Adrenal haemorrhage due to heparin-induced thrombocytopenia

2013 ◽  
Vol 109 (04) ◽  
pp. 669-675 ◽  
Author(s):  
Siva Ketha ◽  
Patrick Smithedajkul ◽  
Adrian Vella ◽  
Rajiv Pruthi ◽  
Waldemar Wysokinski ◽  
...  
Keyword(s):  
Natural History ◽  
Time Frame ◽  
Antiphospholipid Antibody ◽  
Thrombotic Complication ◽  
Antiphospholipid Antibody Syndrome ◽  
Adrenal Haemorrhage ◽  
Heparin Induced Thrombocytopenia ◽  
Joint Replacement Surgery ◽  
History Of ◽  
Heparin Exposure

SummaryAdrenal haemorrhage (AH) is a rare but potentially devastating complication of heparin-induced thrombocytopenia (HIT). Neither the prevalence nor the natural history of AH due to HIT are known. The objectives of this study were to identify the spectrum of AH causes, to characterise the frequency of AH due to HIT and determine the natural history of HIT-associated AH. All patients with incident adrenal haemorrhage from January 2002 through June 2012 seen at the Mayo Clinic were identified. Over this time frame, there were a total of 115 patients with AH of which 11 cases (10%; mean age 67 ± 8 years; 73% female) were associated with HIT. Of these, all but one occurred in the postoperative setting and involved both adrenal glands (89%) with acute adrenal insufficiency at the time of diagnosis. Cases were found incidentally during an evaluation for fever, shock, abdominal pain or mental status changes. All HIT patients experienced venous thrombosis at other locations including deep venous thromboses (n=14), pulmonary emboli (n= 4) and arterial thrombosis (n=2). Four patients undergoing total knee arthroplasty had “spontaneous HIT” with AH in the absence of identifiable heparin exposure. Other causes of AH included trauma (29%), sepsis (15%), antiphospholipid antibody syndrome (10%), and metastatic disease (12%). In conclusion, AH is an important but seldom recognised presumed thrombotic complication of HIT, which usually occurs in the postoperative period, especially after orthopaedic procedures. This syndrome can occur in the apparent absence of heparin exposure, especially following major joint replacement surgery.

scholarly journals Antiphospholipid Antibody Syndrome Presenting with Hemichorea

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Yezenash Ayalew ◽  
Fazlihakim Khattak
Keyword(s):  
First Trimester ◽  
Anticardiolipin Antibodies ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Blurred Vision ◽  
Significant Family History ◽  
History Of ◽  
The Right ◽  
Time Of Presentation ◽  
Underlying Pathophysiology

A 25-year-old Bangladeshi lady presented to neurology with a three-month history of involuntary movements of her right arm, associated with loss of power. There was progression to the right leg, and she subsequently developed episodes of slurred speech and blurred vision. At the time of presentation, she was 12 weeks pregnant and the symptoms were reported to have started at conception. Past medical history was unremarkable apart from one first trimester miscarriage and there was no significant family history suggestive of a hereditary neurological condition. MRI of the head revealed no abnormalities but serology showed positive antinuclear antibodies (ANAs) at a titre of 1/400. Further investigations revealed strongly positive anticardiolipin antibodies (>120) and positive lupus anticoagulant antibodies. The patient had a second miscarriage at 19 weeks gestation strengthening the possibility that the chorea was related to antiphospholipid antibody syndrome and she was started on a reducing dose of Prednisolone 40 mg daily and aspirin 300 mg daily. Six months later, she had complete resolution of neurological symptoms. There are several reports of chorea as a feature of antiphospholipid syndrome, but no clear consensus on underlying pathophysiology.

Pyoderma Gangrenosum Mimicking Antiphospholipid Antibody Syndrome in a Child With Juvenile Systemic Lupus Erythematosus

2020 ◽  
Author(s):  
metin kaya gürgöze ◽  
Aslıhan Kara ◽  
Mehmet yusuf sarı ◽  
İlknur Çalık ◽  
Saadet Akarsu
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Skin Biopsy ◽  
Pyoderma Gangrenosum ◽  
Lupus Erythematosus ◽  
Anticoagulation Therapy ◽  
Anticardiolipin Antibody ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Systemic Lupus ◽  
History Of

Abstract Background: Although pyoderma gangrenosum (PG) -like lesions have been rarely described in adults with the antiphospholipid antibody syndrome (APS) and systemic lupus erythematosus (SLE), the occurrence of PG as a preceding manifestation of APS in children with SLE has not been reported until. We present a young girl with SLE and APS who developed progressive extstensive ulcerations that were consistent with PG.Case presentation: A 14-year-old girl with a 2-year history of SLE was admitted to our department, complaining painful crusted ulcerations on her legs. Skin biopsy was reported as PG. However, she did not respond to immunosuppressive therapy administered. When her skin biopsy findings is reassessed in keeping with the positive anticardiolipin antibody results, superficial small vessel microthrombosis was observed. Diagnosis of APS and PG developing secondary to SLE were made. It was resulted in marked clinical improvement with anticoagulation therapy in addition to immunosuppressives as is recommended in APS. Conclusions: Based in clinical, pathological and response to proposed treatment, we can state that PG -like lesions in children with SLE could be considered as a secondary form of APS.

