scholarly journals Life-Threatening Intrapulmonary Hemorrhage due to Vancomycin-Induced Thrombocytopenia: A Case Report

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Haneen Abdalhadi ◽  
Yazan Fahmawi ◽  
Abhijin Das ◽  
Brian Fouty
Keyword(s):  
Atypical Hemolytic Uremic Syndrome ◽  
Kidney Injury ◽  
Ventilator Associated Pneumonia ◽  
Disseminated Intravascular Coagulopathy ◽  
Heparin Induced Thrombocytopenia ◽  
Platelet Antibodies ◽  
Intravascular Coagulopathy ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Life Threatening Complication

Thrombocytopenia is a rare and sometimes life-threatening complication of Vancomycin. A 52-year-old male patient with acute kidney injury was treated with Vancomycin for ventilator-associated pneumonia. Three days later, his platelets decreased from 172×109/L to 3×109/L over a 36-hour period. The patient developed significant intrapulmonary bleeding leading to profound hypoxemia. Workup was negative for thrombotic thrombocytopenic purpura, disseminated intravascular coagulopathy, atypical hemolytic uremic syndrome, heparin-induced thrombocytopenia, and autoimmune diseases. All recently started medications were discontinued, and the patient was started empirically on methylprednisolone and intravenous immunoglobulin. The patient’s platelets increased, and his airway bleeding stopped within 48 hours; his platelet count returned to normal by 18 days. Vancomycin-dependent anti-platelet antibodies were identified in the patient’s serum by flow cytometry. Thrombocytopenia is an underrecognized complication of Vancomycin that can lead to life-threating bleeding. Stopping Vancomycin may be sufficient to reverse the thrombocytopenia in patients with normal renal function, but more aggressive measures such as steroids, IVIG, and dialysis may be required to stop bleeding and reverse thrombocytopenia in patients with underlying kidney injury who cannot effectively excrete Vancomycin.

scholarly journals Ulcerative Colitis and Atypical Hemolytic-Uremic Syndrome: An Unusual But Potentially Life-threatening Complication

2018 ◽  
Vol 25 (4) ◽  
pp. e27-e28 ◽  
Author(s):  
Javier Francisco Viada Bris ◽  
Marta Velasco Rodríguez-Belvís ◽  
Carmen de Lucas Collantes ◽  
Cristina Aparicio López ◽  
Amelia Martínez de Azagra ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Life Threatening Complication

Erratum to Ulcerative Colitis and Atypical Hemolytic-Uremic Syndrome: An Unusual But Potentially Life-threatening Complication

2018 ◽  
Vol 25 (11) ◽  
pp. e151-e151 ◽  
Author(s):  
Javier Francisco Viada Bris ◽  
Marta Velasco Rodríguez-Belvís ◽  
Carmen de Lucas Collantes ◽  
Cristina Aparicio López ◽  
Amelia Martínez de Azagra ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Life Threatening Complication

scholarly journals Life-Threatening Extrarenal Manifestations in an Infant with Atypical Hemolytic Uremic Syndrome Caused by a Complement 3-Gene Mutation

2019 ◽  
Vol 44 (5) ◽  
pp. 1300-1305
Author(s):  
Sa Ra Han ◽  
Myung Hyun Cho ◽  
Jin Soo Moon ◽  
Il Soo Ha ◽  
Hae Il Cheong ◽  
...  
Keyword(s):  
Gastrointestinal Bleeding ◽  
Hemolytic Uremic Syndrome ◽  
Gene Mutation ◽  
Hemolytic Anemia ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Pulmonary Hemorrhage ◽  
Microangiopathic Hemolytic Anemia ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Extrarenal Manifestations

Background: Atypical hemolytic uremic syndrome (aHUS) is a rare, life-threatening disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal impairment caused by uncontrolled activation of the complement system. About 20% of patients show extrarenal manifestations, with central nervous system involvement being the most frequent. We described the clinical course and management of aHUS in an infant, that was caused by a complement 3 (C3) gene mutation with severe extrarenal manifestations. Case Presentation: A 4-month-old girl visited our hospital for jaundice and petechiae. Laboratory tests revealed microangiopathic hemolytic anemia, thrombocytopenia, and hyperazotemia. She was diagnosed with aHUS with a C3 p.E1160K mutation. Daily fresh-frozen plasma (FFP) therapy was administered; however, she experienced the severe extrarenal manifestations of pulmonary hemorrhage and gastrointestinal bleeding. With aggressive treatment, supportive care, and daily FFP transfusion, the patient recovered and was discharged after 72 days of hospital stay, on a regular FFP transfusion. Four months after diagnosis, she was switched to eculizumab treatment. Twenty months have passed since then and she has been relapse-free until now. Conclusion: aHUS is rare but has a devastating course if not properly treated. Severe extrarenal manifestations, such as pulmonary hemorrhage and gastrointestinal bleeding, can develop in aHUS caused by a C3 mutation. In our case, long-term management with eculizumab resulted in relapse-free survival.

