6/19/22, 5:37 PM 5605

Official reprint from UpToDate®

[Link] © 2022 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Overview of hemarthrosis
Author: Peter A Nigrovic, MD
Section Editor: Simon M Helfgott, MD
Deputy Editor: Paul L Romain, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: May 2022. | This topic last updated: Apr 26, 2022.

INTRODUCTION

Bleeding into a joint is referred to as hemarthrosis and is an important cause of monoarticular

joint pain and swelling. Hemarthrosis may be suspected on the basis of a suggestive history,
physical examination, or imaging studies, but definitive diagnosis usually requires joint
aspiration. The management is determined in part by the cause.

An overview of the causes, clinical manifestations, diagnosis, and management of hemarthrosis

is reviewed here. The differential diagnosis of monoarthritis, techniques of joint aspiration
(arthrocentesis), the approach to adults with a bleeding diathesis, and the diagnosis and
management of hemophilia are described in detail separately. (See "Monoarthritis in adults:
Etiology and evaluation" and "Joint aspiration or injection in adults: Technique and indications"
and "Joint aspiration or injection in children: Indications, technique, and complications" and
"Approach to the adult with a suspected bleeding disorder" and "Approach to the child with
bleeding symptoms" and "Clinical manifestations and diagnosis of hemophilia" and "Treatment
of bleeding and perioperative management in hemophilia A and B".)

CAUSES OF HEMARTHROSIS

The range of disorders that may result in hemarthrosis can be broadly grouped into traumatic
and nontraumatic causes; the latter include bleeding disorders, neurologic deficits, arthritis,
neoplasms, vascular damage, and other miscellaneous causes ( table 1). (See 'Traumatic'
below and 'Nontraumatic' below.)

[Link] 1/32
6/19/22, 5:37 PM 5605

Traumatic — Injuries are among the most common causes of hemarthrosis. In patients with
normal sensation and without a bleeding diathesis, joint trauma is generally remembered. The
pain is often severe [1]. However, pain may be minimal or absent immediately following the
event. Patients with impaired sensation from neuropathy or myelopathy may have little or no
pain despite the presence of a fracture. (See 'Knee injury' below and 'Lipohemarthrosis' below
and 'Minimal injuries' below and 'Postoperative' below.)

Following a major injury with intraarticular bleeding, synovial fluid rapidly accumulates within
the joint. The accumulation of bloody fluid is due to soft tissue injury or to bone or
osteochondral fracture. Serious ligamentous, osseous, or cartilage damage may be suspected
when joint swelling occurs within 12 hours after trauma, although swelling is present much
earlier, sometimes within two hours, in many patients [2].

Knee injury — The knee is a frequent site of injury, and the majority of cases of posttraumatic
hemarthrosis of the knee are associated with serious articular injury, often ligamentous and
meniscal damage ( table 2). Thus, evaluation for internal derangement is an important part of
the assessment (see "Approach to the adult with unspecified knee pain"). The most common
mechanism of injury in patients with acute hemarthrosis of the knee is forced twisting of the
loaded joint [2,3].

Anterior cruciate ligament (ACL) tears are the most common cause, occurring in approximately
70 percent of patients with posttraumatic hemarthrosis of the knee [2]. Meniscal tears occur in
10 percent of patients, one-half of whom also have an ACL tear [1]. Patellar subluxation or
dislocation occurs in 10 to 15 percent of patients, and osteochondral fracture fragments are
found in 2 to 5 percent. Patellar subluxation may be a more common mechanism of
hemarthrosis in children, accounting for 48 of 117 cases (41 percent) in one series [4]. Other
lesions, such as posterior cruciate ligament injuries and capsule tears, occur in approximately 5
percent of patients.

Tenderness to palpation of the medial or lateral joint lines or the patella can indicate the site of
injury [1]. Clinical tests for stability are performed with varus (for the lateral collateral ligament),
valgus (for the medial collateral ligament), anterior (drawer test, for the ACL), and posterior
(posterior draw or sag test, for the posterior cruciate ligament) stress ( picture 1A-B). (See
"Physical examination of the knee" and "Approach to acute knee pain and injury in children and
skeletally immature adolescents", section on 'Evaluation'.)

The initial imaging technique of choice is plain film radiography of the involved joint and
adjacent bones. For the knee, we usually obtain anterior-posterior, lateral, patellar, and tunnel
views [5]. When a fracture is strongly suspected but radiographs are negative, computed

[Link] 2/32
6/19/22, 5:37 PM 5605

tomography (CT) may aid in diagnosis. Magnetic resonance imaging (MRI) provides helpful
information about ligamentous and cartilaginous structures that are not typically visible with
plain radiographs or CT.

Arthroscopic evaluation of the knee provides an alternative approach to assessing the severity
of knee damage when injury is accompanied by hemarthrosis, but should generally be
performed only if advanced imaging is not informative. In a prospective study, all injured knees
that had a traumatic hemarthrosis with little or no instability on clinical examination underwent
arthroscopy and examination under anesthesia [6]. One-third of the knees had slight or no pain
at the time of the injury. Some degree of disruption of the ACL of the involved knee was found
in 71 percent of the patients examined, while a torn meniscus was present in 47 percent. A
meniscal tear was frequently associated with injuries of varying severity to other joint
structures. Other damage found during arthroscopy and examination under anesthesia
included minor ligament sprains without laxity, major associated ligament injury, and femoral
cartilage fractures or surface defects [6]. When examined without anesthesia, some patients
with documented ACL tears did not have a positive drawer sign.

Lipohemarthrosis — Lipohemarthrosis, which is the presence of fat and blood in a joint

cavity, is usually caused by intracapsular fractures or extensive intraarticular soft tissue injury
[2]. Lipohemarthrosis can be detected by arthrocentesis, by CT scan or MRI, and/or plain
radiology ( image 1) [2,7]. While a single fluid-fluid level on cross-table plain radiographs is
suggestive of lipohemarthrosis, this finding may also occur due to separation of intraarticular
cellular and fluid components following intraarticular bleeding without the presence of fat in
joint fluid [8]. The finding of a double fluid-fluid level is more specific for lipohemarthrosis [7].
The diagnosis can be suggested also by ultrasonography [9].

Minimal injuries — In patients in whom hemarthrosis occurs after minimal trauma,

coagulation disorders, such as hemophilia, an acquired inhibitor to factor VIII, or other disorder
of blood clotting should be suspected [10] (see "Approach to the adult with a suspected
bleeding disorder"). When hemarthrosis following minimal trauma is not due to a bleeding
diathesis, the most commonly documented injuries are ACL and meniscal tears [8,11].

Postoperative — Recurrent postoperative hemarthrosis is an uncommon complication of total

knee arthroplasty, seen in approximately 1 percent of such patients, and is most often due to
impingement of hypertrophic synovium by the prosthesis [12]. It may present at any point
within the first year after surgery, and can be addressed by operative excision of the affected
tissue or by embolization of feeding vessels. Hemarthrosis is also a potential but unusual
complication after performing lateral releases or after arthroscopy [13-16].

[Link] 3/32
6/19/22, 5:37 PM 5605

Nontraumatic — A variety of hereditary, acquired, and iatrogenic bleeding disorders can result
in hemarthrosis. Other potential causes are neurologic, infectious, and vascular diseases,
arthritis, particularly osteoarthritis with associated chondrocalcinosis, and neoplasms. (See
'Bleeding disorders' below and 'Osteoarthritis' below and 'Neurologic disorders' below and
'Septic arthritis' below and 'Vascular disorders' below and 'Tumors' below.)