scholarly journals Successful Pregnancy Outcome with High dose Heparin Therapy in Antiphospholipid Antibody Syndrome

1970 ◽  
Vol 11 (2) ◽  
pp. 205-206
Author(s):  
MP Ranjith ◽  
Ranjith Divya ◽  
S Meera ◽  
Shabu Bahuleyan ◽  
Roney Joseph Kuryan
Keyword(s):  
Antiphospholipid Antibodies ◽  
Heparin Therapy ◽  
High Dose ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Syndrome Patient ◽  
Successful Pregnancy ◽  
Dose Heparin ◽  
History Of ◽  
Recurrent Abortions

Antiphospholipid antibody syndrome is an autoimmune disease characterized by thrombosis, both arterial andvenous, recurrent spontaneous abortion and the persistence of positive antiphospholipid antibodies. Placentalthrombosis is believed to be the cause of recurrent abortions, characteristic of the syndrome. We report a pregnantwith antiphospholipid antibody syndrome patient with history of recurrent miscarriages and managed successfullywith high dose heparin.Keywords: Antiphospholipid antibody syndrome; recurrent intra uterine death; HeparinDOI: 10.3329/jom.v11i2.5476J MEDICINE 2010; 11 : 205-206

Efficacious and Safe Use of Recombinant Activated Factor VII (rFVIIa) in Patients with Enoxaparin (ENOX)-Induced Bleeding and Pre-Existing Hypercoagulable States.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1054-1054 ◽  
Author(s):  
K. Firozvi ◽  
P. Acs ◽  
S. Baidas ◽  
R. Deveras ◽  
C. M. Kessler
Keyword(s):  
Kidney Biopsy ◽  
Ex Vivo ◽  
Factor Vii ◽  
Bleeding Complications ◽  
Prior History ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Intravenous Bolus ◽  
History Of ◽  
Antifactor Xa

Abstract Introduction: rFVIIa has been touted as a pancoagulant to reverse untoward hemorrhage in various clinical situations. We describe 3 hypercoagulable patients with enox-induced bleeding treated successfully and safely with rFVIIa. Case Summaries: Patient 1, a 58 year old female, received enox 60mg SQ q12 h for a left femoral DVT. On day 2, a bleeding right femoral pseudoaneurysm was detected. On day 3, the patient’s hematocrit fell from 37.5% to 22%, as swelling and pain ensued in the right thigh 4h after receiving her AM dose of enox. The concurrent PT, INR and aPTT were 18.1, 1.72 and 34.2 sec respectively. rFVIIa (20μg/kg) was administered intravenously with rapid cessation of bleeding. Patient 2, a 42 year old male, with a history of SLE, antiphospholipid antibody syndrome, and a distant history of a distal DVT was admitted for acute renal failure (creatinine of 4.2) secondary to lupus nephritis. One day after a kidney biopsy, the patient was placed on coumadin 5mg and continuous infusion of unfractionated heparin which was then changed to enox 70 mg SQ q 12. Both coumadin and enox were held after 4 d, once his PT, INR and aPTT reached 30, 3.97 and 56.2 sec respectively. The next day, a CT scan to evaluate a new abdominal pain revealed a large bleed at the kidney biopsy site. Despite transfusions of 6 bags of red blood cells, 4 bags of fresh frozen plasma, and 10mg of SQ vitamin K1, his hematocrit dropped to 19% and his PT, INR, and aPTT remained elevated at 28, 3.49, and 60.8 sec respectively. Thromboembolization was achieved to terminate bleeding from 2 of his 3 renal biopsy sites, the last of which was technically inaccessible. rFVIIa (30μg/kg) was administered as an intravenous bolus with immediate cessation of active bleeding. The next day, the antifactor Xa level was 0.12 anti-Xa U/ml and the PT, INR, and aPTT were 13.7, 1.09 and 45.1 sec, respectively and remained at these levels for the next 4 days. Patient 3, a 56 year old female with a prior history of multiple PEs and proximal DVTs due to protein S deficiency, was admitted for total knee arthroplasty. Admission labs were all within normal limits. Enox 80mg sq was initiated 24 h post-operatively for DVT prophylaxis. Four h later, brisk bleeding developed acutely from the surgical site. The simultaneous antifactor Xa level was 0.49 anti-Xa U/ml. rFVIIa (20μg/kg) was administered as an intravenous bolus and bleeding from the JP drain ceased instantly. All 3 patients stabilized within hours following administration of rFVIIa for their acute bleeding events; all required multiple transfusions of FFP and packed RBCs before rFVIIa; and all resumed anticoagulation without further bleeding. Discussion: Many clinicians fear that the rare untoward hemorrhage associated with any low molecular weight heparin (LMWH) preparation cannot be efficiently or rapidly reversed as there is no specific or reliable antidote. rFVIIa concentrate has reversed the anti-Xa properties of LMWH in ex vivo plasma-spiking experimental models but experience with use of rFVIIa to reverse LMWH-induced bleeding in vivo is lacking. Conclusion: This report suggests that rFVIIa administered in low doses (20–30μg/kg) reverses clinically significant LMWH-induced bleeding complications effectively, rapidly, and safely and should be considered as an adjunct in the treatment of LMWH-induced bleeding in patients with either hypercoagulable conditions or acute VTE. Clinical trials are needed to confirm the effectiveness of rFVIIa in this clinical scenario.

