Category Archive Health

Knee Joint Examination – Indications, Technique, Result

Knee Joint Examination/The knee examination, in medicine and physiotherapy, is performed as part of a physical examination, or when a patient presents with knee pain or a history that suggests a pathology of the knee joint.

The knee examination, in medicine and physiotherapy, is performed as part of a physical examination, or when a patient presents with knee pain or a history that suggests a pathology of the knee joint. The exam includes several parts: position lighting draping. inspection.

It is important to have a systemic plan for the examination of the knee to arrive at the correct diagnosis, to identify its impact on the patient, to understand the patients’ needs and concerns and then to formulate a treatment plan that is individualized for the particular patient. Thorough knowledge of the normal anatomy, biomechanics of the knee and the pathology of various knee disorders is a must for proper examination of the knee and for the interpretation of physical findings.

First, listen to the patient carefully to understand his concerns and needs and also to gain his confidence.
The involved and the normal knee should be adequately exposed to examine the knee. Always examine the spine and the hip to rule out conditions that lead to referred pain in the knee and any associated hip and spine disorders.
Always compare with the uninvolved side as a wide range of anatomic and functional variations exist.
The examination should be gentle and as painless as possible to avoid worsening of injury and to ensure a cooperative patient. The function of the knee is assessed by the patient’s ability to weight bear, walk, ability to squat, sit cross-legged, run, stair climb and the level of restriction of activities of daily living and occupational and recreational activities.

HISTORY

Presenting complaints – Give the presenting complaints in chronological order.

Pain

  • Duration – How long the pain is present?
  • Onset – How it started? Symptoms may begin after a traumatic event, after unaccustomed activity. It may start suddenly or gradually. Acute onset of symptoms is seen with trauma, infections and crystal deposition disorders.
  • Progress – What has happened to the pain after it started? Has it increased, decreased or remain in the same intensity. Is it constant or intermittent? What is its present status?
  • Site – Ask the patient to pinpoint the site of pain with a single finger. Note down whether in the joint line medially or laterally, around the patella or popliteal fossa. Don’t use vague terms like pain in the hip. Remember that a patient with the hip disease may present with knee pain.
  • Severity – How disabling is the pain? What is its effect on routine activities, self-care, locomotion, occupation and recreational activities?
  • Character – What is the nature of pain? The throbbing pain is due to inflammatory causes, burning pain is due to neuropathic causes.
  • Radiation – Pain of the hip may radiate to the knee or thigh. Pain radiating below the knee is due to sciatica.
  • Aggravating and relieving factors- Mechanical pain due to osteoarthritis or impingement is aggravated by activity and relieved by rest. Pain due to inflammatory arthritis is aggravated by rest and partially relieved by activity.
  • Diurnal variation – Pain of osteoarthritis is more towards the evening and less when a patient gets up in the morning. The pain of inflammatory arthritis is more in the morning and less in the evening. Nocturnal pain that interferes with sleep is an ominous sign of malignancy or infection.

Deformity

  • How long the deformity is present?
  • How did it start?
  • How is it progressing?
  • Any associated symptoms such as giving way, locking, popping, catching, grinding?
  • Is there any history of trauma or infection?
  • Is there any history of patellar instability?

Limb length discrepancy

  • How long it is present?
  • Is it static or progressive?
  • Associated symptoms?
  • Any history of infection or trauma?

History to assess function

  • Walking ability
  • Normal or altered
  • Restricted or unrestricted
  • Aided or unaided
  • If aided; which aid is used
  • Ability to stand, squat and kneel
  • Ability to sit cross-legged
  • Ability to jog, sprint, go up or down the hill, go up or down the stairs
  • Pivoting and cutting ability
  • Ability to stand, squat and kneel

Fever

  • Whether associated with chills and rigour, severity continued or intermittent and the treatment is taken.

History of trauma

  • What was the mechanism of injury? Direct trauma
  • Whether the foot was grounded or not?
  • Any twisting or hyperextension of the knee?
  • What were the symptoms immediately after trauma?
  • Was the patient’s knee deformed?
  • Was there a loud pop?
  • Was he able to walk or use the limb?
  • Was there knee swelling? If yes when it appeared? Effusion of meniscus injury develops late.
  • What was the emergency treatment given?
  • How long the patient was immobilised or advised rest at that time?
  • Did the joint return to pre-injury status after initial treatment?
  • What are the present symptoms? Instability? Locking? Abnormal sounds? Pain? Deformity?
  • What brings the patient now? What does he want?