Bleeding disorders — Bleeding disorders should be considered as the underlying cause when
hemarthrosis occurs with minimal or no trauma. Questions about bleeding during or after
surgical or dental procedures, use of anticoagulant medications [17,18], and rarely,
thrombolysis [19,20] or extreme dietary restriction (vitamin C deficiency) may help uncover the
presence of a bleeding diathesis or its cause.

Initial laboratory tests include a complete blood count, prothrombin time (PT), and activated
partial thromboplastin time (aPTT) ( table 3). A bleeding time may be helpful if the history or
physical examination suggests a platelet disorder; however, joint bleeding is typically seen with
deficiencies in coagulation factors, rather than platelet abnormality ( table 4). Unexplained
abnormalities of any of these tests require further investigation, which is described in detail
separately. (See "Approach to the adult with a suspected bleeding disorder".)

Hemarthrosis is the most common musculoskeletal manifestation of hemophilia [21]. Severe

hemophilia (defined as less than 1 percent of normal factor activity) causes hemarthrosis in 75
to 90 percent of patients. The first attack usually occurs between two or three years of age. The
knee is the most common joint involved, followed by the elbow, ankle, hip, and shoulder.
Bleeding commonly recurs in a subset of joints, referred to as "target joints," that are at highest
risk for permanent injury. Bilateral involvement is not uncommon [21]. (See "Clinical
manifestations and diagnosis of hemophilia", section on 'Hemophilic arthropathy'.)

Three forms of hemarthrosis are recognized in patients with hemophilia: acute, subacute, and
chronic.

● In acute hemarthrosis, the affected joint is painful, swollen, and warm, and range of
motion is reduced. The clinical manifestations vary by age. In infants, early signs of
bleeding include irritability and decreased use of the affected limb. In older children and
adults, hemarthrosis is manifested by prodromal stiffness and, in some patients, by a
characteristic "aura" (often a sensation of tingling or warmth), which is followed by acute
pain and swelling [22]. One joint is usually affected at a time, but multiple bleeding sites
are not uncommon. Symptoms respond rapidly to plasma and factor replacement, and as
the effusion is reabsorbed, mobility returns.

[Link] 4/32
6/19/22, 5:37 PM 5605

● Untreated hemorrhage can lead to intraarticular damage in the subacute stage. In this
stage, the toxic effects of blood products lead to synovial hypertrophy, fibrosis, and
impaired joint movement. Despite marked internal derangement, joint pain is not
prominent at this time.

● Repeated attacks or persistent hemorrhage for more than six months can lead to chronic
disabling arthropathy, with symptoms sometimes mimicking osteoarthritis. Chronic
arthropathy can affect 20 percent or more of patients with hemophilia [23].

The histopathology of hemophilic arthropathy is complex [24,25]. In early disease, the histology
reveals synovial hypertrophy and fibrosis, changes similar to rheumatoid arthritis. Late disease
is characterized by disruption of cartilage and by subchondral bone cyst formation. Cyst
formation appears to reflect the combined effects of degeneration and interosseous bleeding
[26-28]. Cartilage and bone destruction in affected patients appears to be the result of direct
toxic effects of blood products, mechanical effects, and cytokines [26]. Iron, in the form of ferric
citrate, stimulates human synovial fibroblasts to proliferate in vitro [29]. In vitro data suggest
that blood can be toxic to human cartilage after as little as two days, a conclusion supported by
studies of induced hemarthrosis in hemophilic rats [30,31]. Interestingly, susceptibility to joint
injury may reflect in part the impaired wound healing observed in hemophilia, since wild-type
animals subjected to experimental hemarthrosis exhibited more rapid clearance of joint
bleeding than mice with inherited coagulation defects and were correspondingly protected
from associated structural injury [32]. Murine studies suggest that blood vessel hyperplasia
occurs in reaction to hemarthrosis, potentially predisposing to recurrent bleeding in a subset of
joints characteristic of each patient ("target joints," defined as joints affected by at least three
bleeding episodes within six months) [22,33]. Growing cartilage is most susceptible to blood-
induced damage [34]. Thus, children with hemarthrosis should be treated aggressively to
minimize joint injury.

Radiologically, five stages of hemophilic arthropathy are recognized [21]:

● Stage 1: Soft tissue swelling – Swelling secondary to direct bleeding, both into the joint
and into the adjacent tissues.

● Stage 2: Osteoporosis – Development of osteoporosis and/or epithelial overgrowth

associated with inflammatory hyperemia, especially marked in the knee and elbow.

● Stage 3: Osseous lesions – Disorganization of the joint with overgrowth of the epiphysis,
squaring of the patella, and widening of the articular notch of the knee and the trochlea of
the ulna; the articular cartilage remains intact.

[Link] 5/32
6/19/22, 5:37 PM 5605

● Stage 4: Cartilage destruction – Cartilage injury and secondary joint space narrowing.

● Stage 5: Joint disorganization – Complete loss of cartilage spaces with associated bony
erosion and irregularity.

Radiographic assessment of hemophilic arthropathy tends to underestimate the joint

destruction. MRI and CT allow for early evaluation of joint damage, subchondral cysts, and
cartilage or synovial lesions.

Treatment of hemarthrosis in the setting of hemophilia is discussed separately. (See "Treatment

of bleeding and perioperative management in hemophilia A and B", section on 'Hemarthroses'.)

Osteoarthritis — Hemarthrosis of the knee can occur as a result of osteoarthritis; however,

this is uncommon as osteoarthritis usually only causes a small amount of bleeding, and should
be regarded as a diagnosis of exclusion. The origin of bleeding in several reported cases was
presumed to be from the peripheral arteries of the posterior horn of the lateral meniscus,
which were found to have degenerative tears [35].

Neurologic disorders — Recurrent episodes of hemarthrosis can occur in patients with

neuropathic arthropathy (Charcot joints). Note that Charcot joints are often still somewhat
painful. (See "Diabetic neuroarthropathy".)

Septic arthritis — Hemarthrosis may occur without associated trauma in patients with
bacterial arthritis, though this is rare [36]. (See "Septic arthritis in adults".)

Vascular disorders — Vascular fragility due to vitamin C deficiency may lead to hemarthrosis
and subperiosteal bleeding [37] (see "Overview of water-soluble vitamins", section on 'Vitamin C
(ascorbic acid)'). Peripheral arterial aneurysms or, more commonly, procedure-related
pseudoaneurysms may rupture, resulting in intraarticular hemorrhage [38].

Tumors — The neoplasms most often associated with hemarthrosis are generally benign. Two
important types are synovial hemangiomas (see 'Synovial hemangioma' below) and
tenosynovial giant cell tumor (TCGT), historically known as pigmented villonodular synovitis
(PVNS) (see 'Tenosynovial giant cell tumor/pigmented villonodular synovitis' below). Malignant
tumors, both metastatic and those arising de novo in or near a joint, can lead to bloody
effusions.

Synovial hemangioma — A synovial hemangioma is a rare benign vascular tumor that

can occur in a joint, usually the knee. Children are more likely to have intraarticular
hemangiomas than adults. Affected patients present with a recurrent painful monoarticular
hemarthrosis [39].
[Link] 6/32
6/19/22, 5:37 PM 5605

Plain film radiography is normal in half of the patients or shows joint effusion, soft tissue
swelling, and/or erosions. The presence of phleboliths is suggestive of hemangioma, but MRI is
the modality of choice for diagnosis [40,41].

