Paradoxical embolism is defined as a systemic arterial embolism requiring the passage of a venous thrombus into the arterial circulatory system through a right-to-left shunt. It is a relatively rare phenomenon, representing about 2% of all cases of arterial embolism. We report a case of a 79-years-old woman admitted to hospital because of dyspnea and lower left limb pain. CT scan revealed multiple thrombi to kidney, lower limb and superior mesenteric artery during acute pulmonary embolism. Echocardiogram documented a patent foramen ovale with a right-to-left shunt. The patient was treated with thrombolytic therapy and heparin with progressive improvement of symptoms and resolution of pulmonary embolism and peripheral thrombosis. Patent foramen ovale closure was not performed because a life-long anticoagulation therapy was necessary, a tunnel-type patent foramen ovale may increases difficulty in realizing device implantation and there are no clear evidence-based guidelines to date addressing treatment in presence of a patent foramen ovale.
Cystic fibrosis is usually associated with chronic pulmonary sepsis and frequent infective exacerbations. We report a very unusual cause of severe hypoxaemia in a woman with cystic fibrosis caused by thrombus formation in the right atrium.
A 21-year-old Caucasian woman with cystic fibrosis and a totally implantable venous access device presented with severe hypoxaemia. This was initially treated with antibiotics but her oxygen levels did not improve significantly. Subsequently, a transient ischaemic attack occurred. Further investigations, including a contrast echocardiogram and a cardiac magnetic resonance scan, revealed the presence of a large right atrial thrombus and right-to-left intracardiac shunt through a patent foramen ovale.
This case highlights the need to consider a right-to-left shunt in chronic respiratory diseases when hypoxaemia is out of proportion to the degree of lung function impairment. Totally implantable venous access devices should always be considered as a source of thrombus formation.
Currently, the only widely accepted indication for thrombolysis in cases of pulmonary embolism is hemodynamic instability. However, the presence of a right-heart thrombus along with pulmonary embolism is a poor prognostic indicator, and the use of thrombolytic agents should also be considered in this circumstance. Furthermore, despite a risk of distal embolization, thrombolytic therapy may be implemented if the intracardiac thrombus also straddles a patent foramen ovale.
Herein, we present the case of a 92-year-old woman who presented at our institution after a syncopal event and multiple recent episodes of amaurosis fugax. Transthoracic echocardiography revealed a mobile right-heart thrombus that extended through a patent foramen ovale into the left atrium. Computed tomography of the chest showed a saddle pulmonary embolus. We used thrombolytic therapy to treat the patient, and imaging showed complete resolution of the thrombus and the embolism 2 days later.
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Heart diseases/complications/mortality/therapy; pulmonary embolism/complications; thrombolytic therapy; thrombosis/complications/drug therapy
Thrombosis due to heparin-induced thrombocytopenia (HIT) is rare but has a severe prognosis. Its management is not always easy, particularly in old patients with renal insufficiency. A 95-year-old woman was hospitalized for dyspnea. Curative treatment with unfractionated heparin was started because pulmonary embolism was suspected. Disseminated intravascular coagulation was then suspected because of thrombocytopenia, hypoprothrombinemia, hypofibrinogenemia, and a positive ethanol gelation test. The first immunoassay for HIT was negative. On the 12th day of hospitalization, bilateral cyanosis of the toes occurred associated with recent deep bilateral venous and arterial thrombosis at duplex ultrasound. New biological tests confirmed HIT and led us to stop heparin and to start argatroban with a positive clinical and biological evolution. Venous and arterial thrombosis associated with thrombocytopenia during heparin treatment must be considered HIT whatever the biological test results are. Argatroban is a good alternative treatment in the elderly.
Heparin is one of the most frequently used anticoagulants. It is easy to use, but can be associated with life-threatening side effects. One of these is heparin-induced thrombocytopenia syndrome (HITS), which develops in about 3–5% of patients exposed to heparin and is associated with thrombosis in 1% of cases. We report here the successful treatment of five patients with HITS who were treated with alternative anticoagulants namely danaparoid or hirudin. The median time between their exposure to heparin and onset of symptoms and or signs was 10.2 days (range 7–14 days). Platelet counts decreased to a mean of 38.4 x 109 /l (12–82 x 109/l). All five patients had evidence of thrombosis; four patients had clinical and radiological evidence of pulmonary emboli, one patient had confirmed deep vein thrombosis (DVT) and one patient had extensive skin necrosis of the thighs and abdomen. Platelet aggregation test were positive in two patients, inconclusive in one patient and negative in two patients. Two patients were anticoagulated with danaparoid and three with hirudin until their platelet counts returned to normal between 4 and 14 days (average 6 days) following the recognition of the syndrome. Our patients had significant morbidity, but no mortality. Immediate withdrawal of heparin is of paramount importance and introduction of alternative anticoagulant is necessary in the presence of thrombosis.
