scholarly journals Digital Vessel Thrombosis After Early Cessation of Heparin Therapy Following Reimplantation: Two Case Reports

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Kevin McGarry ◽  
Michael Larsen ◽  
Mitchell A. Pet ◽  
Amy M. Moore
Keyword(s):  
Case Reports ◽  
Heparin Therapy ◽  
Vessel Thrombosis

Heparin-Induced Thrombotic Thrombocytopenia

1994 ◽  
Vol 28 (1) ◽  
pp. 43-46 ◽  
Author(s):  
David E. Phillips ◽  
D. Keith Payne ◽  
Glenn M. Mills
Keyword(s):  
Case Reports ◽  
Data Extraction ◽  
Oral Anticoagulants ◽  
Disease Onset ◽  
Insulin Dependent Diabetes Mellitus ◽  
Heparin Therapy ◽  
University Teaching ◽  
Dependent Diabetes Mellitus ◽  
Oliguric Renal Failure ◽  
Presentation Time

OBJECTIVE: To report a case of heparin-induced thrombotic thrombocytopenia (HITTS) and discuss the incidence, possible mechanisms, complications, and treatment for this syndrome. DATA SOURCES: Case reports and review articles identified by MEDLINE from 1980 through 1991. Older articles located by manual searches. DATA EXTRACTION: Data were extracted and reviewed from published sources. Cases were selected on the basis of case presentation, time of disease onset, pathophysiology of disease, and therapeutic options. SETTING: A 600-bed university teaching hospital and an affiliated community hospital. PATIENT: A 36-year-old woman with insulin-dependent diabetes mellitus, sepsis, adult respiratory distress syndrome, diabetic ketoacidosis, oliguric renal failure developed HITTS and subsequent gangrene of her right arm. INTERVENTION: Immediate cessation of all heparin use and amputation of the patient's right arm. RESULTS: The patient's condition improved progressively over the following 60 days and she was discharged to outpatient care. CONCLUSIONS: Heparin has been associated with thrombocytopenia and thrombotic events. Laboratory tests for HITTS are unreliable and the diagnosis is usually suspected by the clinical presentation of the patient. Platelet counts should be monitored closely during heparin use. In the event of a marked decrease in platelet count associated with venous or arterial thrombosis, heparin therapy should be stopped immediately. If further anticoagulation is necessary, oral anticoagulants such as warfarin may be used instead. As the onset of warfarin may take several days to become therapeutic, aspirin, dipyridamole, or both may be used effectively. Healthcare workers should be aware that in these patients, the use of even small amounts of heparin can produce catastrophic results.

A Case against Heparin Therapy of Intravascular Coagulation

1975 ◽  
Vol 33 (01) ◽  
pp. 107-112 ◽  
Author(s):  
P. W Straub
Keyword(s):  
Clinical Benefit ◽  
Serum Proteins ◽  
Case Reports ◽  
Critical Evaluation ◽  
Heparin Therapy ◽  
Controlled Clinical Trials ◽  
Intravascular Coagulation ◽  
Therapeutic Procedures ◽  
Proteolytic Action ◽  
Theoretical Considerations

SummaryAdministration of a potentially dangerous drug like heparin should not be based on theoretical considerations and innumerable case reports but 1) on a firm diagnosis and 2) on a critical evaluation of the clinical benefit.The validity of criteria for the diagnosis of intravascular coagulation (IC) is discussed. It is emphasized in particular that loss of fibrinogen into extravascular spaces can only be excluded by assays of the level and disappearance rate of serum proteins not subject to the proteolytic action of thrombin or plasmin.Even when the diagnosis can be reasonably established, heparin therapy in a particular condition should only be advocated if its clinical benefit has been demonstrated in controlled clinical trials.Our conviction that heparin has as yet a small if any place in the management of patients with so-called intravascular coagulations is based mainly on two sets of arguments, one stemming from a critique of the diagnosis of IC, the other from a general attitude in the evaluation of therapeutic procedures.

Heparin-induced Thrombocytopenia: Pathophysiology, Diagnosis, and Review of Pharmacotherapy

2009 ◽  
Vol 22 (2) ◽  
pp. 149-157 ◽  
Author(s):  
Abir O. Kanaan ◽  
A. Samer Al-Homsi
Keyword(s):  
Myocardial Infarction ◽  
Adverse Drug Reaction ◽  
Randomized Trials ◽  
Clinical Presentation ◽  
Case Reports ◽  
Heparin Therapy ◽  
Thrombin Inhibitors ◽  
Limb Amputation ◽  
Direct Thrombin Inhibitors ◽  
Heparin Induced Thrombocytopenia

Heparin-induced thrombocytopenia is an adverse drug reaction to heparin therapy leading to devastating clinical outcomes including venous thromboembolism, myocardial infarction, stroke, and limb amputation. Heparin cessation alone is not sufficient for the management of heparin-induced thrombocytopenia. Direct thrombin inhibitors, such as argatroban and lepirudin, are considered the mainstay for the management of heparin-induced thrombocytopenia. Case reports support the use of fondaparinux in the management of heparin-induced thrombocytopenia; however, randomized trials are still lacking. This article will review the pathophysiology, clinical presentation, complications, diagnosis, and pharmacotherapy management of heparin-induced thrombocytopenia.