Past history

  • History of similar episodes in the past
  • Past injuries and their treatment
  • Hypertension
  • Diabetes mellitus
  • Inflammatory arthropathy
  • Septic arthritis
  • Tuberculosis
  • Umbilical sepsis
  • H/o prolonged IV infusion in childhood
  • Blood Dyscrasias
  • Frequent episodes of bleeding
  • Frequent episodes of infection
  • H/o Childhood limping
  • Previous hospital admission
  • Previous surgery
  • Previous trauma

Personal history

  • Prolonged drug intake
  • Alcohol abuse
  • Smoking
  • Diet
  • Menstrual history
  • Occupational history
  • Recreational activities
  • Treatment History
  • Family history
  • Any family history of dwarfism
  • Any family history of angular deformities
  • Metabolic disorders
  • Similar illness
  • Tuberculosis

GENERAL EXAMINATION

Head to foot examination

  • Eyes- Blue sclera, iritis, uveitis, squint, microphthalmos, cornea, pigmentation of the sclera.
  • Pinna- Low set, blackish discolouration.
  • Cheeks- Malar rash.
  • Mouth – Normal dental hygiene, arch of the palate.
  • Hair Line- Normal or low
  • Neck – Webbing, thyroid swelling.
  • Nipples- Normal level or not.
  • The shape of the chest wall- Pectus carinatum/ excavatum.
  • Abdomen- Protuberant , undescended testis , hernias.
  • Nails- Pitting.
  • Palms and soles- Hyperkeratosis.
  • Thickening of lower end radius, malleoli and costochondral junctions.
  • Ligamentous laxity (Wynne-Davis Criteria- 3 out of 5 needed for diagnosing generalized laxity)
  • Apposition of thumb to flexor aspect of the forearm?
  • Passive extension of fingers so that they lie parallel to the forearm.
  • Hyperextension of elbow at least 10 degrees
  • Hyperextension of knee at least 10 degrees
  • Excessive passive dorsiflexion of ankle (45 degrees) with eversion of the foot.
  • Neurocutaneous markers

INSPECTION

  • Watch how the patient walks into the examination room. Is the gait normal? Is it painful? Is any deformity or shortening? Is there any incoming?
  • Make the patient stand with his feet and knee together. Look for any varus or valgus deformity by observing the patient from the front. Observe from the side to identify any flexion deformity or hyperextension deformity. Look at the popliteal fossa from behind. Observe muscle bulk and symmetry especially of the quadriceps.
  • Make the patient sit on a chair with the knee bend to 90 degrees. Observe the position of the patella. In the normal, the anterior surface of the patella will be at an angle of 45 degrees to the floor and it will be placed centrally within the femoral trochlea. In patella Alta, it will be more horizontal and in patella infra, it will be more vertical.
  • Make the patient lie supine on a couch. Look suprapatellar and parapatellar fullness. Observe the position of the tibial tuberosity.
  • Look at the shape of the bones of the knee and the soft tissues to detect any swelling or muscle wasting.
  • Observe the medial and lateral surfaces of the knee from either side.
  • Make the patient prone and observe the back of the thigh, popliteal fossa and the calf.

PALPATION

  • First feel for elevated temperature with the dorsum of examiners fingers at the joint line, patella, suprapatellar pouch, femoral and tibial condyles, popliteal fossa and the calf. Many times it helps to pinpoint the area of pathology.
  • When palpating anatomic structures, feel for tenderness, break in continuity, swelling, thickening and their position in relation to normal location.
  • First, flex the knee to 90 degrees to locate the joint line. Palpate the joint line on the medial and lateral side, palpate the medial and lateral femoral condyles, then palpate the tibial condyles and the tibial tuberosity. From the tibial tuberosity palpate up the patellar tendon to the inferior pole of the patella. Extend the knee, displace the patella laterally and medially and then insinuate the examiner’s fingers to feel the undersurface of patella.
  • Palpate the superior border of patella and then roll the fingers superolaterally and superomedially to detect synovial thickening. Palpate the suprapatellar pouch for any synovial thickening and loose bodies. Milk the suprapatellar pouch down to evacuate the fluid to the area beneath the patella and do the Patellar tap test
  • Palpate down towards the tibia. Palpate the fibular head and the common peroneal nerve winding around it. Place the knee into the figure 4 position and feel the cord like fibular collateral ligament from the fibular head to the lateral epicondyle.
  • Make the patient prone, palpate the back of thigh, popliteal fossa and the calf. Palpate the hamstrings and feel for the popliteal pulse.