Unfractionated heparin; Low-molecular weight heparin; Heparin-induced thrombocytopenia; Hirudin; Danaparoid; Case report; Oman
OBJECTIVE--To compare the efficacy and safety of low molecular weight heparins and unfractionated heparin in the initial treatment of deep venous thrombosis for the reduction of recurrent thromboembolic events, death, extension of thrombus, and haemorrhages. DESIGN--Meta-analysis of results from 16 randomised controlled clinical studies. SUBJECTS--2045 patients with established deep venous thrombosis. INTERVENTION--Treatment with low molecular weight heparins or unfractionated heparin. MAIN OUTCOME MEASURES--Incidences of thromboembolic events (deep venous thrombosis or pulmonary embolism, or both); major haemorrhages; total mortality; and extension of thrombus. RESULTS--A significant reduction in the incidence of thrombus extension (common odds ratio 0.51, 95% confidence interval 0.32 to 0.83; P = 0.006) in favour of low molecular weight heparin was observed. Non-significant trends also in favour of the low molecular weight heparins were observed for the recurrence of thromboembolic events (0.66, 0.41 to 1.07; P = 0.09), major haemorrhages (0.65, 0.36 to 1.16; P = 0.15), and total mortality (0.72, 0.46 to 1.4; P = 0.16). CONCLUSIONS--Low molecular weight heparins seem to have a higher benefit to risk ratio than unfractionated heparin in the treatment of venous thrombosis. These results, however, remain to be confirmed by using clinical outcomes in suitably powered clinical trials.
Paradoxical embolism (PDE) occurs after embolic material passes from the venous to the arterial circulation through a right-to-left shunt, which is frequently a patent foramen ovale (PFO). We describe the case of a patient with deep venous thrombosis and an intracardiac thrombus straddling a PFO and who was successfully treated with an emergency surgery.
Paradoxical embolism; Patent foramen ovale; Economy class syndrome; Pulmonary embolism
Heparin-induced thrombocytopenia (HIT) is an immunologic drug reaction characterized by paradoxical association with venous and arterial thrombosis. The syndrome is caused by IgG antibodies that are reactive against complexes of platelet factor 4 and heparin. Fondparinux does not bind to platelet factor 4, is structurally too short to induce an antibody response, and could in theory be a useful agent to treat HIT. A 69-year-old white female presented with a lower extremity extensive iliofemoral deep vein thrombosis after a right total knee arthroplasty and was subsequently found to have a pulmonary embolism. The patient was noted to have heparin flushes during her operation. Her platelet drop decreased >50% from baseline during initiation of antithrombotic therapy. She was started on subcutaneous fondaparinux 7.5 mg once daily injection. Her serotonin release assay and enzyme-linked immunosorbent assay for heparin antibodies were positive for HIT. Her platelet count nadir was 60 × 03/mm3 on day 5 and the platelet count rebounded after 8 days of fondaparinux therapy. No recurrent thrombotic or bleeding events were noted throughout her therapy. Anecdotal reports have shown that fondaparinux can be a useful agent to treat HIT with or without thrombosis.
fondaparinux; heparin-induced thrombocytopenia with thrombosis (HITT)
A 45-year-old female presented with 8 hours of right lower extremity pain and dyspnea. She was tachycardic and her right lower extremity was dusky, cold, and pulseless.
Computerized tomography of the venous and arterial systems revealed massive pulmonary embolism and right lower extremity arterial and left lower extremity venous thromboses. Management included intra-arterial thrombolytics, right lower extremity arterial embolectomy, and anticoagulation. Echocardiogram revealed a patent foramen ovale (PFO) with a right-to-left shunt.
