Upper-extremity deep venous thrombosis (DVT), although not as common as
its lower-extremity counterpart, is a clinical entity with potentially
devastating complications. Approximately 1% to 4% of all DVT cases involve the
upper extremity, with 9% to 14% of these cases complicated by pulmonary
embolism. Prompt diagnosis with duplex ultrasonography and subsequent
anticoagulation are the gold standards for identification and treatment. The
majority of these cases are secondary to medical comorbidities such as
malignancy, hypercoagulable states, and indwelling catheters. Although rare,
several case reports of orthopedic-related upper-extremity DVT are present in
the literature. This article reports a case of upper-extremity DVT in a humeral
shaft fracture treated nonoperatively.
A 58-year-old man presented with right elbow pain after a fall from
scaffolding. Radiographs demonstrated a distal humeral shaft fracture at the
tip of a previously placed intramedullary nail. Initial treatment consisted of
closed reduction in a coaptation splint. The patient re-presented 4 days later
with increasing forearm pain and swelling. An ultrasound revealed an extensive
thrombus of the right brachial vein. A coaptation splint was replaced and the
patient was admitted to the hospital for therapeutic anti-coagulation. After
hematology consultation and a short hospitalization, the patient was discharged
home on a 3-month course of Warfarin. The goal of treatment of upper-extremity
venous thrombosis is to improve the patients acute symptoms and prevent
both pulmonary embolism and post-thrombotic syndrome. Post-thrombotic syndrome
is a chronic, potentially debilitating condition that occurs in approximately
15% of upper-extremity DVT cases with symptoms consisting of pain, swelling,
paresthesias, and functional limitation.
Deep venous thrombosis (DVT) is a well-known clinical entity seen in the
orthopedic trauma patient population, most often occurring in the lower
extremities following pelvic and long-bone fractures. These patients are
frequently affected due to the tissue trauma suffered from the initial injury
and the subsequent period of immobilization. This trauma sequence exposes
patients to all 3 components of Virchows triad: interrupted blood flow
(venous stasis), endothelial vessel wall damage, and hypercoagulability.
However, it must be recognized that long-bone fractures of the upper extremity
also carry a risk of DVT and the possibility of a subsequent life-threatening
Upper-extremity DVT most frequently occurs secondary to a variety of
medical comorbidities; however, several case reports of orthopedic-related
upper-extremity DVT are present in the literature. This article reports a case
of upper-extremity DVT in a humeral shaft fracture treated nonoperatively.
A 58-year-old, right-hand-dominant man presented with right elbow pain
after a 6-foot fall from scaffolding 24 hours prior to evaluation. The
patients past medical history was significant for a similar fall
approximately 9 months prior, where he sustained a right proximal humeral shaft
fracture treated with a locked intramedullary nail. He had an uneventful
recovery from this operation and had returned to full-time work. Also of note,
the patient was a long-time smoker.
On examination, the patient was noted to have gross deformity, swelling,
and ecchymosis at the right distal humerus with intact skin. His hand was
neurologically intact with a strongly palpable radial pulse. Radiologic
examination revealed a completely displaced spiral distal humeral shaft
fracture at the tip of the previously placed intramedullary nail (Figure 1).
|Figure 1: Pre-reduction AP (A)
and lateral (B) radiographs of the right humerus, identifying a distal
one-third humeral shaft fracture at the tip of an intramedullary nail.
Figure 2: Post-reduction AP (A) and lateral (B) radiographs of the right
Closed reduction was performed using a coaptation splint with the
forearm wrapped, leaving the fracture in approximately 10° of varus
alignment (Figure 2). Post-reduction examination revealed 4/5 strength of wrist
extensors and extensor pollicis longus, but otherwise neurovascularly intact at
the hand. The patient was discharged to home with appropriate follow-up.
Four days after his original injury the patient re-presented to the
emergency room with increasing right forearm and hand swelling. The coaptation
splint was removed and the patient was noted to have swelling about the distal
humerus down to the hand. He was noted to have 0/5 extensor pollicis longus
strength, 2/5 wrist extensor strength, decreased sensation in the radial nerve
distribution, and a strong palpable radial pulse. Ultrasound revealed a near
occlusive thrombus of the right brachial vein extending from the level of the
mid-arm to the brachial/axillary vein junction (Figure 3).
|Figure 3: Duplex ultrasound of the right
brachial vein identifying limited flow, consistent with a nearly occlusive
The coaptation splint was replaced resulting in acceptable alignment.