Synovial hemangiomas may be congenital, appearing as solitary neoplasms that infiltrate local
tissue and adjacent neurologic structures. The margins of the mass are typically composed of
both large and small vessels. Hemangiomas do not metastasize or undergo malignant
transformation. Pathologic examination of hemangiomas shows spaces of various sizes,
ranging from capillaries to cavernous sinusoids, which are lined by endothelium.

Tenosynovial giant cell tumor/pigmented villonodular synovitis — Tenosynovial giant

cell tumor (TGCT), historically known as pigmented villonodular synovitis (PVNS), is a slow-
growing, benign, but locally invasive tumor of the synovium. It most commonly involves the
knee, but can also occur in the hip, ankle, and elbow. Episodic acute attacks of pain and swelling
are associated with spontaneous hemarthrosis, but hemarthrosis may also be identified
unexpectedly upon joint aspiration performed as part of the evaluation of a chronically swollen
joint.

Most patients with knee involvement have difficulty in ambulation, and may experience locking
and catching of the joint. This tumor-like growth may be driven by overexpression of colony
stimulating factor 1 (CSF1, also known as macrophage-CSF [M-CSF]) by a minority of cells,
driving recruitment and expansion of CSF1-responsive neighboring cells [42]. (See "Treatment
for tenosynovial giant cell tumor and other benign neoplasms affecting soft tissue and bone",
section on 'Tenosynovial giant cell tumor'.)

The synovial fluid classically is dark brown or hemorrhagic. A synovial biopsy may be diagnostic.
The histopathology of TGCT can mimic rheumatoid arthritis, but TGCT affects few joints and
rarely in a symmetrical fashion. It usually presents as a monoarticular hemarthrosis and it may
exist in a diffuse or nodular form [43].

The diffuse form is characterized by a history of swelling that is not preceded by trauma. On
physical examination, the majority of patients have distension of the suprapatellar pouch and a
large effusion. As many as 40 percent may have a palpable diffuse synovial mass. This can be
accompanied by periarticular erosions on plain radiographs.

The nodular form is less common and does not show the same destructive changes as the
diffuse form. It can cause recurrent hemarthrosis, but the aspirate may be of normal color and
not show the classic changes or radiographic findings.

[Link] 7/32
6/19/22, 5:37 PM 5605

The most common feature of TGCT on MRI is the presence of intraarticular nodules or masses.
MRI findings are very useful in the diagnosis of TGCT, because hemosiderin in the tissues
renders TGCT "dark" on all MRI sequences due to a characteristic lack of signal on both T1 and
T2 images.

The treatment of TGCT is described in detail separately. (See "Treatment for tenosynovial giant
cell tumor and other benign neoplasms affecting soft tissue and bone", section on
'Tenosynovial giant cell tumor'.)

CLINICAL MANIFESTATIONS

Symptoms and physical findings — The presentation of hemarthrosis varies with the etiology
and is particularly influenced by the acuity or chronicity of bleeding (see 'Causes of
hemarthrosis' above). Pain, stiffness, reduced range of motion, swelling, and warmth are
typically present but can range from very mild to severe.

As an example, acute intraarticular bleeding, as occurs with trauma or from an acute

hemophilic bleed, typically occurs immediately and is often intensely painful. However,
subacute bleeding that occurs with articular tumors such as tenosynovial giant cell tumor
(TGCT) may be identified as an unexpected finding upon joint aspiration performed as part of
the diagnostic evaluation of a swollen joint. In such cases, joint swelling, stiffness, and mild to
moderate discomfort may be the only presenting symptoms. (See 'Traumatic' above and
'Bleeding disorders' above and 'Tenosynovial giant cell tumor/pigmented villonodular synovitis'
above.)

Patients with hemophilia may report a vague sensation of tingling or warmth at the onset of
acute bleeding, termed an aura, followed by tightness and reduced motion, which is typically
accompanied by increasing pain, warmth, and acute swelling. Knees are most commonly
affected in this group, but elbows and ankles are commonly affected as well. (See 'Bleeding
disorders' above.)

Synovial fluid analysis and other laboratory findings — Synovial fluid obtained from a
patient with hemarthrosis may appear red, pink, or brown. Other abnormalities of the fluid may
be noted that depend upon the cause of bleeding. As an example, the presence of lipid globules
strongly suggests an intraarticular fracture, resulting in leakage of marrow fat into the synovial
fluid (see 'Lipohemarthrosis' above). A true bloody effusion usually fails to clot due to chronic
fibrinolysis, while blood from a traumatic aspiration generally does coagulate [36].

[Link] 8/32
6/19/22, 5:37 PM 5605

Following centrifugation of joint fluid, the aspirate from a patient with hemarthrosis will
generally exhibit xanthochromia from lysis of the resident erythrocytes. This characteristic can
help to distinguish a bloody or blood-tinged fluid due to a traumatic arthrocentesis from true
hemarthrosis. (See 'Differential diagnosis' below and "Synovial fluid analysis".)

Laboratory findings on testing of peripheral blood depend upon the presence of comorbid
conditions, but otherwise hemarthrosis alone does not cause changes in general laboratory
testing.

Imaging — Standard plain radiography often suggests soft tissue swelling and joint effusion; in
patients with chronic, recurrent hemarthrosis (eg, in hemophilia) additional changes may occur
over time, including in cartilage and bone (see 'Bleeding disorders' above and "Clinical
manifestations and diagnosis of hemophilia", section on 'Hemophilic arthropathy'). Rarely,
patients with large effusions may exhibit a blood-fluid level that is evident on radiography.

Computed tomography (CT) is most sensitive to the detection of acute blood but does not
provide soft tissue or cartilage information. Hemosiderin is easily identified as low signal
intensity on joint magnetic resonance imaging (MRI). Echogenic intraarticular fluid seen on
ultrasound also indicates articular hemorrhage.

Imaging, especially MRI, may provide clues to other etiologies for hemarthrosis including
fracture, intraarticular vascular malformation, and tenosynovial giant cell tumor (pigmented
villonodular synovitis).

DIAGNOSIS

The diagnosis of hemarthrosis is usually made by joint aspiration, which typically reveals joint
fluid that is overtly and uniformly sanguineous, although with chronicity, the fluid can become
rusty or brown in color. Centrifugation discloses xanthochromia (yellow-tinged discoloration) of
the supernatant, from ruptured red blood cells, distinguishing hemarthrosis from bleeding due
to trauma incurred during the procedure itself. By contrast, in a traumatic tap, the fluid will
typically change color from less to more sanguineous over the course of the procedure, while
the supernatant of a centrifuged sample will disclose typical straw-colored fluid.

Arthrocentesis is generally not required for diagnosis when the underlying cause is already
known with confidence (eg, patients with hemophilia and a history of hemarthrosis, or patients
with acute trauma and known intraarticular injury), and when important alternate diagnoses
such as septic arthritis can be excluded clinically.

[Link] 9/32
6/19/22, 5:37 PM 5605

Aspiration of larger effusions should be performed using a needle of sufficient gauge (eg, 18-
gauge) to permit evacuation to relieve capsular distension and pain. If there is diagnostic
uncertainty, fluid should be sent for cytology to evaluate potential malignancy in addition to
routine synovial fluid studies (cell count, differential, Gram stain, culture, and, if indicated,
crystal analysis).

In patients with plain radiographic evidence of trauma, the diagnosis of hemarthrosis is further
supported by the appearance of a blood-fluid level in larger effusions, which is occasionally
present.