We hypothesize that our patient developed deep venous thrombosis that led to major pulmonary embolization and increased right-sided pressures. In the setting of a patent foramen ovale, a later venous embolus transversed the PFO and lodged in the femoral artery. Our case illustrates the importance of a high index of suspicion for a paradoxical embolus in patients with arterial thrombosis.
paradoxical embolism; deep venous thrombosis; patent foramen ovale
Traditionally, acute deep venous thrombosis (DVT) is treated with intravenous heparin followed by oral anticoagulants. With the advent of the low-molecular-weight heparins (LMWHs), this strategy is changing dramatically. LMWHs are compounds derived from standard unfractionated heparin that offer distinct clinical advantages over unfractionated heparin, including better bioavailability, longer half-life, and a more predictable anticoagulant response that obviates the need for laboratory monitoring. The common side effects of unfractionated heparin, including bleeding, thrombocytopenia, and osteoporosis, may be less common with LMWH. For the treatment of established venous thromboembolism, LMWH is at least as safe and effective as unfractionated heparin. Recent studies demonstrate that home therapy of DVT with LMWH, compared with inpatient therapy with unfractionated heparin, produces comparable clinical outcomes and patient satisfaction, with dramatic cost savings. With careful patient selection, home therapy of venous thromboembolism is quickly becoming the new standard of care.
Heparin-induced thrombocytopenia (HIT) is a thromboembolic complication that can occur with unfractionated heparin (UFH) or low molecular weight heparin (LMWH). Our objective was to determine and compare the incidence of IgG-class HIT antibodies in patients undergoing total hip arthroplasty (THA) or total knee arthroplasty (TKA) with different antithrombotic prophylaxis therapies and their contributions to the occurrence of venous thromboembolism (VTE).
A prospective observational study was performed for 374 Japanese patients undergoing THA or TKA to determine the incidence of VTE. IgG-class anti-PF4/heparin antibodies were measured using IgG-specific EIA before and after the operation.
In the clinical outcome, the incidence of symptomatic deep vein thrombosis (DVT) was 15.0% (56/374, TKA; 35, THA; 21) and pulmonary emboli (PE) were not observed. The total seroconversion incidence of IgG-class PF4/heparin antibodies was 19.8% (74/374). The seroconversion incidence of IgG-class PF4/heparin antibodies was higher in patients receiving UFH (32.7%) compared to those receiving LMWH (9.5%) or fondaparinux (14.8%). Furthermore, the seroconversion incidence was significantly higher in patients undergoing TKA compared to those undergoing THA. Based on multivariate analysis, seroconversion of the IgG-class PF4/heparin antibodies was independent a risk factor for symptomatic DVT.
Our findings show that the seroconversion of IgG-class anti-PF4/heparin antibodies differed with various anti-thrombotic prophylaxis therapeutics and was associated with the risk of DVT in a subset of patients undergoing total joint arthroplasty (TKA and THA).
Venous thromboembolism (VTE) is a frequent complication among acutely ill medical patients hospitalized for congestive heart failure, acute respiratory insufficiency, rheumatologic disorders, and acute infectious and/or inflammatory diseases. Based on robust data from randomized controlled studies and meta-analyses showing a reduced incidence of VTE by 40% to about 60% with pharmacologic thromboprophylaxis, prevention of VTE with low molecular weight heparin (LMWH), unfractionated heparin (UFH), or fondaparinux is currently recommended in all at-risk hospitalized acutely ill medical patients. In patients who are bleeding or are at high risk for major bleeding, mechanical prophylaxis with graduated compression stockings or intermittent pneumatic compression may be suggested. Thromboprophylaxis is generally continued for 6 to 14 days or for the duration of hospitalization. Selected cases could benefit from extended thromboprophylaxis beyond this period, although the risk of major bleeding remains a concern, and additional studies are needed to identify patients who may benefit from prolonged prophylaxis. For hospitalized acutely ill medical patients with renal insufficiency, a low dose (1.5 mg once daily) of fondaparinux or prophylactic LMWH subcutaneously appears to have a safe profile, although proper evaluation in randomized studies is lacking. The evidence on the use of prophylaxis for VTE in this latter group of patients, as well as in those at higher risk of bleeding complications, such as patients with thrombocytopenia, remains scarce. For critically ill patients hospitalized in intensive care units with no contraindications, LMWH or UFH are recommended, with frequent and careful assessment of the risk of bleeding. In this review, we discuss the evidence for use of thromboprophylaxis for VTE in acutely ill hospitalized medical patients, with a focus on (low-dose) fondaparinux.