Fludrocortisone for the Treatment of Heparin-Induced Hyperkalemia

2000 ◽  
Vol 34 (5) ◽  
pp. 606-610 ◽  
Author(s):  
Deb S Sherman ◽  
Carrie L Kass ◽  
Douglas N Fish
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Case Reports ◽  
Alternative Therapy ◽  
Heparin Therapy ◽  
Zona Glomerulosa ◽  
Vein Thrombosis ◽  
Case Summary ◽  
Heparin Administration ◽  
Distal Tubules

OBJECTIVE: To report the use of fludrocortisone for heparin-induced hyperkalemia and to briefly review the available literature relating to heparin-induced hyperkalemia. CASE SUMMARY: A 34-year-old African-American man was admitted to the hospital for pneumococcal pneumonia and sepsis. His hospital course was complicated by the development of acute respiratory distress syndrome, severe sepsis, acute renal failure, placement of a tracheostomy, and recurrent nasopharyngeal bleeding. The patient also developed a subclavian vein thrombosis with extension to the cephalic and basilic veins secondary to placement of a pulmonary artery catheter; anticoagulation with heparin was required. On day 9 of heparin therapy, the patient developed symptomatic hyperkalemia refractory to conventional therapies. Oral fludrocortisone 0.1 mg/d was initiated with resolution of the hyperkalemia within 24 hours despite the continued administration of heparin. DATA SOURCES: A MEDLINE (1966–October 1999) search was performed to identify case reports and clinical trials discussing heparin-induced hyperkalemia or the use of fludrocortisone for hyperkalemia. DISCUSSION: Heparin has the potential to induce hyperkalemia by several mechanisms, including decreased aldosterone synthesis, reduction in number and affinity of aldosterone II receptors, and atrophy of the renal zona glomerulosa. Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. In this patient, fludrocortisone resulted in a significant and rapid decrease in serum potassium even with continued heparin administration and acute renal failure. CONCLUSIONS: This case suggests that fludrocortisone is a reasonable alternative therapy for patients with hyperkalemia secondary to heparin therapy when the continued administration of heparin is necessary.

Case Reports Link ADHD Stimulants to Skin Eruptions

2011 ◽  
Vol 45 (12) ◽  
pp. 10
Author(s):  
SHERRY BOSCHERT
Keyword(s):  
Case Reports

Bowel ischaemia after endovascular aneurysm repair

VASA ◽  
2018 ◽  
Vol 47 (4) ◽  
pp. 273-277
Author(s):  
Christopher Lowe ◽  
Oussama El Bakbachi ◽  
Damian Kelleher ◽  
Imran Asghar ◽  
Francesco Torella ◽  
...  
Keyword(s):  
Case Reports ◽  
Endovascular Aneurysm Repair ◽  
Artery Occlusion ◽  
Bibliographic Databases ◽  
Bowel Ischaemia ◽  
Prophylactic Measures ◽  
Increased Risk ◽  
Prisma Statement ◽  
Meta Analyses ◽  
Aneurysm Repair

Abstract. The aim of this review was to investigate presentation, aetiology, management, and outcomes of bowel ischaemia following EVAR. We present a case report and searched electronic bibliographic databases to identify published reports of bowel ischaemia following elective infra-renal EVAR not involving hypogastric artery coverage or iliac branch devices. We conducted our review according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement standards. In total, five cohort studies and three case reports were included. These studies detailed some 6,184 infra-renal elective EVARs, without procedure-related occlusion of the hypogastric arteries, performed between 1996 and 2014. Bowel ischaemia in this setting is uncommon with an incidence ranging from 0.5 to 2.8 % and includes a spectrum of severity from mucosal to transmural ischaemia. Due to varying reporting standards, an overall proportion of patients requiring bowel resection could not be ascertained. In the larger series, mortality ranged from 35 to 80 %. Atheroembolization, hypotension, and inferior mesenteric artery occlusion were reported as potential causative factors. Elderly patients and those undergoing prolonged procedures appear at higher risk. Bowel ischaemia is a rare but potentially devastating complication following elective infra-renal EVAR and can occur in the setting of patent mesenteric vessels and hypogastric arteries. Mortality ranges from 35 to 80 %. Further research is required to identify risk factors and establish prophylactic measures in patients that have an increased risk of developing bowel ischaemia after standard infra-renal EVAR.

Cannabis-associated arteritis

VASA ◽  
2010 ◽  
Vol 39 (1) ◽  
pp. 43-53 ◽  
Author(s):  
Grotenhermen
Keyword(s):  
Systematic Review ◽  
Case Reports ◽  
Case Series ◽  
Cardiovascular Effects ◽  
Causative Factor ◽  
Cannabis Use ◽  
Thromboangiitis Obliterans ◽  
Pathological Features ◽  
Scientific Support ◽  
Clinical And Pathological Features

Background: To investigate the hypothesis that cases of arteritis similar to thromboangiitis obliterans (TAO) and associated with the use of cannabis were caused by cannabis or THC (dronabinol), or that cannabis use is a co-factor of TAO. Patients and methods: A systematic review on case reports and the literature on so-called cannabis arteritis, TAO, and cardiovascular effects of cannabinoids was conducted. Results: Fifteen reports with 57 cases of an arteritis associated with the use of cannabis and two additional case series of TAO, in which some patients also used cannabis, were identified. Clinical and pathological features of cannabis-associated arteritis do not differ from TAO and the major risk factor of TAO, tobacco use, was present in most, if not in all of these cases. The proposed pathophysiological mechanisms for the development of an arteritis by cannabis use are not substantiated. Conclusions: The hypothesis of cannabis being a causative factor or co-factor of TAO or an arteritis similar to TAO is not supported by the available evidence. The use of the term “cannabis arteritis” should be avoided until or unless more convincing scientific support is forthcoming.

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