DIFFERENTIAL DIAGNOSIS

A wide variety of infectious and inflammatory conditions may cause an acute monoarthritis and
could clinically mimic hemarthrosis. The history and physical examination frequently help to
suggest the presence of a cause of likely hemarthrosis, such as trauma or hemophilia, or
another articular disorder. The finding of hemorrhagic joint fluid on synovial fluid analysis is the
key finding that distinguishes hemarthrosis from other disorders causing similar symptoms and
physical findings. The differential diagnosis of acute monoarticular joint pain and swelling is
reviewed in detail separately. (See "Monoarthritis in adults: Etiology and evaluation".)

The principal mimickers of hemarthrosis include traumatic arthrocentesis, resulting in bloody

"contamination" of synovial fluid; many conditions that may cause arthritis that can present
with acute joint pain and swelling; and chronic hemophilic arthritis, which can present in a
clinical setting typically associated with acute hemarthrosis. The major conditions of importance
in the differential diagnosis include:

● Traumatic arthrocentesis – A traumatic arthrocentesis is the most likely cause of a

bloody synovial fluid sample when the aspiration is not initially bloody, but fresh blood
appears after some synovial fluid has been withdrawn. In this case, centrifugation of the
specimen to examine the appearance of the resultant supernatant is useful. A serous
appearance of the synovial fluid supernatant suggests that fresh blood has been mixed
with previously nonbloody fluid. A true bloody effusion usually fails to clot due to chronic
fibrinolysis, while blood from a traumatic aspiration generally does coagulate. The
aspirate from a patient with hemarthrosis will generally exhibit xanthochromia from lysis
of the resident erythrocytes. (See 'Synovial fluid analysis and other laboratory findings'
above and "Synovial fluid analysis", section on 'Categories of joint effusions'.)

[Link] 10/32
6/19/22, 5:37 PM 5605

● Acute monoarthritis – A number of medical conditions may present with similar clinical
symptoms to hemarthrosis, but the major differentiating factor is nonhemorrhagic joint
effusions, in addition to the history and physical examination findings that typify other
disorders. Major conditions that may also cause acute pain and joint swelling, similar to
hemarthrosis, can be excluded by history and synovial fluid analysis. These conditions
include:

• Bacterial septic arthritis – Bacterial septic arthritis typically presents with

concomitant fever, and the diagnosis of septic arthritis can be confirmed with synovial
fluid analysis and culture (see 'Septic arthritis' above and "Septic arthritis in adults"). In
hemarthrosis, body temperature is often not elevated, there are minimal white blood
cells in the synovial fluid, and the culture should be negative.

• Crystal arthropathy – The diagnosis of a crystal arthropathy (gout or calcium

pyrophosphate deposition disease) is often suggested by the medical history and made
by the identification of crystals on synovial fluid analysis. Occasionally, calcium
pyrophosphate crystal deposition (CPPD) disease can present as "pseudo-
hemarthrosis," with recurrent bleeding particularly affecting the shoulder, especially in
the context of concomitant osteoarthritis [44]. (See "Clinical manifestations and
diagnosis of gout" and "Clinical manifestations and diagnosis of calcium
pyrophosphate crystal deposition (CPPD) disease".)

• Reactive arthritis – Reactive arthritis can generally be distinguished by the

characteristic history of antecedent infection and differentiated from hemarthrosis by
synovial fluid analysis. (See "Reactive arthritis".)

• Lyme arthritis – Lyme arthritis may be characterized, like hemarthrosis, by large joint
mono- or oligoarthritis, especially of the knee, but occurs in an endemic region and
may have other typical historical and physical features such as a prior tick bite and
typical rash; the diagnosis of Lyme disease can generally be confirmed (or excluded) by
serologic testing. (See "Musculoskeletal manifestations of Lyme disease" and
"Diagnosis of Lyme disease".)

• Primary inflammatory arthropathies – Primary inflammatory arthropathies (which

may also present with a mono- or oligoarthritis), such as rheumatoid arthritis, juvenile
idiopathic arthritis, and spondyloarthritis, can mimic hemarthrosis when only one or a
few joints are involved, but can be distinguished by medical history, examination, and
synovial fluid analysis. (See "Diagnosis and differential diagnosis of rheumatoid
arthritis" and "Oligoarticular juvenile idiopathic arthritis" and "Polyarticular juvenile

[Link] 11/32
6/19/22, 5:37 PM 5605

idiopathic arthritis: Clinical manifestations, diagnosis, and complications" and

"Systemic juvenile idiopathic arthritis: Clinical manifestations and diagnosis" and
"Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis
and nonradiographic axial spondyloarthritis) in adults" and "Clinical manifestations and
diagnosis of peripheral spondyloarthritis in adults".)

● Chronic hemophilic arthropathy – In patients with hemophilia and recurrent

intraarticular bleeding, it may be difficult to distinguish new hemarthrosis from
exacerbations of pain from underlying chronic joint injury. In both cases, patients present
with pain, limited motion, swelling, stiffness, and joint warmth, although an acute painful
episode combined with overt joint fullness (ie, substantial effusion) and a patient report of
new tenseness in the joint should suggest hemarthrosis [45]. In some cases, patients with
hemarthrosis report an aura (tingling or warmth) in the joint prior to new swelling and
pain, providing another potentially helpful clue [45]. (See "Clinical manifestations and
diagnosis of hemophilia", section on 'Hemophilic arthropathy'.)

POSTDIAGNOSTIC EVALUATION

Once the diagnosis of hemarthrosis has been established, the further management depends in
part upon the cause; for example, orthopedic management should be undertaken for acute
injuries or factor replacement should be administered in hemophiliacs. Thus, in patients in
whom no cause is immediately evident on history, examination, and synovial fluid analysis,
additional studies, such as further history, laboratory testing, imaging, and/or cytology, may be
required to evaluate the possibility of a more subtle intraarticular lesion, intraarticular
neoplasm, or other disorder.

In patients with bleeding that occurs with minor or no trauma, evaluation for coagulopathy
should be undertaken if that diagnosis has not been previously established. Patients suspected
of a coagulopathy should be referred to a hematologist with expertise in coagulation disorders.

TREATMENT

Treatment of hemarthrosis can be divided into interventions that are generally useful for any
patient with acute hemarthrosis, and more specific treatments directed toward the underlying
disorder. (See 'General approach' below and 'Cause-specific interventions' below.)

General approach — The goals of initial treatment are to limit further joint injury and optimize
patient comfort. We advise the following approach, based upon case series and expert opinion
[Link] 12/32
6/19/22, 5:37 PM 5605

[46-48]:

● Initial/acute therapy

• Patients with acute posttraumatic hemarthrosis should be treated initially by

immobilization of the affected joint, application of ice, and compression.

• In patients with a tense effusion and those in whom the diagnosis is uncertain,
aspiration of the joint may help provide pain relief.

• Potent analgesics may be required while the diagnostic evaluation proceeds, but most
nonselective nonsteroidal antiinflammatory drugs, other than cyclooxygenase (COX) 2
selective agents that don't affect platelet function, should be avoided in the first 48 to
72 hours because of the increased risk of bleeding associated with their use. The
decision regarding whether to use opioid analgesics in patients unresponsive to
nonopioid agents, and the type of agent in patients receiving such therapy, should be
made on an individualized basis taking the patient's history of analgesic use into
account.

● Postacute phase interventions

• Nonsteroidal antiinflammatory drugs (NSAIDs) may be employed when the acute

hemorrhage risk has receded, 48 to 72 hours after the injury, unless coagulopathy
evaluation or immediate surgical intervention is planned. The presence of a
coagulopathy influences drug choices. (See 'Coagulation disorders/hemophilia' below.)