venous thromboembolism; medical patient; hospitalization; fondaparinux; heparin
A 34-year-old man was admitted to our hospital’s department of neurology because he had experienced a cryptogenic stroke followed by a transient ischaemic attack. The patient suffered from congenital hydrocephalus which was treated by ventriculoatrial shunt at 8 months of age. Twelve months later, because of recurrent infections, the catheter was partially removed and the distal segment was left in place. At admission, the transoesophageal echocardiogram showed severe pulmonary hypertension (80 mm Hg confirmed by invasive measurement). The distal tip of the catheter had migrated into the left atrium through a patent foramen ovale inducing a massive right-to-left shunt. We surgically removed the catheter and closed the interatrial defect. At 1 and 6 months follow-up the patient was asymptomatic with a reduced pulmonary hypertension (50 mm Hg). Since there was no other clinical finding responsible for the recurrent thromboembolic events, both at the pulmonary and cerebral level, the catheter was removed to prevent further complications.
Skin necrosis and limb gangrene are occasional thrombotic manifestations of anticoagulation therapy. We report a man heterozygous for the Factor V Leiden (FVL) mutation, and with a history of recurrent deep venous thrombosis, who initially presented with a necrotic skin lesion of the right flank while on warfarin therapy with a therapeutic international normalized ratio. Warfarin was discontinued and he received intravenous heparin. Thereafter he developed thrombocytopenia and pedal erythema and was diagnosed with heparin-induced thrombocytopenia (HIT). Heparin was replaced with argatroban. He ultimately underwent bilateral below-knee amputations for the thrombotic complications of the HIT. The initial necrotic lesion healed with antibiotics and wound care. Pathologic examination of multiple biopsy specimens revealed two separate lesions. One was necrotic tissue infiltrated with methicillin resistant Staphylococcus aureus having features of ecthyma gangrenosum. The second showed thrombotic changes consistent with HIT. The case illustrates the differential diagnosis of skin necrosis and limb gangrene in patients on warfarin and heparin, and also the clinical complexities that can occur in a FVL heterozygote.
Factor V Leiden; ecthyma gangrenosum; heparin induced thrombocytopenia; deep vein thrombosis.
A 78 year old woman with congestive cardiac failure developed pulmonary embolism. Cross sectional echocardiography detected an undulating fusiform mass attached to the lateral wall of the right atrium and protruding through the tricuspid valve. Serial cross sectional echocardiograms showed a reduction in the size of the mass, and by three months the mass was immobile and attached by a broad base to the lateral atrial wall. The mass was assumed to be a thrombus, and treatment with heparin and oral anticoagulants appeared to prevent the development of further pulmonary emboli.
Deep venous thrombosis prophylaxis is essential to the appropriate management of multisystem trauma patients. Without thromboprophylaxis, the rate of venous thrombosis and subsequent pulmonary embolism is substantial. Three prophylactic modalities are common: pharmacologic anticoagulation, mechanical compression devices, and inferior vena cava filtration. A systematic review was completed using PRISMA guidelines to evaluate the potential complications of DVT prophylactic options. Level one evidence currently supports the use of low molecular weight heparins for thromboprophylaxis in the trauma patient. Unfortunately, multiple techniques are not infrequently required for complex multisystem trauma patients. Each modality has potential complications. The risks of heparin include bleeding and heparin induced thrombocytopenia. Mechanical compression devices can result in local soft tissue injury, bleeding and patient non-compliance. Inferior vena cava filters migrate, cause inferior vena cava occlusion, and penetrate the vessel wall. While the use of these techniques can be life saving, they must be appropriately utilized.
Right sided heart thrombi may develop within the right heart chambers or they may be peripheral venous clots that on their way to the lungs, accidentally lodge in a patent foramen ovale, tricuspid chordae or Chiaris network. Type A thrombi have a worm-like shape and are extremely mobile. These pleomorphic thrombi are mainly localized in the right atrium, frequently move back and forth through the tricuspid orifice and may cause cardiovascular collapse when entrapment occurs. Type B thrombi attach to the atrial or ventricular wall indicating that they are probably of local origin. We describe the case of a middle age man (48 years old) with no cardiovascular history and a massive pulmonary embolism where transthoracic echocardiography revealed many type A thrombi in both right atrium and ventricle. He presented with acute dyspnea, diaphoresis and hemodynamical instability. He was treated with thrombolysis and after three hours was greatly improved and the thrombi were disappeared. After ten days of hospitalization he was discharged. Thrombi were originated in the popliteal region of the inferior vena cava of both legs and were totally treated.
pulmonary embolism; right heart thromboemboli; thrombolysis
An elderly gentleman presented to the emergency department with a recent history of dyspnoea, collapse and transient neurological symptoms. He was noted to be hypoxic with a significantly elevated D Dimer. A computer tomography pulmonary angiogram demonstrated a large embolus with a further filling defects within the left and the right atria, abutting the inter-atrial septum. Suspicion of a paradoxical pulmonary embolus was raised and the patient subsequently underwent echocardiography which confirmed a patent foramen ovale (PFO). He was commenced on warfarin therapy. In patients with elevated right heart pressure, a PFO can be unmasked and give rise to cerebral emboli. Clinical suspicion should be raised in patients with pulmonary emboli or deep venous thrombosis if there is a concomitant history of focal neurological symptoms.