MOVEMENTS

  • Movements of the knee occur in the sagittal plane. Normal range of movements of the knee is from 5-10 degrees of hyperextension to 135 degree flexion. Movements should be assessed actively and passively and should be measured with a goniometer. During passive movements the amount of joint play and the quality of end point should be assessed. The end point may be of six types; tissue approximation, capsular feel spasm, springy block, empty feel or bone to bone.
  • If movement is painful then the relationship between the appearance of pain and the resistance to the movement should be noted. In acute conditions, the pain appears before resistance to movement. The appearance of pain and resistance to movement appear together in subacute conditions. Resistance to movement occurs before the appearance of pain in chronic conditions.

MEASUREMENTS

Q Angle

  • It is the angle between the axis of the pull of the quadriceps and the axis of the patellar tendon. Normally is 10-200. It should be measured in full extension, 300 flexions and in the sitting position with knee flexed to 900 (tubercle-sulcus angle). Mark the centres of the patella, tibial tuberosity and the anterior superior iliac spine (ASIS). Draw a line from the centre of ASIS through the centre of the patella and beyond. Draw another line from the centre of tibial tuberosity to the centre of the patella and beyond. Measure the angle between the lines.

Circumference

Measure the circumference at the following levels.

  • At the joint line
  • 2- 5 cm above the joint line to assess effusion or vastus medialis obliquus wasting=
  • 3- 15 cm above the joint line to assess quadriceps bulk
  • 4- 15 cm below the joint line to assess the calf muscle bulk

SPECIAL TESTS

Special tests are done to detect specific disorders or to detect injury to specific anatomic structures. Four sets of tests are usually done; one set each for evaluation of knee joint effusion, patellofemoral disorders, meniscus or articular cartilage lesions and ligamentous instability.

Special tests to detect knee effusion

Patellar tap test

  • Patient position – Supine.
  • Joint position – Knee maximally extended. Quadriceps relaxed.
  • Procedure – Milk the suprapatellar pouch to displace the fluid collected there into the retropatellar area. Sharply tap the patella posteriorly towards the femoral trochlea.
  • Interpretation – If there is moderate effusion the patella will be floating with no contact with the femur. When tapped it will move posteriorly till it contacts the femur and bounces back. It needs about 50 ml of fluid within the joint to make the patellar tap test positive.

Fluctuation test

  • Patient position- Supine.
  • Joint position- Knee maximally extended. Quadriceps relaxed.
  • Procedure- Milk the suprapatellar fossa to displace the maximal amount of fluid into the rest of the joint cavity. Place index finger and thumb of one hand on either side of patella superiorly. Place the index finger and thumb of another hand on either side of the patella inferiorly. Alternatively, press the fingers of either hand to elicit fluctuation.
  • Interpretation- In presence of effusion, fluctuation can be elicited between the fingers.

Stroke test

  • Patient position- Standing.
  • Joint position- Knee fully extended. Quadriceps relaxed.
  • Procedure- Gently stroke the lateral aspect of the knee from the superolateral aspect of the patella to the lateral joint line. Observe the medial side for a wave-like displacement of fluid. Repeat the same on the medial side.
  • Interpretation- Will be positive in presence of effusion. Effusion is graded as follows.
  • Zero – No wave produced on downstroke
  • Trace – Small wave on the medial side with a downstroke
  • 1+ – Larger bulge on the medial side with dowstroke\2+ – Effusion spontaneously returns to the medial side after upstroke (no downstroke necessary)\3+ – So much fluid that it is not possible to move the effusion out of the medial aspect of the knee

Special tests for patellofemoral disorders

Fairbank Apprehension Test

  • Patient position- Supine on the examination couch.
  • Joint position- Knee extended. Quadriceps relaxed.
  • Procedure- Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to displace the patella. Note the response of the patient.\
  • Interpretation- Discomfort or apprehension during the test indicates patellar instability.

Patellar glide test

  • Patient position – Supine on the examination couch
  • Joint position – Knee flexed to 300. Quadriceps relaxed.
  • Procedure – Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to displace the patella medially and laterally. Note the amount of displacement possible as the percentage patellar width or in millimetres.
  • Interpretation – If the medial glide is less than 25% or <5mm, then there is tightness of the lateral patellar retinaculum. If the medial or lateral glide is more than 75%, then there is a laxity of the parapatellar retinaculum. Discomfort or apprehension during the test indicates patellar instability.