• Depending upon the rate and extent of the clinical response to initial measures, some
patients may require immobilization, the application of ice, and compression for up to
a week.

• Joint lavage is generally not indicated, other than potentially in patients with
hemophilia with recurrent hemarthrosis (see 'Coagulation disorders/hemophilia'
below), because an isolated episode of bleeding into the joint is unlikely to cause
lasting injury.

Cause-specific interventions — In patients in whom a definite cause for the hemarthrosis can
be identified, interventions specific to the particular etiology can be employed. (See 'After major
trauma' below and 'Coagulation disorders/hemophilia' below and 'Patients receiving
anticoagulation' below and 'Postoperative' below and 'Vascular causes' below and 'Benign
tumors' below.)

[Link] 13/32
6/19/22, 5:37 PM 5605

After major trauma — Patients with major trauma and hemarthrosis should be evaluated and
managed in collaboration with an orthopedic surgeon; such patients are at risk for significant
bone and soft tissue injuries. (See 'Traumatic' above and 'Knee injury' above.)

The involved joint should be completely immobilized until radiographs have been obtained; in
patients with evidence of a fracture or suspicion of an internal derangement, orthopedic
consultation should be obtained. Although not all intraarticular fractures require operative
intervention, the patient and radiographic findings should be reviewed with a clinician
experienced in fracture care. Ligamentous and meniscal injuries generally do not require
immediate operative intervention.

Coagulation disorders/hemophilia — The prevention and treatment of acute and chronic

hemarthrosis in patients with known clotting factor deficiency is described in detail separately.
(See 'Bleeding disorders' above and "Synovectomy for inflammatory arthritis of the knee" and
"Treatment of bleeding and perioperative management in hemophilia A and B", section on
'Hemarthroses' and "Chronic complications and age-related comorbidities in people with
hemophilia", section on 'Arthropathy' and "Hemophilia A and B: Routine management including
prophylaxis", section on 'Prophylaxis versus on-demand therapy'.)

In hemophilic patients with recurrent hemarthrosis, the role of lavage to avoid the long-term
consequences of recurrent hemarthrosis is uncertain, although observational but uncontrolled
data suggest good outcomes with prompt arthrocentesis, saline lavage, and glucocorticoid
instillation [49].

Use of the selective cyclooxygenase (COX) 2 inhibitors celecoxib and etoricoxib is safe and
effective in patients with hemophilic arthropathy [50,51]. Since the selective COX-2 inhibitors do
not interfere with platelet function and may be less likely to cause gastroduodenal damage
than nonselective NSAIDs, this approach may be useful for treating chronic joint pain in those
with clotting factor deficiencies who require an NSAID [48,52]. The use and safety of celecoxib
are described separately. (See "Overview of COX-2 selective NSAIDs" and "NSAIDs: Adverse
cardiovascular effects", section on 'Aspirin and other antithrombotic agents'.)

One small series reported reduction of both recurrent hemarthrosis and synovitis in three
hemophilia patients treated with tumor necrosis factor (TNF) inhibitors for concurrent
inflammatory arthritis, providing anecdotal support for this approach [53]. Further support
comes from murine studies that have implicated TNF as a mediator of hemophilia-associated
joint inflammation and injury [54,55].

Patients receiving anticoagulation — Clinically important hemarthrosis in patients receiving

therapeutic anticoagulation is rare. Diagnostic or therapeutic arthrocentesis is usually well
[Link] 14/32
6/19/22, 5:37 PM 5605

tolerated in these patients despite the use of such therapies [56]. In most patients, temporary
immobilization and analgesics will be the only treatment necessary after correction, if needed,
of excessive anticoagulation. In the unusual event of persistent or recurrent hemarthrosis, an
anatomic cause should be sought [57]. If the patient is not at immediate risk of
thromboembolism, reversal of anticoagulation may be appropriate, provided that the benefits
outweigh the risks of thromboembolism. (See "Management of warfarin-associated bleeding or
supratherapeutic INR" and "Joint aspiration or injection in adults: Technique and indications",
section on 'Approach to the patient on anticoagulants' and "Management of bleeding in
patients receiving direct oral anticoagulants".)

Postoperative — Patients with recurrent postoperative hemarthrosis may require revision

surgery and should be referred to their orthopedic surgeon for further evaluation and
management (see 'Postoperative' above). In one reported case, angiographically guided
embolization controlled recurrent bleeding into the knee in a patient who required chronic
anticoagulation [58].

Vascular causes — In patients with an aneurysm or pseudoaneurysm as the cause of

intraarticular bleeding, surgical intervention is often required. In patients in whom surgical
treatment is not feasible, endovascular treatment with arterial embolization may be an option
[38,59]. (See 'Vascular disorders' above.)

Benign tumors — In patients with benign tumors that lead to hemarthrosis, arthroscopic or
surgical synovectomy is usually the treatment of choice to prevent recurrent episodes of
hemarthrosis. (See 'Tumors' above and "Synovectomy for inflammatory arthritis of the knee".)

PROGNOSIS

The prognosis of hemarthrosis varies with the specific cause. For trauma and tumors, the
prognosis is typically that of the inciting process. Repeated intraarticular hemorrhage in
hemophilia carries a high risk of chronic hemophilic arthropathy, experienced by 20 percent or
more of patients even in the era of factor replacement [60-62]. (See "Clinical manifestations and
diagnosis of hemophilia", section on 'Hemophilic arthropathy'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Hemophilia A and B".)

[Link] 15/32
6/19/22, 5:37 PM 5605

SUMMARY AND RECOMMENDATIONS

● Hemarthrosis, or bleeding into a joint, can occur from a variety of causes ( table 1) and
results in monoarticular pain and swelling. Diagnosis usually requires joint aspiration,
which reveals red, pink, or brown synovial fluid; arthrocentesis is needed whenever septic
arthritis is suspected. Arthrocentesis is generally not required for diagnosis when the
underlying cause is known with confidence (eg, patients with hemophilia and a history of
hemarthrosis, acute trauma), and when important alternate diagnoses such as septic
arthritis can be excluded clinically. Other abnormalities of the fluid depend upon the cause
of the bleeding. (See 'Causes of hemarthrosis' above and 'Diagnosis' above.)

● A true bloody effusion usually fails to clot due to chronic fibrinolysis, while blood from a
traumatic aspiration generally does coagulate. Traumatic arthrocentesis is most likely if
the aspiration is not bloody initially, but fresh blood appears after some synovial fluid has
been withdrawn. (See 'Causes of hemarthrosis' above and 'Diagnosis' above.)

● Injuries are among the most common causes of hemarthrosis. The pain is often severe but
may be minimal or absent immediately following the event. Patients with impaired
sensation from neuropathy or myelopathy may have little or no pain despite the presence
of a fracture. The rapid accumulation of bloody fluid that follows a major injury with
intraarticular bleeding is due to soft tissue injury or bone/osteochondral fracture. (See
'Traumatic' above.)

● The knee is a frequent site of injury, and evaluation for internal derangement is an
important part of the evaluation. The most common mechanism of injury in patients with
acute hemarthrosis of the knee is forced twisting of the loaded joint. The initial imaging
technique of choice is plain film radiography. If a fracture is strongly suspected but
radiographs are negative, computed tomography (CT) may aid in diagnosis; however,
magnetic resonance imaging (MRI) also provides helpful information about ligamentous
and cartilaginous structures. Arthroscopic evaluation of the knee may be helpful in some
patients. (See 'Knee injury' above.)