scholarly journals CRITICAL ANALYSIS OF JATAHARINIES WSR TO ANTIPHOSPHOLIPID ANTIBODY SYNDROME

2020 ◽  
pp. 95-102
Author(s):  
Sushma
Keyword(s):  
Critical Analysis ◽  
Recurrent Miscarriage ◽  
Intrauterine Fetal Death ◽  
Antiphospholipid Antibody ◽  
Antiphospholipid Antibody Syndrome ◽  
Intrauterine Death ◽  
Still Birth ◽  
Neonatal Deaths ◽  
History Of ◽  
Ayurvedic Treatment

Acharya Kashyapa in Revatikalpa adhyaya explained about the Jataharinies, as a group of demons who has divine vision, attack women to destroy or to produce serious problems of menstrual cycle, recurrent abortions, still birth, intrauterine fetal death, neonatal deaths or severe disorders which decreases the life span of the fetus. As recurrent miscarriage, intrauterine death of an infant or death at birth has always been a devastating experience for the mother and of concern in clinical practice. All these mortality remains a challenge in the care of pregnant women worldwide, particularly for those who had history of adverse outcome in previous pregnancies (BOH). Antiphospholipid antibody syndrome (Hughes syndrome) is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. Pregnancy related complications are miscarriage, still birth, preterm delivery, IUD etc. This is one of the few treatable causes of pregnancy loss, and successful pregnancy rates of 70% or more can be achieved with appropriate treatment. Description of Jataharinies resemble with APLA, hence critical analysis will help to emphasize on management of Jataharinies by Ayurvedic treatment principles.

Rapid onset heparin-induced thrombocytopenia (HIT) without history of heparin exposure: A new case of so-called ‘spontaneous’ HIT

2012 ◽  
Vol 107 (04) ◽  
pp. 795-797 ◽  
Author(s):  
Damien Barraud ◽  
Marie Toussaint-Hacquard ◽  
Pierre-Edouard Bollaert ◽  
Thomas Lecompte ◽  
Julien Perrin
Keyword(s):  
Rapid Onset ◽  
Heparin Induced Thrombocytopenia ◽  
History Of ◽  
Heparin Exposure

scholarly journals How I treat patients with a history of heparin-induced thrombocytopenia

Blood ◽  
2016 ◽  
Vol 128 (3) ◽  
pp. 348-359 ◽  
Author(s):  
Theodore E. Warkentin ◽  
Julia A. M. Anderson
Keyword(s):  
Oral Anticoagulants ◽  
Chronic Hemodialysis ◽  
Short Term ◽  
Heparin Induced Thrombocytopenia ◽  
Coronary Syndrome ◽  
History Of ◽  
Minimum Interval ◽  
Direct Acting ◽  
Or History ◽  
Heparin Exposure

Abstract Heparin-induced thrombocytopenia (HIT) is a relatively common prothrombotic adverse drug reaction of unusual pathogenesis that features platelet-activating immunoglobulin G antibodies. The HIT immune response is remarkably transient, with heparin-dependent antibodies no longer detectable 40 to 100 days (median) after an episode of HIT, depending on the assay performed. Moreover, the minimum interval from an immunizing heparin exposure to the development of HIT is 5 days irrespective of the patient’s previous heparin exposure status or history of HIT. This means that short-term heparin reexposure can be safely performed if platelet-activating antibodies are no longer detectable at reexposure baseline and is recommended when heparin is the clear anticoagulant of choice, such as for cardiac or vascular surgery. The risk of recurrent HIT 1 to 2 weeks after heparin reexposure is ∼2% to 5% and is attributable to formation of delayed-onset (or autoimmune-like) HIT antibodies that activate platelets even in the absence of pharmacologic heparin. Some studies suggest that longer-term heparin reexposure (eg, for chronic hemodialysis) may also be reasonable. However, for other antithrombotic indications that involve patients with a history of HIT (eg, treatment of venous thromboembolism or acute coronary syndrome), preference should be given to non-heparin agents such as fondaparinux, danaparoid, argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

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