Patellar tilt test

  • Patient position- Supine on the examination couch
  • Joint position- Knee kept in extension. Quadriceps relaxed.
  • Procedure- Hold the patella by placing the examiner’s fingers on the medial and lateral border of the patella. Try to lift the medial border of the patella off the femur while depressing the lateral border and vice versa. Note the amount of tilt possible.
  • Interpretation- Normally lateral border can be tilted slightly beyond the horizontal. If the lateral border can be tilted less than normal then there is tightness of the lateral patellar retinaculum. If the medial border can be tilted more if there is laxity of the medial patella retinaculum.

Clarke’s patellar grind test

  • Patient position- Supine on the examination couch
  • Joint position- Knee extended. Quadriceps relaxed.
  • Procedure- Examiner places his hand on the patella and compresses the patella against the femur. Ask the patient to contract his quadriceps muscle actively.
  • Interpretation- Pain indicates disease of the articular cartilage of the patella.

McConnell’s test

  • Patient position- Seated on the couch with legs hanging down the edge of the table.
  • Joint position- Knee bend to 90 degrees.
  • Procedure- Ask the patient to externally rotate the limb while performing resisted isometric contractions of the quadriceps at 0, 30, 600, 90 and 120 degrees. During these resisted isometric quadriceps contractions, apply a medially directed pressure and laterally directed pressure on the patella.
  • Interpretation- Pain or discomfort during isometric contractions when applying laterally directed pressure indicates symptoms due to patellar maltracking.

Patellar tracking

  • Patient position- Seated with the knee flexed and limb hanging freely
  • Procedure- Ask the patient to move the knee joint actively through the entire arc of flexion extension several times. Observe the movement of the patella.
  • Interpretation- Normally the patella progressively becomes engaged in the trochlea with increasing degrees of knee flexion. Patella is pulled axially by the rectus femoris and the vastus intermedius and obliquely by the vastus lateralis and the vastus medialis. Static stabilization is provided by the medial and lateral parapatellar retinaculum. The shape of the trochlea and the position of the patella and the location of tibial tuberosity also influence patellar tracking. J sign is seen if the patella was laterally subluxated in full extension and suddenly moves medially and engages the trochlea during flexion.

Special tests for meniscus pathology

McMurray’s test

  • Patient position- supine on the examination couch.
  • Joint position- Knee flexed fully. Quadriceps relaxed. Procedure- Hold the foot of the patient with one hand. On the other hand, stabilize the knee and keep one finger on the joint line. To test for medial meniscus, apply valgus and external rotation stress on the knee. Gradually extend the knee fully. To test lateral meniscus, apply a varus and internal rotation stress.
  • Interpretation- If clicks or thud from the joint, or if the patient complains of pain then the test is positive for the meniscus injury.

Bragard’s test

  • Patient position – supine on the examination couch
  • Joint position – Knee flexed to 90 degrees.
  • Procedure – Palpate the medial joint line for tenderness in neutral rotation. Extend the knee and externally rotate the knee and palpate for medial joint line tenderness. Interpretation- If there is no tenderness in flexion and neutral rotation and if there is tenderness in the medial joint line on extension and external rotation, the test is positive for the medial meniscus injury. The reason is that the medial meniscus becomes more anterior in extension and external rotation.

Steinman’s first test

  • Patient position – Supine
  • Joint position – Hip flexed. Knee flexed to 90.
  • Procedure – Rotate the tibia externally and internally. Interpretation- Pain on external rotation indicate medial meniscus injury and pain on external rotation indicate lateral meniscus injury.

Bounce home test

  • Patient position – Supine.
  • Joint position – Knee fully flexed.
  • Procedure – Keep the heel of the patient’s foot in the palm and allow the knee to extend.
  • Interpretation – Normally the knee will extend fully. Limitation of full extension with a rubbery end feel is suggestive of a locked knee due to bucket handle tear of the meniscus.

Steinman’s second test

  • Patient position – supine on the examination couch.
  • Joint position – Knee flexed fully.
  • Procedure – Palpate the joint line for tenderness with the knee in flexion and in extension.
  • Interpretation – If the area of tenderness moves posteriorly with knee flexion and anteriorly with knee extension then the test is positive for the meniscus Injury.