Eculizumab Modifies Outcomes in Adults with Atypical Hemolytic Uremic Syndrome with Acute Kidney Injury

2018 ◽  
Vol 48 (3) ◽  
pp. 225-233 ◽  
Author(s):  
Mercedes Cao ◽  
Bruna N. Leite ◽  
Tamara Ferreiro ◽  
María Calvo ◽  
Constantino Fernández ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Hemolytic Uremic Syndrome ◽  
Kidney Function ◽  
Case Reports ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Kidney Injury ◽  
Complete Recovery ◽  
Genetic Abnormalities ◽  
Uremic Syndrome ◽  
Meta Analyses

Background: Atypical hemolytic uremic syndrome (aHUS) is a rare disease associated with congenital or acquired genetic abnormalities that result in uncontrolled complement activation, leading to thrombotic microangiopathy and kidney failure. Until recently, the only treatment was plasma exchange or plasma infusion (PE/PI), but 60% of patients died or had permanent kidney damage despite treatment. Eculizumab, a complement inhibitor, has shown promising results in aHUS. However, data are mainly extracted from case reports or studies of heterogeneous cohorts, and no direct comparison with PE/PI is available. Methods: An observational retrospective study of adult, dialysis-dependent aHUS patients with acute kidney injury (AKI) who were treated with either PE/PI alone or with second-line eculizumab in our center. We compared the effect of PE/PI and eculizumab on kidney function, hypertension, proteinuria, hematologic values, relapse, and death. Results: Thirty-one patients were included (females, 18; sporadic aHUS, 29; mean age, 46 ± 20 years). Twenty-six patients were treated with PE/PI alone, and 5 were deemed to be plasma-resistant and received eculizumab after stopping PE/PI. Among patients receiving eculizumab, 80% attained complete recovery of kidney function, 100% stopped dialysis, 20% had decreased proteinuria, and no patient relapsed (vs. 38.5, 50, 15.4, and 11.5%, respectively, of patients receiving only PE/PI). At 1-year of follow-up, no deaths had occurred in either group. Conclusion: Eculizumab shows greater efficacy than PE/PI alone for the treatment of adult aHUS patients with AKI. Prospective studies and meta-analyses are warranted to confirm our findings and set guidelines for treatment, monitoring, and maintenance.

scholarly journals Atypical Hemolytic Uremic Syndrome Presenting as Acute Heart Failure—A Rare Presentation: Diagnosis Supported by Skin Biopsy

2019 ◽  
Vol 7 ◽  
pp. 232470961984290
Author(s):  
Asim Kichloo ◽  
Savneek Singh Chugh ◽  
Sanjeev Gupta ◽  
Jay Pandav ◽  
Praveen Chander
Keyword(s):  
Heart Failure ◽  
Skin Biopsy ◽  
Hemolytic Uremic Syndrome ◽  
Thrombotic Microangiopathy ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Systolic Heart Failure ◽  
Kidney Injury ◽  
Rare Presentation ◽  
History Of ◽  
Uremic Syndrome

Atypical hemolytic uremic syndrome (aHUS) is a rare disorder of uncontrolled complement activation that manifests classically as anemia, thrombocytopenia, and renal failure, although extrarenal manifestations are observed in 20% of the patient most of which involving central nervous system, with relatively rare involvement of the heart. In this article, we report the case of a 24-year-old male with no history of heart disease presenting with acute systolic heart failure along with microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Given his presentation of thrombotic microangiopathy (TMA), along with laboratory results significant for low haptoglobin, platelets, hemoglobin, C3, C4, CH50, and normal ADAMTS13 levels, with no diarrhea and negative STEC polymerase chain reaction in stool, aHUS diagnosis was established with strong clinical suspicion, and immediate initiation of treatment was advised. Kidney biopsy to confirm diagnosis of aHUS was inadvisable because of thrombocytopenia, so the skin biopsy of a rash on his arm was done, which came to be consistent with thrombotic microangiopathy. Our case highlights a relatively rare association between aHUS and cardiac involvement, and the use of skin biopsy to support diagnosis of aHUS in patients who cannot undergo renal biopsy because of thrombocytopenia.

scholarly journals A life-threatening case of pregnancy-related atypical Haemolytic uremic syndrome and successful treatment with Eculizumab

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Prianka Puri ◽  
Anida Hanxhiu ◽  
Daniel V. O’Hara ◽  
Danny Hsu ◽  
Mirna Vucak-Dzumhur
Keyword(s):  
Kidney Injury ◽  
Rare Condition ◽  
Foetal Death ◽  
Case Presentation ◽  
Haemolytic Uremic Syndrome ◽  
Genetic Sequencing ◽  
Planned Pregnancy ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Antenatal Visits