● Additional concerns in patients with traumatic hemarthrosis include lipohemarthrosis,

recurrent postoperative hemarthrosis following total knee arthroplasty, and coagulation
disorders, which should be suspected in patients in whom hemarthrosis occurs after
minimal trauma. When hemarthrosis following minimal trauma is not due to a bleeding
diathesis, the most commonly documented injuries are anterior cruciate ligament (ACL),

[Link] 16/32
6/19/22, 5:37 PM 5605

meniscal tears, and patellar subluxations. (See 'Lipohemarthrosis' above and 'Minimal
injuries' above and 'Postoperative' above.)

● A variety of hereditary, acquired, and iatrogenic bleeding disorders can result in

hemarthrosis. Bleeding disorders should be considered when hemarthrosis occurs with
minimal or no recollected trauma. Hemarthrosis is typically seen with deficiencies in
coagulation factors, rather than platelets ( table 4). Three forms of hemarthrosis due to
hemophilia and other coagulopathies are recognized: acute, subacute, and chronic; and
five stages of hemophilic arthropathy have been identified. (See 'Bleeding disorders'
above.)

● Potential causes of hemarthrosis other than bleeding disorders and trauma include
neurologic, infectious, and vascular disorders; inflammatory, degenerative, and crystalline
arthritis; and neoplasms, including tenosynovial giant cell tumor (formerly termed
pigmented villonodular synovitis). (See 'Nontraumatic' above and 'Osteoarthritis' above
and 'Neurologic disorders' above and 'Septic arthritis' above and 'Vascular disorders'
above and 'Tumors' above.)

● The treatment of hemarthrosis includes interventions that are generally useful for any
patient with an acute hemarthrosis and more specific treatments directed toward the
underlying disorder. Treatments of general benefit include immobilization, ice, and
compression initially; analgesia; and arthrocentesis. Lavage is generally not required but
can be considered (together with glucocorticoid instillation) for recurrent hemarthrosis
associated with hemophilia. Nonsteroidal antiinflammatory drugs (NSAIDs) that interfere
with platelet function should be avoided, and thus the use of cyclooxygenase (COX) 2
inhibitors is encouraged. Specific treatment can be employed when a definite cause for
the hemarthrosis can be identified. (See 'General approach' above and 'Cause-specific
interventions' above and 'After major trauma' above and 'Postoperative' above and
'Vascular causes' above and 'Benign tumors' above.)

● The approach to patients treated with anticoagulation is variable, depending upon the risk
of reduced anticoagulation therapy. The treatment of patients with known clotting factor
deficiency is described in detail separately. (See 'Coagulation disorders/hemophilia' above
and "Treatment of bleeding and perioperative management in hemophilia A and B".)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

[Link] 17/32
6/19/22, 5:37 PM 5605

1. Baker CL. Acute hemarthrosis of the knee. J Med Assoc Ga 1992; 81:301.
2. Maffulli N, Binfield PM, King JB, Good CJ. Acute haemarthrosis of the knee in athletes. A
prospective study of 106 cases. J Bone Joint Surg Br 1993; 75:945.
3. Visuri T, Koskenvuo M, Dahlström S. Hemarthrosis of the clinically stable knee due to sports
and military training in young recruits: an arthroscopic analysis. Mil Med 1993; 158:378.
4. Askenberger M, Ekström W, Finnbogason T, Janarv PM. Occult Intra-articular Knee Injuries
in Children With Hemarthrosis. Am J Sports Med 2014; 42:1600.

5. Allum R. The management of acute traumatic haemarthrosis of the knee. Br J Hosp Med
1997; 58:138.
6. Bomberg BC, McGinty JB. Acute hemarthrosis of the knee: indications for diagnostic
arthroscopy. Arthroscopy 1990; 6:221.
7. Ryu KN, Jaovisidha S, De Maeseneer M, et al. Evolving stages of lipohemarthrosis of the
knee. Sequential magnetic resonance imaging findings in cadavers with clinical correlation.
Invest Radiol 1997; 32:7.
8. Lugo-Olivieri CH, Scott WW Jr, Zerhouni EA. Fluid-fluid levels in injured knees: do they
always represent lipohemarthrosis? Radiology 1996; 198:499.
9. Bianchi S, Zwass A, Abdelwahab IF, et al. Sonographic evaluation of lipohemarthrosis:
clinical and in vitro study. J Ultrasound Med 1995; 14:279.
10. Ames PR, Maffulli N, Capasso G, Brancaccio V. Minimal trauma knee hemarthrosis. Bull
Hosp Jt Dis 1996; 54:258.

11. Lu KH, Hsiao YM, Lin ZI. Arthroscopy for acute knee haemarthrosis in road traffic accident
victims. Injury 1996; 27:341.
12. Saksena J, Platts AD, Dowd GS. Recurrent haemarthrosis following total knee replacement.
Knee 2010; 17:7.
13. Worland RL, Jessup DE. Recurrent hemarthrosis after total knee arthroplasty. J Arthroplasty
1996; 11:977.
14. Ballard WT, Clark CR, Callaghan JJ. Recurrent spontaneous hemarthrosis nine years after a
total knee arthroplasty. A presentation with pigmented villonodular synovitis. J Bone Joint
Surg Am 1993; 75:764.
15. Oishi CS, Elliott ML, Colwell CW Jr. Recurrent hemarthrosis following a total knee
arthroplasty. J Arthroplasty 1995; 10 Suppl:S56.

16. Schneider T, Fink B, Abel R, et al. Hemarthrosis as a major complication after arthroscopic
subcutaneous lateral retinacular release: a prospective study. Am J Knee Surg 1998; 11:95.

[Link] 18/32
6/19/22, 5:37 PM 5605

17. Wild JH, Zvaifler NJ. Hemarthrosis associated with sodium warfarin therapy. Arthritis
Rheum 1976; 19:98.
18. Jaffer AM, Schmid FR. Hemarthrosis associated with sodium warfarin. J Rheumatol 1977;
4:215.

19. Birnbaum Y, Stahl B, Rechavia E. Spontaneous hemarthrosis following thrombolytic therapy

for acute myocardial infarction. Int J Cardiol 1993; 40:289.
20. Finlayson J, Dunsmuir RA. Haemarthrosis following thrombolytic therapy for acute
myocardial infarction. Injury 1997; 28:146.
21. Lan HH, Eustace SJ, Dorfman D. Hemophilic arthropathy. Radiol Clin North Am 1996;
34:446.
22. Blanchette VS, Key NS, Ljung LR, et al. Definitions in hemophilia: communication from the
SSC of the ISTH. J Thromb Haemost 2014; 12:1935.
23. Soucie JM, Cianfrini C, Janco RL, et al. Joint range-of-motion limitations among young males
with hemophilia: prevalence and risk factors. Blood 2004; 103:2467.

24. Arnold WD, Hilgartner MW. Hemophilic arthropathy. Current concepts of pathogenesis and
management. J Bone Joint Surg Am 1977; 59:287.
25. van Vulpen LFD, Holstein K, Martinoli C. Joint disease in haemophilia: Pathophysiology, pain
and imaging. Haemophilia 2018; 24 Suppl 6:44.
26. Roosendaal G, Vianen ME, Marx JJ, et al. Blood-induced joint damage: a human in vitro
study. Arthritis Rheum 1999; 42:1025.