Apley’s grinding test

  • Patient position – Prone
  • Joint position – Knee flexed to 90 degrees.
  • Procedure – Fix the limb by placing the knee of the examiner on the patient’s thigh. Hold the foot of the patient. Distract the knee and rotate internally and externally. Give axial compression and rotate internally and externally. Note any restriction or excessive rotation and pain during these manoeuvres.
  • Interpretation – More pain during compression indicate meniscus injury and more pain during distraction indicate ligamentous injury.

Bohler’s test

  • Patient position – supine on the examination couch.
  • Joint position – Knee extended.
  • Procedure – Apply valgus stress and varus stress.
  • Interpretation – Pain felt at the medial joint line on varus stress indicate medial meniscus injury and pain felt at the lateral joint line on valgus stress indicate lateral meniscus injury.

Thessaly test

  • Patient position – Standing on the affected limb. Another limb is off the ground. The examiner supports the patient by holding extended hands.
  • Joint position – Knee flexed to 5 degrees and then to 20 degrees.
  • Procedure – Ask the patient to twist the body to the left and the right side to rotate the weight-bearing knee internally and externally.
  • Interpretation – Pain felt at the joint line indicate meniscus or chondral lesion.
  • Reliability of Thessaly test – Sensitivity of 90.3%, specificity of 97.7%, the positive predictive value of 98.5%, the negative predictive value of 86.0%, the likelihood ratio for a positive test of 39.3, likelihood ratio for a negative test of 0.09, and diagnostic accuracy of 88.8%.
  • Harrison BK, Abell BE, Gibson TW – The Thessaly test for detection of meniscal tears: validation of a new physical examination technique for primary care medicine. Clin J Sports Med.  2009 Jan;19(1):9-12. doi: 10.1097/JSM.0b013e31818f1689.

Squat test (Ege’s test)

  • Patient position – Standing on both lower limbs.
  • Joint position – Hip and knee extended.
  • Procedure – Ask the patient to squat first with the foot turned in internal rotation and then in external rotation.
  • Interpretation – Pain on squatting with the foot externally rotated indicate medial meniscus lesion and pain with a foot in internal rotation indicate lateral meniscus lesion.

Duck walking test (Childress test)

  • Patient position – Sitting in the deep squatting position.
  • Joint position – Hip and knee in maximum flexion.
  • Procedure – Ask the patient to duck walk in deep knee flexion.
  • Interpretation – Pain felt at the joint line suggestive of meniscus lesion.

Merkel’s test

  • Patient position – Standing on the affected lower limb with the other limb off the ground.
  • Joint position – Knee in extension.
  • Procedure – Ask the patient to slightly bend the knee and then rotate the body to the left and right.
  • Interpretation – Pain felt at the joint line indicate meniscus pathology.

Peyer’s test

  • Patient position – Sitting in the cross-legged sitting position (Turkish or Indian sitting position)
  • Joint position – Hip in flexion and external rotation. Knee fully flexed.
  • Procedure – Ask the patient to sit in the Turkish sitting position.
  • Interpretation – Pain on the medial aspect of the knee indicate medial meniscus lesion.

Helfet’s test

  • Patient position – Seated on the couch with a limb hanging over the edge of the couch.
  • Joint position – Knee flexed to 90 degrees.
  • Procedure – Ask the patient to extend the knee. Note the position of the tibial tuberosity in relation to the midline of the patella.
  • Interpretation – During extension, the tibia externally rotates during the final degrees of knee extension as the medial femoral condylar articular surface is longer than the lateral femoral condyle. Hence the tibial tuberosity becomes more laterally placed in full extension. If the normal external rotation is absent it indicates injury to the medial meniscus.

Tests for ligamentous instability

Valgus stress test

  • Purpose – To assess the structural integrity of the medial collateral ligament.
  • Patient position – supine on the examination couch.
  • Joint position – Initially the knee is flexed to 30 degrees. Then the knee is kept in 0-degree extension.
  • Procedure – Hold the leg with one hand at the ankle. With the other hand hold the knee in such a way that the thumb is over the medial joint line to detect the amount of opening of the joint and the other fingers are on the lateral side to act as the fulcrum for the application of valgus stress. Bend the knee to 30 degrees and apply valgus stress. Note the amount of widening of the medial joint line. Repeat the test at 0-degree extension. Do the test on the other limb and compare the amount of widening.
  • Interpretation – If there is widening of the medial joint space in excess to the normal side in 30-degree flexion of the knee there is an injury to the medial collateral ligament. If there is excessive opening up of medial joint space in 0 extensions as well as in 30-degree flexion, then there is an injury to the MCL and the cruciate ligaments. The laxity is graded as follows. 0-5mm opening in comparison to the opposite side. 5-10mm opening >10mm opening

