Introduction:
Internal jugular (IJ) thrombosis refers to an intraluminal thrombus that develops somewhere from the intracranial internal jugular vein to the junction of the internal jugular vein and the subclavian vein that eventually forms the brachial vein. It can occur as a complication of head and neck infections, surgery, central venous access, local malignancies, erythrocytosis, hyperhomocysteinemia, cervical massage, and intravenous (IV) substance abuse. The condition is vastly underdiagnosed. It has also been reported to occur spontaneously. Given the widespread use of IJ veins for venous access, central venous catheters are currently the most common root cause of IJ thrombosis. Of concern is the tendency to reflect an increase in the number of IV drug users who develop IJ thrombosis due to repeated direct drug injections into the internal jugular vein.
What Is the Anatomy of Internal Jugular Vein?
The internal jugular vein (IJV) begins at the jugular foramen, travels to the lateral neck, and ends at the brachial vein. One of the carotid artery's four parts is the IJV, along with the common carotid artery, internal carotid artery, vagus nerve, and deep cervical lymph node. It runs inside the sternocleidomastoid muscle of the carotid triangle. IJV thrombosis is the formation of a blood clot located within the lumen of an IJV. Inherited and acquired risk factors for thrombosis include injectable drug use, factor V Leiden mutations, malignant tumors, hormone replacement therapy, sedation, trauma, and pregnancy.
What Is Internal Jugular Vein Thrombosis?
Internal jugular vein thrombosis most commonly results from long-term central venous catheterization, cervical trauma, infections, ovarian hyperstimulation syndrome (OHSS), and intravenous drug abuse.
The classic triad that predisposes to intravascular thrombosis was first described by Virchow and included:
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Injured blood vessels.
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Congestion in the bloodstream.
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Hypercoagulation.
What Causes Internal Jugular Vein Thrombosis?
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A cross-sectional study suggests that cancer and central venous catheters are the most common causes of internal jugular vein thrombosis.
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A systematic review and meta-analysis found that 7.5% of the 5636 cancer patients developed catheter-related venous thrombosis. When investigating catheter-related venous thrombosis, researchers considered many factors, including the history of deep vein thrombosis, the site of insertion, and the location of the tip of the catheter.
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Patients with factor V Leiden or another hyper coagulant have been found to have a three-fold increased risk of developing upper limb thrombosis.
What Are the Symptoms Seen With Internal Jugular Vein Thrombosis?
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Internal jugular vein thrombosis is asymptomatic in the majority of patients. Due to its subtle symptoms, it is difficult for clinicians to diagnose. However, patients may show typical signs of deep vein thrombosis, such as erythema, tenderness, and warmth.
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A physical examination may reveal swelling of the left neck, mandibular angle, or anterior edge of the sternocleidomastoid muscle.
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Internal jugular vein thrombosis, fever, headache, swelling of the neck, and jaw angle with impaired opening are also possible symptoms associated with an infection known as Lemierre's syndrome (a necrotizing bacterial disease).
How Is Internal Jugular Vein Thrombosis Diagnosed?
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Laboratory tests may show elevated levels of D-dimer, a fibrin degradation product that is sensitive and non-specific to venous thrombosis.
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Elevated levels of D-dimer are associated with malignancies, sepsis, recent surgery or trauma, and pregnancy and are often associated with internal jugular vein thrombosis.
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Doppler compression ultrasonography with 96 % sensitivity and 93 % specificity is the best diagnostic test.
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Venography is the gold standard for diagnosing IJV thrombosis, but bedside ultrasound is non-invasive and rapid and may show hyperechoic thrombosis within the IJV.
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A CT scan may indicate an intraluminal filling defect in the jugular vein wall. CT scans may be better than ultrasound because they have a better assessment of the veins under the soft tissue.
How Is Internal Jugular Vein Thrombosis Treated?
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The risk of bleeding should be carefully assessed. Anticoagulant therapy is customized for each patient. Tools like HAS-BLED help assess the risk of bleeding in adults. However, there are no clear indicators or tools that can reliably predict the risk of bleeding in patients with internal jugular vein thrombosis.
[HAS-BLED stands for:
- Hypertension
- Abnormal renal and liver function.
- Stroke.
- Bleeding.
- Labile INR (international normalized ratio).
- Elderly.
- Drugs or alcohol].
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It is important to remove the catheter in patients using an indwelling catheter. However, if for some reason the catheter cannot be removed, an anticoagulant should be given.
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Patients at no risk of bleeding may have a low molecular weight (LMW) Heparin and Warfarin dual therapy, LMW Heparin followed by direct thrombin inhibitor or factor Xa inhibitor dual therapy, or factor Xa inhibitor monotherapy. There is a requirement for therapy.
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For patients at high risk of thrombophilia, some studies suggest that the INR (international normalized ratio) is maintained between 2.5 and 3.0. Long-term treatment with Warfarin may also be considered.
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However, there is a lack of clinical research on anticoagulant therapy for internal jugular vein thrombosis. Internal jugular vein thrombosis is often found by accident in most patients. Therefore, many patients remained untreated.
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Alteplase and other intravenous thrombolytic infusion regimens have been reported to be beneficial in treating IJV thrombosis.
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Thrombolysis is not recommended as first-line treatment in patients diagnosed with catheter-induced IJV thrombosis, as there is little evidence that thrombolysis provides better results than anticoagulant therapy.
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Patients rarely require surgical intervention.
What Is the Prognosis for People Suffering From Internal Jugular Vein Thrombosis?
Results are generally good but show morbidity and mortality similar to subclavian and axillary vein thrombosis. Pulmonary embolism can occur but is rare if complete systemic anticoagulant therapy is in place. The prevalence of pulmonary embolism is about 0.5 % for isolated IJ venous thrombosis and 2.4 % for a combination of IJ veins and subclavian or axillary venous thrombosis. Mortality was reported to be 14 % in one month, 33 % in three months, and 42% in 12 months.
Conclusion:
Anticoagulant therapy is the best treatment for patients with internal jugular vein thrombosis, and this therapy prevents serious complications such as pulmonary embolism. Anticoagulant therapy is recommended for patients with asymptomatic IJV thrombosis because delayed treatment increases the risk of potentially life-threatening embolisms. Anticoagulant management requires individual adjustments with the experience of a physician. The anticoagulant period ranges from four to 12 weeks. It is standard practice to have an imaging test before discontinuing anticoagulant therapy.