Abstract Background Pregnancy-related Atypical Haemolytic Uremic Syndrome (P-aHUS) is a rare condition affecting genetically predisposed women during pregnancy. It is often difficult to diagnose and has a significant impact on maternal and foetal outcomes. It is characterised by microangiopathic haemolytic anaemia and kidney injury from thrombotic microangiopathy. Case presentation A 27-year-old female of Lebanese descent presented at 36 weeks’ gestation with foetal death in-utero (FDIU) with placental abruption on a background of previously normal antenatal visits. She was coagulopathic and anaemic with anuric acute kidney injury, requiring emergency Caesarean section, intubation and dialysis. Her coagulopathy rapidly resolved, however, her anaemia and renal dysfunction persisted. A diagnosis of P-aHUS was made, and she was empirically treated with Eculizumab. Her ADAMTS13 level was normal, effectively excluding thrombotic thrombocytopenic purpura. Within 2 weeks of treatment her haematological parameters improved, and her renal function began to recover and within 2 months she became dialysis independent. Conclusion This case highlights the challenges of a timely diagnosis of P-aHUS from other pregnancy-related diseases. Although our patient is dialysis-independent, her risk of relapse remains high with subsequent pregnancies. Currently we are awaiting her genetic sequencing to complete her assessment for underlying mutations and are determining the safest approach to a future planned pregnancy.

А case of heparin-induced thrombocytopenia in a patient with a novel coronaviral infection, features of diagnosis and treatment in a naval hospital conditions

2021 ◽  
Vol 7 (3) ◽  
pp. 71-77
Author(s):  
I. D. Shapovalov ◽  
V. E. Makarchenko ◽  
O. Yu. Kartina ◽  
T. L. Belousova
Keyword(s):  
Clinical Practice ◽  
Platelet Activation ◽  
Clinical Case ◽  
Diagnosis And Treatment ◽  
Review Of The Literature ◽  
Heparin Induced Thrombocytopenia ◽  
Frequency Of Use ◽  
Life Threatening ◽  
Life Threatening Complication ◽  
Naval Hospital

The heparin-induced thrombocytopenia is a severe, potentially life-threatening complication of heparinotherpapia associated with thrombosis, develops as a result of antibody-mediated platelet activation. In the context of the SARS CoV-2 pandemic, the frequency of use of heparin in clinical practice has significantly increased, as a result of which the doctors have become more likely to face this complication. The article presents a review of the literature, describes the pathogenesis, modern algorithms for diagnosis and treatment, demonstrates a clinical case of heparin-induced thrombocytopenia in a patient with the SARS CoV-2, and discusses the features of diagnosis and treatment of this complication in a naval hospital.

Complement and the prothrombotic state

Blood ◽  
2021 ◽  
Author(s):  
Christoph Q Schmidt ◽  
Hubert Schrezenmeier ◽  
David Kavanagh
Keyword(s):  
Complement Activation ◽  
Ex Vivo ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Protein Losing Enteropathy ◽  
Mortality And Morbidity ◽  
Life Threatening ◽  
Uremic Syndrome ◽  
Clinical Conditions ◽  
Distinct Features

In 2007 and 2009 the regulatory approval of the first-in-class complement inhibitor Eculizumab has revolutionized the clinical management of two rare, life-threatening clinical conditions: paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS). While being completely distinct diseases affecting blood cells and the glomerulus, PNH and aHUS remarkably share several features in their etiology and clinical presentation. An imbalance between complement activation and regulation at host surfaces underlies both diseases precipitating in severe thrombotic events that are largely resistant to anti-coagulant and/or anti-platelet therapies. Inhibition of the common terminal complement pathway by Eculizumab prevents the frequently occurring thrombotic events responsible for the high mortality and morbidity observed in patients not treated with anti-complement therapy. While many in vitro and ex vivo studies elaborate numerous different molecular interactions between complement activation products and hemostasis, this review focuses on the clinical evidence that links these two fields in humans. Several non-infectious conditions with known complement involvement are scrutinized for common patterns concerning a prothrombotic statues and the occurrence of certain complement activation levels. Next to PNH and aHUS, germline encoded CD59 or CD55 deficiency (the latter causing the disease Complement Hyperactivation, Angiopathic thrombosis, and Protein-Losing Enteropathy; CHAPLE), autoimmune hemolytic anemia (AIHA), (catastrophic) anti-phospholipid syndrome (APS, CAPS) and C3 glomerulopathy are considered. Parallels and distinct features among these conditions are discussed against the background of thrombosis, complement activation, and potential complement diagnostic and therapeutic avenues.

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