
Yoshiaki Takemoto ◽  
Ako Hanaoka ◽  
Junji Uchida ◽  
Tatsuya Nakatani
Keyword(s):  
Kidney Transplantation ◽  
Plasma Exchange ◽  
Fresh Frozen Plasma ◽  
Partial Substitution ◽  
Fresh Frozen ◽  
Frozen Plasma

scholarly journals Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge

2015 ◽  
Vol 2015 ◽  
pp. 1-5
Author(s):  
Mohsin Ijaz ◽  
Naeem Abbas ◽  
Dmitry Lvovsky
Keyword(s):  
Basement Membrane ◽  
Plasma Exchange ◽  
Glomerular Basement Membrane ◽  
Metabolic Alkalosis ◽  
Fresh Frozen Plasma ◽  
Maintenance Hemodialysis ◽  
Positive Serology ◽  
Aged Woman ◽  
Fresh Frozen ◽  
Intravenous Steroids

Metabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture’s syndrome treated with plasma exchange who developed severe metabolic alkalosis. High citrate load in plasma exchange fluid is the underlying etiology. Citrate metabolism generates bicarbonate and once its level exceeds the excretory capacity of kidneys, the severe metabolic alkalosis ensues. Our patient presented with generalized weakness, fever, and oliguria and developed rapidly progressive renal failure. Patient had positive serology for antineutrophilic cytoplasmic antibodies myeloperoxidase (ANCA-MPO) and anti-glomerular basement membrane antibodies (anti-GBM). Renal biopsy showed diffuse necrotizing and crescentic glomerulonephritis with linear glomerular basement membrane staining. Patient did not respond to intravenous steroids. Plasma exchange was started with fresh frozen plasma but patient developed severe metabolic alkalosis. This metabolic alkalosis normalized with cessation of plasma exchange and initiation of low bicarbonate hemodialysis. ANCA-MPO and anti-GBM antibodies levels normalized within 2 weeks and remained undetectable at 3 months. Patient still required maintenance hemodialysis.

Plateletpheresis during Plasma Collection

1993 ◽  
Vol 16 (5_suppl) ◽  
pp. 139-142
Author(s):  
M. Rubertelli ◽  
F. Marafioti ◽  
C. Mazzon ◽  
G. Rossetti ◽  
G. Gosetti ◽  
...  
Keyword(s):  
Fresh Frozen Plasma ◽  
Minimum Amount ◽  
Platelet Concentrate ◽  
Competitive System ◽  
Platelet Poor Plasma ◽  
Normal Plasma ◽  
Fresh Frozen ◽  
Plasma Collection ◽  
Frozen Plasma

New systems for collection of platelet concentrate (PC) and platelet poor plasma (PPP) are presently available. The aim of our work was to test the possibility of preparing PC routinely from normal plasma donors in a minimum amount of time and, at the same time, providing a second product that can be used as source-plasma or fresh-frozen plasma. Over a 3 year period (from 1990 to 1992) we performed 3503 procedures using 2 Haemonetics PCS machines (1236 procedures) and 3 Autopheresis-C (2267 procedures). With the PC produced we were able to satisfy all the requests coming from the hospitals of our region. The platelet yield was 1.95x10″ with PCS and 3.2x10″ with Auto-C in a PC volume of 150 and 200 ml respectively; collection times were quite similar (56 and 63 min). The results show that plasma-plateletpheresis is an efficient and competitive system. Regarding platelet yield, the best results were obtained with the Auto-C.

scholarly journals Caution in diagnosing angioedema as anaphylaxis

2019 ◽  
Vol 12 (9) ◽  
pp. e230329 ◽  
Author(s):  
Shivam Patel ◽  
Roshan Mathew ◽  
Sanjeev Bhoi
Keyword(s):  
Ace Inhibitor ◽  
Fatal Outcome ◽  
Fresh Frozen Plasma ◽  
Definitive Treatment ◽  
Common Presentation ◽  
Good Outcome ◽  
Fresh Frozen ◽  
Life Threatening ◽  
The Common ◽  
Frozen Plasma

Angioedema is one of the commonest life-threatening conditions with good outcome timely definitive treatment. However, failure to recognise the common presentation of an uncommon bradykinin-mediated angioedema in time may lead to fatal outcome in the emergency department (ED). We report a case of a 79-year-old male patient who presented to ED with features of ACE inhibitor-induced angioedema which was identified and resuscitated by the emergency physician with use of fresh frozen plasma (FFP) leading to prompt recovery and good outcome.

scholarly journals Effects of fresh-frozen plasma and its cryosupernatant fraction on von Willebrand factor multimeric forms in chronic relapsing thrombotic thrombocytopenic purpura

Blood ◽  
1985 ◽  
Vol 65 (5) ◽  
pp. 1232-1236 ◽  
Author(s):  
JL Moake ◽  
JJ Byrnes ◽  
JH Troll ◽  
CK Rudy ◽  
SL Hong ◽  
...  
Keyword(s):  
Plasma Exchange ◽  
Fresh Frozen Plasma ◽  
Plasma Samples ◽  
Fresh Frozen ◽  
Normal Human ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Frozen Plasma

Abstract Remission plasma samples of some patients with chronic relapsing thrombotic thrombocytopenic purpura (TTP) contain unusually large von Willebrand factor (vWF) multimers similar to those produced by normal human endothelial cells in culture. The infusion of the cryosupernatant fraction of normal plasma is as effective as normal fresh-frozen plasma (FFP) in the treatment or prevention of TTP episodes in patients with the chronic relapsing form of TTP. Three patients with chronic relapsing TTP during remission have unusually large vWF multimers present in their plasma. Two of the patients were transfused once with FFP, one of the two received cryosupernatant on three occasions, and the third patient was studied before and immediately after plasma exchange. Unusually large vWF multimers decreased or disappeared from patient plasma samples within 1/2 to 1 1/2 hours following the transfusion of FFP (on two occasions) or cryosupernatant (on two of three occasions), and immediately after plasma exchange (on one occasion). The patient who received cryosupernatant was studied serially after the infusions. Unusually large vWF multimers returned to her plasma within ten to 24 hours and persisted thereafter. Unusually large vWF multimers did not disappear from patient remission plasma samples, or from the culture medium removed from normal human endothelial cells, when these fluids were incubated in vitro with either normal FFP or cryosupernatant. We conclude that an activity in FFP, and its cryosupernatant fraction, promoted the rapid in vivo disappearance of unusually large vWF multimers from the plasma of two patients with chronic relapsing TTP in remission, and plasma exchange reversed the abnormality in a third patient who was in partial remission. Neither FFP nor cryosupernatant directly converted unusually large multimers to smaller vWF forms in vitro in the fluid phase. These results indicate that an activity in the cryosupernatant fraction of normal plasma is involved in vivo in controlling the metabolism of unusually large vWF multimers, and that this process is defective in some chronic relapsing TTP patients.

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