The patient was admitted and started on therapeutic enoxaparin as a bridge to
Warfarin. Hematology consultation attributed his upper-extremity DVT to local
trauma with subsequent immobilization and did not feel that patient required a
After an uneventful hospital course, the patient was discharged on day
4, with plans for 3 months of Warfarin therapy. At 2-month follow-up, the
patient was doing well with significantly decreased pain. He exhibited 4/5
strength in his wrist extensors, radiographs revealed abundant callus formation
at the fracture site with only slight varus malalignment, and he had begun
therapy for range of motion exercises. He exhibited no further clinical
sequelae from his DVT.
An estimated 1% to 4% of all DVT cases involve the upper
extremity.1 While the vast majority of these are related to comorbid
medical conditions, the orthopedic literature has included several case reports
for shoulder arthroscopy, shoulder dislocation, proximal humerus fracture,
clavicle fracture, and following open reduction and internal fixation of a
Upper-extremity DVT can be categorized into 2 subdivisions: primary and
secondary. Primary is uncommon (2 per 100,000 person years), consisting of
either effort dependent thrombosis (Paget Schroetter Syndrome) or
idiopathic.7 Paget Schroetter Syndrome is a rare entity whereby
affected individuals suffer microtrauma to upper-extremity vessel wall intima,
often during strenuous exercise, which initiates the coagulation cascade
resulting in thrombosis.7 These patients also often have a
congenitally narrow thoracic inlet that puts them at increased risk for primary
venous thrombosis, secondary to stasis and vessel intimal wall damage (2/3 of
Virchows triad). The idiopathic subdivision refers to patients for which
no identifiable cause of the thrombosis can be identified. This is a diagnosis
of exclusion, although many feel that the patients that receive this diagnosis
have an occult malignancy causing a hypercoagulable state.7
Secondary upper-extremity DVTs have an underlying trigger or disease
process that increases the risk of subsequent thrombosis. The most common is
malignancy, particularly lung, breast, and colorectal, which generate a
hypercoagulable state. The second most frequent is thrombosis secondary to
indwelling catheters including central lines, port systems, peripheral lines,
and pacemakers.7 Our patient fits into this classification with
upper-extremity trauma, treated with immobilization, resulting in venous stasis
and clot formation.
Patients with upper-extremity DVTs present classically with vague arm,
shoulder, or neck pain, depending on the location and extent of thrombosis.
They can also have swelling, edema, and occasionally a palpable tender
cord.7 Systemically, these patients can have mild tachycardia and
low-grade fevers. High fevers are concerning for a septic thrombophlebitis.
When tachycardia is accompanied by cyanosis, concern exists for development of
a pulmonary embolism, which can complicate 9% to 14% of identified
Duplex ultrasound has become the imaging modality of choice for the
diagnosis of upper-extremity DVT, as it is noninvasive with high sensitivity
and specificity.7 The known limitation of this study is the acoustic
shadowing produced by the clavicle, which can obstruct complete visualization
of the subclavian vein.7 Second-line imaging choices include
contrast venography, computed tomography angiography, and magnetic resonance
angiography. Each of these include a contrast load and its possible resulting
complications (allergic reaction and nephrotoxicity). These secondary imaging
modalities may be required if upper-extremity DVT suspicion persists despite a
The treatment goal is improving the patients acute symptoms and
prevention of both pulmonary embolism and post-thrombotic syndrome.7
Pulmonary embolism can complicate upper-extremity DVT in 9% to 14% of cases,
although the actual percentage may be higher, as frequently emboli are
asymptomatic. Post-thrombotic syndrome is a chronic, potentially debilitating
condition that occurs in approximately 15% of patients with upper-extremity
DVT.1 This syndrome is characterized by pain, swelling, heaviness,
paresthesias, and functional limitation of the arm. Post-thrombotic syndrome
can be functionally debilitating in the upper extremity.7 Our
patient has shown no evidence of this syndrome.
The mainstay of venous thrombosis treatment is anticoagulation. Acutely,
unfractionated, or low-molecular-weight heparin are used as a bridge to
long-term Warfarin therapy. The goal of anti-coagulation therapy is to prevent
further clot propagation, while allowing natural thrombolysis to occur.