Pulmonary embolus; Paradoxical embolus; Computer tomography pulmonary angiogram; Patent foramen ovale; Stroke
Antibodies to the heparin-platelet factor-4 (HPF-4) complex (HIT antibodies) have been observed in patients with heparin-induced thrombocytopenia (HIT). These antibodies are thought to be involved in thrombosis through activation of platelet/endothelial cells. This prospective study was conducted to determine the incidence of post-operative HIT antibodies to assess the associated risk of deep vein thrombosis (DVT) in patients undergoing total knee arthroplasty (TKA) or total hip arthroplasty (THA).
We studied 104 patients who underwent unilateral primary TKA (n = 44) and primary THA (n = 60) with short-duration prophylaxis (1–2 days of a fixed dose of unfractionated heparin). HIT antibodies were assayed using a sandwich-type ELISA before the operation and after heparin treatment (post-operative day 7).
In the clinical outcome, the incidence of symptomatic DVT was 15.4% (16/104, TKA; 10, THA 6) and pulmonary embolism (PE) was not observed. The total seroconversion rate of HIT antibodies at post-operative day 7 was 34.6% (36/104). Among 36 seroconverted patients, 11 (30.6%) developed symptomatic DVT and 5 out of 68 of the non-seroconverted patients (7.4%) developed symptomatic DVT. The incidence for DVT was significantly higher in the seroconverted patients compared with that of the non-seroconverted patients (odds ratio 5.5, 95%CI: 1.7–17.6 p = 0.0028). Furthermore, in the patients with symptomatic DVT, the titer of HIT antibodies at post-operative day 7 was significantly higher compared with those without symptomatic DVT.
Our data therefore suggest that seroconversion for HIT antibodies generated by heparin is associated with a risk of DVT in patients undergoing total joint replacement.
The objective of this study was to evaluate the efficacy of unfractionated heparin, warfarin and low molecular weight heparins (LMWH) used for the prevention of venous thromboembolism in arthroplastic surgery of the knee joint.
In this prospective study from August 2002 to November 2004, 60 patients were included and divided into three groups with equal numbers, with each group receiving different treatment protocol. Postoperatively, the occurrence of symptomatic deep vein thrombosis (DVT) or pulmonary embolism (PE) was recorded during the first 30 days after surgery and at a routine follow-up visit.
A significantly lower prevalence of DVT and PE was found in patients using warfarin and LMWH as prophylaxis in comparison with patients using unfractionated heparin.
Warfarin and low molecular weight heparins are more beneficial and effective than unfractionated heparin for DVT and PE prophylaxis in arthroplastic knee surgeries.
Arthroplasty; Deep vein thrombosis (DVT); Prophylaxis; Low Molecular Weight Heparin; Warfarin
Patent foramen ovale (PFO) is present in approximately 25% of the general population. PFO is characterized by intermittent shunting of blood from the right to the left atrium, especially in the context of increased right-sided filling pressures, with risk of paradoxical embolism. We describe a 69-year-old woman presenting with acute chest pain, severe dyspnoea, and acute inferolateral ST-segment elevation on the electrocardiogram. The patient was diagnosed with myocardial infarction and failure of the right cardiac ventricle, which was considered to be secondary to extensive pulmonary embolism leading to increased filling pressures and paradoxical coronary embolism. The patient underwent emergent percutaneous interventions with coronary thrombus extraction and pulmonary thrombus fragmentation and local thrombolysis. The patient was free of symptoms at follow up 6 months later and echocardiography showed substantially improved right ventricular function. We discuss issues related to the diagnosis, treatment, and secondary prevention for patients with concomitant pulmonary and coronary arterial thrombosis.
