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Superior Vena Cava Syndrome: Treatment & Medication
Updated: Dec 31, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
- Prehospital caregivers are aware of the superior vena cava syndrome (SVCS) diagnosis only on occasion.
- The usual attention to airway, breathing, and circulation (ABCs) is required.
- SVCS only rarely manifests as a life-threatening entity; therefore, other causes for the symptomatology must be sought.
Emergency Department Care
- SVCS only rarely manifests as an acute emergency.
- Attention to the ABCs is essential.
- If patients are allowed to sit upright, they may experience some relief of the usual dyspnea.
- Stabilize the airway, as needed, and consider steroids.
- If cerebral/airway edema is present, consider diuretics; however, diuretics have not shown consistent benefit in the emergency department (ED).
- Endovascular shunts are being used increasingly often, as are thrombolytics if a thrombotic cause is present.
- After a tissue diagnosis, radiation and chemotherapy may be initiated.
Consultations
Over the last 10 years, considerable experience with endovascular stenting of superior vena cava syndrome has been achieved. At many centers, endoprostheses have become the initial choice for palliative treatment of superior vena cava syndrome.
- Emergent consultation with radiation therapy may be necessary, depending upon the acuteness of the presentation.
- Because most causes of SVCS are related to lung cancer, a pulmonary or oncology consultation may be obtained.
- Generally, considering the diagnosis in the ED is important.
- If the diagnosis is made de novo in the ED, only rarely is emergent consultation necessary.
- Exceptions include sudden airway compromise or acute SVC thrombosis, which may occur from an indwelling catheter.
Medication
Steroids and diuretics have been the mainstays of ED management. However, superior vena cava syndrome (SVCS) rarely presents as an acute life-threatening emergency. As such, considering the diagnosis may be more important than the actual definitive care when making therapeutic decisions.
Glucocorticoids
These agents decrease the inflammatory response to tumor invasion and edema surrounding the tumor mass. They have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.
Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)
One of several steroids that may be given in ED. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Adult
Loading dose: 125-250 mg IV
Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d
Pediatric
Loading dose: 2 mg/kg IV
Maintenance dose: 0.5-1 mg/kg/dose IV q6h for up to 5 d
Digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor for hypokalemia in patients taking diuretics
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Possible complications include hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, infections
Prednisone (Deltasone, Orasone, Sterapred)
Useful in treatment of inflammatory and autoimmune reactions. By reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity, may decrease inflammation.
Adult
5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve
Pediatric
4-5 mg/m2/d PO; alternatively, 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve
Estrogens may decrease clearance; digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral, fungal, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
Diuretics
These agents may decrease venous return to the heart by decreasing preload, relieving the increased pressure in the SVC.
Furosemide (Lasix)
Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
Dose must be individualized. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1 mg/kg/dose increments until satisfactory effect achieved.
Adult
20-80 mg PO once; repeat in 6-8 h prn; alternatively, increase dose by 20-40 mg and do not give sooner than 6-8 h after previous dose
Pediatric
Infants: Titrate with 1 mg/kg/dose increments PO until satisfactory effect achieved
Children: 1-2 mg/kg PO once; do not administer more frequently than q6h; not to exceed 6 mg/kg/dose
Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; aminoglycosides increase auditory toxicity—hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin; may increase plasma lithium levels and toxicity
Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter
More on Superior Vena Cava Syndrome |
| Overview: Superior Vena Cava Syndrome |
| Differential Diagnoses & Workup: Superior Vena Cava Syndrome |
 Treatment & Medication: Superior Vena Cava Syndrome |
| Follow-up: Superior Vena Cava Syndrome |
| Multimedia: Superior Vena Cava Syndrome |
| References |
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References
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Dhaliwal RS, Das D, Luthra S, et al. Management of superior vena cava syndrome by internal jugular to femoral vein bypass. Ann Thorac Surg. Jul 2006;82(1):310-2. [Medline].
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Courtheoux P, Alkofer B, Al Refai M, et al. Stent placement in superior vena cava syndrome. Ann Thorac Surg. Jan 2003;75(1):158-61. [Medline].
Lanciego C, Chacon JL, Julian A, et al. Stenting as first option for endovascular treatment of malignant superior vena cava syndrome. AJR Am J Roentgenol. Sep 2001;177(3):585-93. [Medline].
Leggio L, Abenavoli L, Vonghia L, et al. Superior vena cava thrombosis treated by angioplasty and stenting in a cirrhotic patient with peritoneovenous shunt. Ann Thorac Cardiovasc Surg. Feb 2008;14(1):60-2. [Medline].
Link MS, Pietrzak MP. Aortic dissection presenting as superior vena cava syndrome. Am J Emerg Med. May 1994;12(3):326-8. [Medline].
Madan AK, Allmon JC, Harding M, et al. Dialysis access-induced superior vena cava syndrome. Am Surg. Oct 2002;68(10):904-6. [Medline].
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Further Reading
Keywords
SVCS, superior vena cava syndrome, superior vena cava, SVC, bronchogenic carcinoma, endovascular stenting, endoprostheses, malignancy-associated SVCS, non-malignancy–associated SVCS, obstruction of superior vena cava, obstruction of SVC, compression of superior vena cava, compression of SVC, low intravascular pressure, interstitial edema, retrograde collateral flow, thrombus formation