27. Rodriguez-Merchan EC. The destructive capabilities of the synovium in the haemophilic
joint. Haemophilia 1998; 4:506.
28. Roosendaal G, Tekoppele JM, Vianen ME, et al. Articular cartilage is more susceptible to
blood induced damage at young than at old age. J Rheumatol 2000; 27:1740.
29. Wen FQ, Jabbar AA, Chen YX, et al. c-myc proto-oncogene expression in hemophilic
synovitis: in vitro studies of the effects of iron and ceramide. Blood 2002; 100:912.
30. Jansen NW, Roosendaal G, Bijlsma JW, et al. Exposure of human cartilage tissue to low
concentrations of blood for a short period of time leads to prolonged cartilage damage: an
in vitro study. Arthritis Rheum 2007; 56:199.
31. Christensen KR, Kjelgaard-Hansen M, Nielsen LN, et al. Rapid inflammation and early
degeneration of bone and cartilage revealed in a time-course study of induced
haemarthrosis in haemophilic rats. Rheumatology (Oxford) 2019; 58:588.

32. Sun J, Hua B, Livingston EW, et al. Abnormal joint and bone wound healing in hemophilia
mice is improved by extending factor IX activity after hemarthrosis. Blood 2017; 129:2161.
[Link] 19/32
6/19/22, 5:37 PM 5605

33. Bhat V, Olmer M, Joshi S, et al. Vascular remodeling underlies rebleeding in hemophilic
arthropathy. Am J Hematol 2015; 90:1027.

34. Feldman BM. Preventing joint damage from hemophilia. J Rheumatol 2000; 27:1579.
35. Kawamura H, Ogata K, Miura H, et al. Spontaneous hemarthrosis of the knee in the elderly:
etiology and treatment. Arthroscopy 1994; 10:171.
36. Dougados M. Synovial fluid cell analysis. Baillieres Clin Rheumatol 1996; 10:519.

37. Mowad CM, Howe KL, Guzzo CA. Unexplained hemothorax, hemarthrosis, and palpable
purpura. Hosp Pract (Off Ed) 1995; 30:55.
38. Klein GE, Raith J, Passler J, et al. Spontaneous recurrent hemarthrosis of the knee joint:
endovascular treatment of a ruptured aneurysm with platinum microcoils. A case report. J
Bone Joint Surg Am 1997; 79:594.

39. Wirth T, Rauch G, Rüschoff J, Griss P. Synovial haemangioma of the knee joint. Int Orthop
1992; 16:130.
40. Frick MA, Wenger DE, Adkins M. MR imaging of synovial disorders of the knee: an update.
Radiol Clin North Am 2007; 45:1017.
41. Larbi A, Viala P, Cyteval C, et al. Imaging of tumors and tumor-like lesions of the knee.
Diagn Interv Imaging 2016; 97:767.
42. West RB, Rubin BP, Miller MA, et al. A landscape effect in tenosynovial giant-cell tumor from
activation of CSF1 expression by a translocation in a minority of tumor cells. Proc Natl Acad
Sci U S A 2006; 103:690.
43. Frassica FJ, Bhimani MA, McCarthy EF, Wenz J. Pigmented villonodular synovitis of the hip
and knee. Am Fam Physician 1999; 60:1404.

44. Zhang W, Doherty M, Pascual E, et al. EULAR recommendations for calcium pyrophosphate
deposition. Part II: management. Ann Rheum Dis 2011; 70:571.

45. Sierra Aisa C, Lucía Cuesta JF, Rubio Martínez A, et al. Comparison of ultrasound and
magnetic resonance imaging for diagnosis and follow-up of joint lesions in patients with
haemophilia. Haemophilia 2014; 20:e51.
46. Hanley J, McKernan A, Creagh MD, et al. Guidelines for the management of acute joint
bleeds and chronic synovitis in haemophilia: A United Kingdom Haemophilia Centre
Doctors' Organisation (UKHCDO) guideline. Haemophilia 2017; 23:511.
47. Simpson ML, Valentino LA. Management of joint bleeding in hemophilia. Expert Rev
Hematol 2012; 5:459.

[Link] 20/32
6/19/22, 5:37 PM 5605

48. Gualtierotti R, Tafuri F, Arcudi S, et al. Current and Emerging Approaches for Pain
Management in Hemophilic Arthropathy. Pain Ther 2022; 11:1.

49. Manners PJ, Price P, Buurman D, et al. Joint Aspiration for Acute Hemarthrosis in Children
Receiving Factor VIII Prophylaxis for Severe Hemophilia: 11-year Safety Data. J Rheumatol
2015; 42:885.

50. Rattray B, Nugent DJ, Young G. Celecoxib in the treatment of haemophilic synovitis, target
joints, and pain in adults and children with haemophilia. Haemophilia 2006; 12:514.

51. Tsoukas C, Eyster ME, Shingo S, et al. Evaluation of the efficacy and safety of etoricoxib in
the treatment of hemophilic arthropathy. Blood 2006; 107:1785.
52. Nissen SE, Yeomans ND, Solomon DH, et al. Cardiovascular safety of celecoxib, naproxen,
or ibuprofen for arthritis. N Engl J Med 2016; 375:2519.
53. Melchiorre D, Morfini M, Linari S, et al. Anti-TNF-α therapy prevents the recurrence of joint
bleeding in haemophilia and arthritis. Rheumatology (Oxford) 2014; 53:576.
54. Haxaire C, Hakobyan N, Pannellini T, et al. Blood-induced bone loss in murine hemophilic
arthropathy is prevented by blocking the iRhom2/ADAM17/TNF-α pathway. Blood 2018;
132:1064.
55. Zhang F, Xu M, Yang Q, et al. A Translational Study of TNF-Alpha Antagonists as an
Adjunctive Therapy for Preventing Hemophilic Arthropathy. J Clin Med 2019; 9.

56. Thumboo J, O'Duffy JD. A prospective study of the safety of joint and soft tissue aspirations
and injections in patients taking warfarin sodium. Arthritis Rheum 1998; 41:736.

57. Son KM, Kim JK, Seo YI, Kim HA. A case of bilateral hemarthrosis due to pseudoaneurysms
in a patient on anticoagulation therapy. J Clin Rheumatol 2013; 19:206.
58. Katsimihas M, Robinson D, Thornton M, Langkamer VG. Therapeutic embolization of the
genicular arteries for recurrent hemarthrosis after total knee arthroplasty. J Arthroplasty
2001; 16:935.
59. Omary R, Stulberg SD, Vogelzang RL. Therapeutic embolization of false aneurysms of the
superior medial genicular artery after operations on the knee. A report of two cases. J Bone
Joint Surg Am 1991; 73:1257.
60. Wyseure T, Mosnier LO, von Drygalski A. Advances and challenges in hemophilic
arthropathy. Semin Hematol 2016; 53:10.

61. Goren R, Pullenayegum E, Blanchette VS, et al. Patterns of joint damage in severe
haemophilia A treated with prophylaxis. Haemophilia 2021; 27:666.

62. Stimec J, Dover S, Pullenayegum E, et al. Magnetic resonance imaging in boys with severe
hemophilia A: Serial and end-of-study findings from the Canadian Hemophilia Primary
[Link] 21/32
6/19/22, 5:37 PM 5605

Prophylaxis Study. Res Pract Thromb Haemost 2021; 5:e12565.