Myocardial infarction; patent foramen ovale; percutaneous coronary intervention; pulmonary artery intervention; pulmonary embolism; right heart failure
In the prenatal heart, right-to-left atrial shunting of blood through the foramen ovale is essential for proper circulation. After birth, as the pulmonary circulation is established, the foramen ovale functionally closes as a result of changes in the relative pressure of the two atrial chambers, ensuring the separation of oxygen depleted venous blood in the right atrium from the oxygenated blood entering the left atrium. Little is known regarding the process of anatomical closure of the foramen ovale in the postnatal heart. Genetically engineered mouse models are powerful tools to study heart development and to reveal mechanisms underlying cardiac anomalies, including defects in atrioventricular septation. Using three-dimensional reconstructions of serial sectioned hearts at early postnatal Days 2–7, we show a progressive reduction in the size of the interatrial communication throughout this period and complete closure by postnatal Day 7. Furthermore we demonstrate that fusion of the septum primum and septum secundum occurs between 4 weeks and 3 months of age. This study provides a standard timeline for morphological closure of the right– left atrial communication and fusion between the atrial septa in normal mouse hearts.
mouse; heart defects; congenital; ASD; PFO
The case is described of a potentially life threatening complication relating to the use of a totally implantable venous access device (Port- a-Cath) in a 28 year old patient with cystic fibrosis. The device was inserted in 1990 and used repeatedly for antibiotic therapy without any complications. In 1995, during assessment for double lung transplantation, a 3 cm thrombus was found at the tip of the catheter in the right atrium. Embolisation of the thrombus to the pulmonary arteries occurred after the infusion of recombinant tissue plasminogen activator (rt-PA). Thrombus formation may be associated with totally implantable venous access devices and thromboembolism may occur following the use of thrombolytic agents in the treatment of such thrombosis.
Heparin-induced thrombocytopenia is a rare and serious reaction to unfractionated heparin and low-molecular-weight heparins in children. Quick recognition, discontinuation of heparin, and subsequent treatment with an alternative anticoagulant are essential steps to prevent serious complications such as thrombus and limb amputation. The purpose of this review is to describe the clinical features of heparin-induced thrombocytopenia in children and to summarize the data available for its management. This paper summarizes data and relates the use of direct thrombin inhibitors with clinical outcomes. A literature search was conducted with Ovid, using the key terms argatroban, bivalirudin, hirulog, danaparoid, lepirudin, direct thrombin inhibitor, heparin-induced thrombocytopenia, thrombosis, warfarin, and fondaparinux. Articles were excluded if they were classified as editorials, review articles, or conference abstracts or if they involved patients 18 years of age or older or described disease states not related to thrombosis. Nineteen articles containing 33 case reports were identified and evaluated for this review. Of the 33 cases, 14, 10, 4, and 2 cases described the use of lepirudin, danaparoid, argatroban, and bivalirudin, respectively. Two cases did not report the type of anticoagulant used, and 1 case used aspirin. The most commonly reported complication was bleeding.
children; direct thrombin inhibitor; heparin-induced thrombocytopenia; low-molecular-weight heparin; unfractionated heparin
Heparin induced thrombocytopenia (HIT) is a serious complication associated with heparin use. HIT usually develops between 5–14 days after starting heparin. Delayed-onset HIT can still occur 9–45 days after heparin had been discontinued. In patients with delayed HIT, the patient might be admitted to the hospital for new thrombosis and reexposure to heparin further worsens the patient’s condition.
Our patient is a 71-year old female readmitted for worsening dyspnea 2 weeks after she was discharged from the hospital. On her previous hospitalization, she was diagnosed with bronchiolitis obliterans organizing pneumonia (BOOP). She had received prophylactic doses of LMWH. Dyspnea was initially thought to be secondary to CHF exacerbation secondary to atrial fibrillation with rapid ventricular response. She was started on a heparin. However, the patient’s clinical condition deteriorated and she needed to be intubated. Her platelet counts also decreased rapidly. After CT angiography of the chest showed pulmonary embolism, HIT was strongly considered. All forms of heparin were discontinued and argatroban was started. However, the patient did not improve and she subsequently expired on the 7th hospital day. Heparin-induced antibodies came back positive that same day.
HIT is an immune-mediated disorder characterized by formation of antibodies against heparin-platelet factor 4 complex. The major clinical presentation of HIT is arterial and venous thrombosis. Once HIT is suspected, immediate cessation of any form of heparin is needed. Alternative anticoagulation must be started. Early treatment decreases the incidence of new thrombosis and stroke, and improves survival and cost savings.
heparin induced thrombocytopenia; thrombosis; argatroban; leupridin