McMurray’s Test Meniscal Tear

McMurray’s test is a commonly used test in orthopaedic examination to test for tears of the meniscus. The McMurray’s test is a rotational maneuver of the knee that is frequently used in the examination of the patient to help in the diagnosis of meniscal tears. Meniscus injuries are very common. When the patient sustains an injury of the knee and has a meniscal tear, usually the patient complains of knee pain localized to the medial or lateral side of the knee. The patient may also have locking and clicking. Sometimes the patient will have an effusion and sometimes this effusion is small (swelling of the knee). Joint line tenderness is the most sensitive finding. Joint line tenderness can be on the medial side (medial meniscal tear) or on the lateral side (lateral meniscal tear). There will be minimal swelling of the knee and possible extension lag (locked knee) due to a displaced bucket handle tear of the meniscus. Pain at a higher level than the joint is usually associated with medial collateral ligament tear. If an MCL tear is present, it is usually avulsed from the medial femoral condyle. The MCL is rarely avulsed from the tibia. Pain at a lower level is usually associated with the pes anserine bursitis. McMurray’s test is a knee examination test that shows pain or a painful click as the knee is brought from flexion to extension with either internal or external rotation of the knee. The McMurray’s test uses the tibia to trap the meniscus between the femoral condyles of the femur and the tibia. When performing the McMurray’s test, the patient should be lying supine with the knee hyperflexed. The examiner then grasps the patient’s heel with one hand and places the other hand over the knee joint. To test the medial meniscus, the knee is fully flexed, and the examiner then passively externally rotates the tibia and places a valgus force. The knee is then extended in order to test the medial meniscus. To test the lateral meniscus, the examiner passively internally rotates the tibia and places a varus force. The knee is then extended in order to test the lateral meniscus. A positive test is indicated by pain, clicking or popping within the knee joint and may signal a tear of either the medial or lateral meniscus when the knee is brought from flexion to extension. There are mixed reviews for the validity of this test. There are other clinical tests that are as good as the McMurray’s test, however MRI is making the diagnosis of a meniscal tear easier. MRI is very sensitive, and it also excludes other associated injuries. I find that the McMurray’s test is valuable in getting insurance approval for performing an MRI. If you state that the McMurray’s test is positive, then the insurance will approve the MRI. Nowadays though, the McMurray’s test does not give us a lot of valuable clinical information, because we get the information from other tests.

Anatomy of the Trapezius Muscle

The trapezius is a large superficial muscle that extends from the back of the skull, back of the neck, and back of the thorax. The upper fibers of the trapezius muscle arise from the external occipital protuberance and the medial third of the superior nuchal line. The middle fibers arise from the ligamentum nuchae and the spinous process of C7. The lower fibers arise from the spinous processes and supraspinous ligaments of all twelve thoracic vertebrae. The trapezius is inserted into the lateral third of the clavicle, and from the acromion process and the spine of the scapula. The trapezius muscle allows for rotation and lift of the scapula. Dysfunction of the trapezius muscle may cause lateral winging of the scapula. Winging can occur after radical neck surgery, but it usually occurs after biopsy or tumor dissection. The spinal accessory nerve will be injured, and the patient will have difficulty with overhead activity. If injury to the spinal accessory nerve occurs early, explore the nerve. If injury is late, do a muscle transfer. The spinal accessory nerve provides motor innervation to the sternocleidomastoid and the trapezius muscle. The spinal accessory nerve courses obliquely across the posterior triangle on the surface of the levator scapula muscle and reaches the trapezius. Within the posterior triangle of the neck, the nerve is vulnerable since it is superficial and only covered by skin and subcutaneous fascia. Extreme caution should be taken for any surgical procedure done in the posterior triangle of the neck.

Neurological Evaluation of the Lumbar Nerve Roots

To study the involvement of any nerve root we look for sensory change, motor changes, reflex changes. A herniated disc at T12-L1 affects the L1 nerve root. The sensory of the L1 nerve root is half the distance between the inguinal ligament and mid-thigh. Motor involvement is hip flexion. There are no reflexes of L1. A herniated disc at L1-L2 affects the L2 nerve root. The sensory of the L2 nerve root is mid-anterior thigh. Motor involvement is hip flexion, hip adduction, and knee extension. There are no reflexes of L2. A herniated disc at L2-L3 affects L3 nerve root. The sensory of the L3 nerve root is distal part of the thigh including the knee area. Motor involvement is hip flexion and knee extension. A herniated disc at L3-L4 affects the L4 nerve root. The sensory of the L4 nerve root is medial side of the leg down to the medial side of the foot. Motor involvement is L4 ankle dorsiflexion (tibialis anterior) and knee extension. L4 reflex changes will be a positive femoral stretch test. The test is positive if pain is felt in the ipsilateral anterior thigh. If the test is positive, it means that there is probably a disc herniation between L3-L4, affecting the L4 nerve root. The patellar reflex is mainly L4. A herniated disc at L4-L5 affects the L5 nerve root. The sensory of the L5 nerve root is dorsum of the foot and leg. Motor involvement is hip abduction (gluteus medius) and extension of the big toe. L5 nerve root is very popular in the exam. If you see a big toe extension, this involves the L5 nerve root (L4, L5 disc herniation). The patient may have Trendelenburg gait due to injury to the L5 nerve root (disc herniation between L4, L5 affecting the L5 nerve root). Both the gluteus medius and minimus muscles are innervated by the L5 nerve root. Straight leg raise can be positive with L5 nerve root irritation. This test is used to determine if the patient with low back pain has an underlying herniated disc irritating the nerves. A herniated disc at L5-S1 affects the S1 nerve root. The sensory of S1 nerve root is lateral and plantar aspects of the foot. Motor involvement is S1 hip extension (gluteus maximus), S1 ankle plantar flexion (gastro-soleus), and S1 foot eversion (peroneus longus and peroneus brevis). Positive straight leg raise examination to determine whether patient with low back pain has an underlying component of a herniated disc or not (stretch test). Reflexes are S1 ankle reflex.

