Wednesday, April 15, 2009

Heamarthrosis of the knee- Causes

The primary diagnostic tool for patients with a knee injury is a clinical examination by a physician well trained in knee evaluation (4). With knowledge of the common causes of Heamarthrosis and understanding of the knee examination, a trained examiner can make an accurate diagnosis 80% to 90% of the time and prescribe the appropriate treatment (1).
Rapid swelling (swelling within minutes-hours) of the knee following a blow or twisting injury is considered a significant injury. The history of trauma coupled with a thorough examination should provide an accurate diagnosis in most patients (1). Aspiration of the fluid may help to establish diagnosis, reduce pain, and prevent capsular damage by the sustained turgid pressure from within the capsule. However, it should not be performed routinely. Splinting and re-evaluation are recommended as the initial treatment of an acute Heamarthrosis (1). However, according to Iobst CA et al treatment algorithm especially for ACL injury must take into account the patient's physiologic maturity, not chronological age (4).
Investigations in Heamarthrosis:
1. X-ray
2. MRI- MR imaging has significant limitations in this younger group. (4)
3. Arthroscopic Evaluation
Early in 1980s, acute Heamarthrosis, was rather a contraindication to arthroscopy, are in fact one of the best indications for use of this procedure (3). Arthroscopy helps to complete the diagnosis or as a means of early surgical intervention.

Causes of Haemarthrosis:
Heamarthrosis is associated with peripheral meniscal tears, anterior cruciate ligament ruptures, tibial tubercle avulsion injuries, and patellar/femoral osteochondral fractures and cannot be ignored (4).
Cazenave A et al Reviewed 161 traumatic Heamarthrosis of the knee cases. These cases ware evaluated clinically, radiologically and arthroscopically.

Anatomical lesions were never benign: they consisted of
1. Ligaments ruptures (65%),
2. Patella dislocations (20.5%),
3. Chondral lesions (41%),
4. Meniscal lesions (31%).

This study confirmed: (1) that a traumatic Heamarthrosis indicates a serious knee injury, and (2) the important contribution of arthroscopy for diagnosis and treatment of these traumatic knees.

Back in 1980 DeHaven KE studied 113 athletes, who had sustained significant acute trauma to the knee with immediate disability and the early onset of Heamarthrosis.

The cases studied had no demonstrable clinical laxity, were examined under anesthesia and had arthroscopy within 3 weeks of injury (the majority within 10 days).

Anatomical lesions were:
1. ACL plus Meniscus lesions were present in 81 (72%)
2. Major meniscus tears without ACL or PCL lesions were found in 17 cases (15%),
3. Osteochondral fractures in 7 cases (6%),
4. PCL tears in 3 cases (3%),
5. No internal derangement in 5 cases (4%).

Analysis of both the above said studies taken together:

The analysis tells us a fact that meniscal lesions with or without associated lesions to other anatomical structures are fairly common & some where between (32-33) % of all acute traumatic heamarthrosis.

Heamarthrosis & Patellar dislocation.
Patella dislocation although do not find a place in the 2nd review; review 1 shows a considerable population may be affected by the patellar dislocation presenting with heamarthrosis. Sillanpää P et al (5) investigated incidence, nature, and risk factors of primary traumatic patellar dislocations. The sample consisted in this study was of 128,714 Finnish male conscripts (median age 20). Heamarthrosis was present in all patients, and when MRI or open surgery was performed, medial retinacular disruption and medial patellofemoral ligament (MPFL) injury were identified. This study concluded that Heamarthrosis and MPFL rupture are the definite signs of an acute traumatic primary patellar dislocation. Height and weight were significant risk factors, whereas poor physical performance was not associated with primary patellar dislocation.

1. Baker CL; J Med Assoc Ga. 1992 Jun;81(6):301-5.
2. Cazenave A; J Chir (Paris). 1990 Nov;127(11):522-7.
3. DeHaven KE; Am J Sports Med. 1980 Jan-Feb;8(1):9-14.
4. Iobst CA et al; Clin Sports Med. 2000 Oct;19(4):621-35, vi.
5. Sillanpää P et al; Med Sci Sports Exerc. 2008 Apr;40(4):606-11.

NB: sorry friends i have missed to provide graphs i have plotted for this article. i dont know how to publish a graph. help wanted in this regard.

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