Similarly to lower-extremity DVT treatment, anticoagulation is recommended for
a 3- to 6-month course, with a goal international normalized ratio of
Thrombolysis is also an option in the early treatment of upper-extremity
DVT. The ideal patient for this therapy is a young, otherwise healthy
individual. The classic thrombolytics are streptokinase, urokinase, and
alteplase (tPA), all of which are delivered intravenously. Following
administration of a thrombolytic, a patient is then begun on a standard course
of anti-coagulation (as previously described). Absolute contraindications for
thrombolysis include allergy to thrombolytics, active or recent internal
bleeding (within the past 6 months), history of hemorrhagic stroke, active
intracranial neoplasm, and recent (<2 months) intracranial surgery or
Surgical interventions for upper-extremity DVT are primarily for
prevention of recurrent thrombosis. This mostly applies to primary
upper-extremity DVT, and the purpose is to alleviate extrinsic sources of
venous compression. These procedures may include partial clavicle resection,
first rib resection, and scalene muscle resection.7
Superior vena cava filters have been successfully used for the
prevention of pulmonary embolism in patients with upper-extremity DVT, for whom
anticoagulation is contraindicated. Using a percutaneous technique, this has
been shown to be a safe and effective method to prevent symptomatic pulmonary
Many reports exist in the literature on central venous thrombosis
resulting in cranial nerve palsies, but rarely has extremity thrombosis
resulting in nerve palsy been reported. Bendszus et al10 reported a
case of peroneal nerve palsy caused by crural vein thrombosis, but otherwise
these reports are scarce in the literature. This patients initial partial
radial nerve palsy was most likely secondary to his humeral shaft fracture, not
his extensive brachial vein thrombosis. A reported 11.8% incidence of radial
nerve palsies is associated with humeral shaft fractures.11
Upper-extremity DVT, although not as common as its lower-extremity
counterpart, is a real clinical entity that must be appropriately diagnosed and
treated to avoid devastating complications, such as pulmonary embolism.
Although seen most frequently in patients with malignancy and central venous
catheters, several case reports exist in the orthopedic literature on both
fracture and postoperative care.
- Elman E, Kahn S. The post-thrombotic syndrome after upper extremity
deep venous thrombosis in adults: A systematic review [published online ahead
of print July 6, 2005]. Thrombosis Research. 2006; 117(6):609-614.
- Creighton RA, Cole B. Upper Extremity deep venous thrombosis after
shoulder arthroscopy: a case report [published online ahead of print September
1, 2006]. J Shoulder Elbow Surg. 2007; 16(1):e20-22.
- Willis A, Verma N, Thornton S, Morrissey N, Warren R. Upper-extremity
deep vein thrombosis after anterior shoulder dislocation and closed reduction.
A case report. J Bone Joint Surg Am. 2005; 87(9):2086-2090.
- Chuter G, Weir D. Upper extremity deep vein thrombosis following a
humeral fracture: a case report and literature review. Injury Extra.
- Adla DN, Ali A, Shahane SA. Upper Extremity deep-vein thrombosis
following clavicular fracture. Eur J Orthop Surg Traumatol. 2004;
- Pearsall AW IV, Stokes DA, Russell GV Jr. Internal jugular deep
venous thrombosis after surgical treatment of a humeral nonunion: a case report
and review of the literature. J Shoulder Elbow Surg. 2004;
- Joffe HV, Goldhaber SZ. Upper-extremity deep vein thrombosis.
Circulation. 2002; 106(14):1874-1880.
- Muñoz FJ, Mismetti P, Poggio R, et al; RIETE Investigators.
Clinical outcome of patients with upper-extremity deep vein thrombosis
[published online ahead of print October 9, 2007]. Chest. 2008;
- Spence L, Gironta M, Malde H, Mickolick C, Geisinger M, Dolmatch B.
Acute upper extremity deep venous thrombosis: safety and effectiveness of
superior vena caval filters. Radiology. 1999; 210(1):53-58.
- Bendszus M, Reiners K, Perez J, Solymosi L, Koltzenburg M. Peroneal
nerve palsy caused by thrombosis of crural veins. Neurology. 2002;
- Shao YC, Harwood P, Grotz MR, Limb D, Giannoudis PV. Radial nerve
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Drs Sawyer and Hayda are from Brown Medical School-Rhode Island
Hospital, Providence, Rhode Island.
Drs Sawyer and Hayda have no relevant financial relationships to
Correspondence should be addressed to: Gregory A. Sawyer, MD, Rhode
Island Hospital, Department of Orthopedics, 593 Eddy St, Providence, RI 02903