Gout, Pseudogout, and Joint Pain

The most common joint affected by gout is the first metatarsophalangeal joint. The most common joint affected by pseudogout is the knee joint. Gout and pseudogout both show a sudden onset of pain, redness, and swelling typically affecting a single joint in 80% of the cases. Gout and pseudogout are similar problems with different causes. Gout is caused by the buildup of uric acid and the deposit of uric acid crystals inside a joint. The best test to diagnose gout is with a joint fluid analysis. Gout crystals are needle shaped and negatively bifringent. When placed under polarized light, they will be yellow. 90% of patients suffering from gout are men between the ages of 40-60 years old. Uric acid buildup in the body occurs by two main mechanisms: excessive urate production and diminished urate clearance. Uric acid is produced from the breakdown of proteins inside the body and from the proteins of food that is eaten. Gout symptoms and signs include joint pain, swelling and arthritis. Patients with gout have periarticular erosions along with the formation of uric acid soft tissue masses in and around the joint which can be seen on x-ray. Soft tissue tophus deposition with periarticular erosions “punch-out” lesions. The tophi occurs due to deposition of uric acid crystals. The tophus aspirate may look like tooth paste. The sudden attack of gout can be brought on by anything that increases the level of uric acid in the blood such as: dehydration, increased consumption of alcohol, eating large amounts of meat or seafood, or trauma/surgery. Other risk factors for gout are obesity, hypertension, and diuretics. Red meats, seafood, liquor, beer, all increase the risk of gout. Vegetables, wine, dairy products, and total proteins do not increase the risk of gout. Aspiration and analysis of the joint fluid is the best method for diagnosis. Elevate uric acid is not diagnostic. 80% of people with elevated uric acid will not get a gouty attack. There are blood tests such as white blood cell count, C-reactive protein, sedimentation rate, and uric acid level that are helpful in supporting the diagnosis if elevated, but if these levels are normal, it cannot definitively rule out gout or pseudogout. Every time you aspirate a joint and you get synovial fluid, you need to analyze it for cell count differential, find out if you have crystals or not and send the fluid for culture and sensitivity if you suspect infection. It might be difficult to differentiate an acute gouty attach from acute septic arthritis. Patients with an acute gouty arthritis may not have an elevated serum uric acid level. A patient with acute gouty arthritis may present with symptoms and a clinical picture that is similar to septic arthritis. Aspirate the joint fluid, and the joint fluid will look like pus, but it could be gout. You will take the fluid and examine it under the microscope (you will find needle shaped, intracellular crystals, and you will think that it is gout). The cell count of the aspirate may be high (may be 50,000-60,000) and the neutrophils may also be high (may be 80%). The incidence of gout and associated septic arthritis of a joint is low (about 1.5%). The incidence of septic arthritis will increase to 11% or more if the cell count is more than 50,000. We aspirate the joint (aspirate will look cloudy, like pus). We look for crystals and if there is crystals, then it is gout, but the presence of uric acid crystals does not exclude septic arthritis. We look at the cell count (will be high, 50,000 or more). The neutrophil count may be 80% or more (we think there is an infection in addition to gout or maybe gout alone). We need to culture the fluid. After we aspirate the fluid and send the fluid for culture, then we give the patient empiric intravenous antibiotics pending the culture result. Remember that gout and septic arthritis can occur together, but the incidence is low. The incidence will increase significantly if the cell count is more than 50,000. Pseudogout or chondrocalcinosis is the deposition of calcium pyrophosphate dihydrate crystals in the hyaline cartilage or fibrocartilage (CPPD). Pseudogout is a metabolic disease where calcium pyrophosphate dehydrate crystals (CPPD) are formed within the joint space. Pseudogout most often affects the knee, occurs more in older patients, and is a calcification of fibrocartilage (chondrocalcinosis). Pseudogout crystals are rhomboid shaped and positively birefringent. Crystals will be blue when placed under polarized light. Associated conditions include hyperparathyroidism, rheumatoid arthritis, and gout. Aspirate to see if it is pseudogout or infection, because you do not want to inject the knee with steroids when there is an infection. You need to look for the rhomboid crystals of pseudogout. X-rays in pseudogout will show thin calcification in the articular cartilage or menisci. Calcifications of the synovium, tendon, and ligaments can also occur. Acute gout can be treated with indomethacin or colchicine if the patient cannot tolerate NSAIDs. Colchicine inhibits the inflammatory mediators and is indicated if the patient cannot tolerate indomethacin. Chronic gout can be treated with allopurinol to prevent buildup of uric acid. Allopurinol is a xanthine oxidase inhibitor. Pseudogout is treated with NSAIDs and intraarticular injections.