Topic 5605 Version 21.0

[Link] 22/32
6/19/22, 5:37 PM 5605

GRAPHICS

Causes of hemarthrosis[1,2]

Trauma
Iatrogenic (traumatic arthrocentesis)

Without bone fracture

With bone fracture (lipohemarthrosis)

Postoperative

Hematologic
Drug-induced

Inherited hematologic disorders, ie, coagulation disorders, sickle cell disease

Acquired hematological disorders, ie, myeloproliferative diseases, essential thrombocytosis, and

thrombocytopenia

Neurologic
Neuropathic (Charcot) arthropathy

Tumors
Tenosynovial giant cell tumor (pigmented villonodular synovitis)

Vascular
Hemangioma

Arteriovenous malformation

Aneurysm

Synovial vascular structural abnormalities

Osteoarthritis
Degenerative tear of the meniscus

Osteoarthritis (other)

Crystal diseases
Gout

Pseudogout (calcium pyrophosphate deposition disease)

Milwaukee shoulder

Nutritional
Scurvy

[Link] 23/32
6/19/22, 5:37 PM 5605

Septic arthritis

References:

1. Dougados M. Synovial fluid cell analysis. Bailliere's Clinical Rheumatology 1996; 10:519.
2. Baker CL. Acute hemarthrosis of the knee. J Med Assoc Ga 1992; 81:301.

Graphic 80811 Version 4.0

[Link] 24/32
6/19/22, 5:37 PM 5605

Causes of acute hemarthrosis of the knee

Injury

Anterior cruciate ligament tear 70-72%

Patellar subluxation or dislocation 10-15%

Peripheral meniscal tear 10%

Osteochondral fracture 2-5%

Posterior cruciate tear, capsular tear, other 5%

Modified with permission from Baker C. Journal of MAG 1992; 81:301.

Graphic 65058 Version 2.0

[Link] 25/32
6/19/22, 5:37 PM 5605

Valgus and varus stress tests of the knee

The valgus stress test (photo A) is used to assess the integrity of the medial
collateral ligament, while the varus stress test (photo B) is used to assess the
lateral collateral ligament.

Courtesy of Anthony Beutler, MD.

Graphic 89745 Version 3.0

[Link] 26/32
6/19/22, 5:37 PM 5605

Anterior drawer test

The anterior drawer test is used to assess the integrity of the

anterior cruciate ligament. With the knee flexed to 90 degrees, the
foot is stabilized by sitting on it. The proximal tibia is grasped firmly
with both hands, and the tibia is forcibly pulled anteriorly, noting
any pain, laxity, or abnormal movement compared with the opposite
side.

Courtesy of Bruce C Anderson, MD.

Graphic 73257 Version 2.0

[Link] 27/32
6/19/22, 5:37 PM 5605

Lipohemarthrosis of the knee: Imaging on plain

radiography and computerized tomography

An anteroposterior view of the left knee (A) shows a depressed

fracture of the lateral tibial plateau (arrow). A tunnel view of the left
knee (B), shows a vertical component of the fracture (arrow). A cross
table lateral view (C) shows a fat-fluid level (arrow). An axial image
from a CT scan (D) at a level above the knee confirms a fat-fluid level
(arrow) with a low-density fat containing supernatant and blood
layering posteriorly. These findings are consistent with a
lipohemarthrosis secondary to a tibial fracture.

CT: Computed tomography

Graphic 88737 Version 3.0

[Link] 28/32
6/19/22, 5:37 PM 5605

Causes of a prolonged prothrombin time (PT) and/or a prolonged activated

partial thromboplastin time (aPTT)

Test result
Causes of test result pattern
PT aPTT

Prolonged Normal Inherited

Factor VII deficiency

Acquired

Mild vitamin K deficiency

Liver disease

Warfarin*

DIC

Normal Prolonged Inherited

Deficiency of factor VIII, IX, or XI

Deficiency of factor XII, prekallikrein, or HMW kininogen (not associated

with a bleeding diathesis)

von Willebrand disease (variable)

Acquired

Heparin, dabigatran, argatroban, direct factor Xa inhibitors (variable)*

Acquired inhibitor of factor VIII, IX, XI, or XII

Acquired von Willebrand syndrome

Lupus anticoagulant (more likely to be associated with thrombosis than

bleeding)

Prolonged Prolonged Inherited

Deficiency of prothrombin, fibrinogen, factor V, or factor X

Combined factor deficiencies

Acquired

Liver disease

DIC

Severe vitamin K deficiency

Anticoagulants (supratherapeutic doses of many anticoagulants,

combined heparin and warfarin, direct thrombin inhibitors,
anticoagulant rodenticide poisoning)*
[Link] 29/32
6/19/22, 5:37 PM 5605

Acquired inhibitor of prothrombin, fibrinogen, factor V, or factor X

Amyloidosis-associated factor X deficiency

Refer to UpToDate topics on use of coagulation tests and on evaluation of patients with bleeding or
specific inherited and acquired conditions for additional details.

PT: prothrombin time; aPTT: activated partial thromboplastin time; DIC: disseminated intravascular
coagulation; HMW: high molecular weight.

* In principle, many anticoagulants affect common pathway factors and can prolong both the PT
and the aPTT if present at high enough levels. As examples:

Warfarin typically prolongs the PT alone, but at high levels warfarin can prolong both tests.
Heparin typically prolongs the aPTT alone (because PT reagents contain heparin-binding
agents that block heparin effect), but at high levels heparin can prolong both tests.
Direct thrombin inhibitors (argatroban, dabigatran) typically prolong both tests, but at low
levels dabigatran may not prolong the PT.
Direct factor Xa inhibitors (apixaban, edoxaban, rivaroxaban) can prolong the PT and aPTT,
although these effects are variable.

Graphic 79969 Version 10.0

[Link] 30/32
6/19/22, 5:37 PM 5605

Clinical features of bleeding disorders

Type of bleeding disorder

Bleeding characteristics
Thrombocytopenia or Clotting factor deficiencies
platelet function disorders or inhibitors

Major sites of bleeding Mucocutaneous (mouth, nose, Deep tissue (joints, muscles) or
gastrointestinal tract, urinary soft tissue hematomas
tract, menorrhagia)

Petechiae Common Uncommon

Ecchymoses Generally small and superficial. May develop large ecchymoses

May be significant, depending
upon the degree of
thrombocytopenia.

Excessive bleeding after minor Yes Not usually

cuts

Excessive bleeding with surgery Often immediate; severity is Often during the procedure.
or invasive procedures variable (no excess bleeding Individuals with factor XIII
with mild thrombocytopenia, deficiency may experience
severe bleeding with certain delayed bleeding.
platelet function disorders such
as GT)

Individuals with mild disorders may not report significant bleeding. Refer to UpToDate for details of
the evaluation of a suspected bleeding disorder and for diagnostic testing for specific disorders.

GT: Glanzmann thrombasthenia.

Graphic 77834 Version 13.0

[Link] 31/32
6/19/22, 5:37 PM 5605

Contributor Disclosures
Peter A Nigrovic, MD Grant/Research/Clinical Trial Support: Novartis [sJIA, IL-1 biology]; Pfizer
[Neutrophil biology]; Bristol Myers Squibb [Genetics]. Consultant/Advisory Boards: Bristol Myers Squibb
[COVID-19]; Novartis [sJIA, IL-1 biology]; Sobi [IL-1 biology]; XBiotech [IL-1 biology]; Simcere [Inflammation
biology]; Cerecor [Inflammation biology]; Quench Bio [Inflammasome biology]; Miach Ortho; Pfizer [Basic
biology]; AbbVie [Uveitis]; Sigilon [Inflammation biology]; Exo Therapeutics. Other Financial Interest:
American Academy of Pediatrics [Royalties]. All of the relevant financial relationships listed have been
mitigated. Simon M Helfgott, MD No relevant financial relationship(s) with ineligible companies to
disclose. Paul L Romain, MD No relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy

[Link] 32/32