Varus stress test

  • Purpose – To assess the structural integrity of the fibular collateral ligament.
  • Patient position – supine on the examination couch.
  • Joint position – Initially the knee is flexed to 30flexion. Then the knee is kept in 0-degree extension.
  • Procedure – Bring the lower limb of the patient beyond the edge of the table. Hold the leg with one hand at the ankle. With the other hand hold the knee in such a way that the thumb is over the lateral joint line to detect the amount of opening of the joint and the other fingers are on the medial side to act as the fulcrum for the application of varus stress. Bend the knee to 30 degrees and apply varus stress. Note the amount of widening of the lateral joint line. Repeat the test at 0-degree extension. Do the test on the other limb and compare the amount of widening.
  • Interpretation – If there is widening of the lateral joint space in excess to the normal side in 30-degree flexion of the knee there is an injury to the lateral collateral ligament. If there is the excessive opening up of lateral joint space in 0-degree extension then there is an injury to the LCL and the cruciate ligaments. The laxity is graded as follows.
  • 0-5mm opening in comparison to the opposite side.
  • 5-10mm opening
  • >10mm opening

Cabot manoeuvre

  • Patient position – Supine.
  • Joint position – Knee kept in figure of 4 position.
  • Procedure – Feel the lateral collateral ligament as a cord-like structure between the lateral epicondyle and fibular head.
  • Interpretation – Inability to feel the lateral collateral ligament as a cord-like structure indicate injury.

Lachmann- Tillat test

  • Patient position – Supine
  • Joint position – Knee flexed to 15 degrees. Slight external rotation of the hip helps in relaxing the quadriceps muscle.
  • Procedure – Stabilize the distal femur with one hand and stabilize the proximal tibia with the other hand. If the patient’s thigh is of large size, then the examiner places his bend knee under the patient’s thigh and one hand over the distal femur to stabilize the knee. Apply anteriorly directed and then posteriorly directed force on the proximal tibia.
  • Interpretation – Excessive anterior translation of tibia when compared to the opposite side with a soft endpoint is suggestive of anterior cruciate ligament injury. Excessive posterior translation of tibia, when compared to the opposite side with a soft endpoint, is suggestive of posterior cruciate ligament injury.
  • Validity – Sensitivity ranges from 80-99%. Specificity under anaesthesia is 95%.

Anterior drawer test

  • Patient position – Supine.
  • Joint position – Hip flexed to 45° and knee flexed to 90°.
  • Procedure – Sit on the patient’s foot in neutral rotation to stabilize it. Palpate the hamstring tendons to ensure that they are relaxed. Observe from the side to rule out any posterior sagging of tibia suggestive of posterior cruciate ligament tear. Place the hands behind the proximal tibia and thumbs on either side of the patellar tendon with the tip of the thumb over the femoral condyles. Apply an anteriorly directed force to the proximal tibia. Should be done in neutral rotation, 30-degree internal rotation and 30-degree external rotation.
  • Interpretation – Increased anterior displacement of tibia when compared with the opposite side is indicative of an anterior cruciate ligament tear. It may be falsely negative in patients with bucket handle meniscus tear with locking. External rotation tightens the PCL and the posterolateral corner and if they are intact the test is negative in external rotation.
  • Validity – Sensitivity increases when performed under anaesthesia. Sensitivity is less in acute injuries. The sensitivity of the test is between 20-40% in acute cases and between 40-70% in chronic cases. The sensitivity of the test is between 60-95% when examined under anaesthesia.

Posterior drawer test

  • Patient position – Supine.
  • Joint position – Hip flexed to 45° and knee flexed to 90°.
  • Procedure – Examiner sits on the subject’s foot in neutral rotation to stabilize it. Palpate the hamstring tendons to ensure that they are relaxed. Place the hands around the proximal tibia and thumbs on the tibial tuberosity. Apply a posteriorly directed force to the proximal tibia.
  • Interpretation – Increased posterior tibial displacement compared with the opposite side is indicative of posterior cruciate ligament tear.
  • Validity-

External rotation recurvatum test

Sag test

  • Patient position – Supine.
  • Joint position – Hip flexed to 45° and knee flexed to 90°. Stabilise the foot in neutral rotation.
  • Procedure – Observe the position of the tibia in relation to the femoral condyles. Normally the tibial tuberosity lies one centimetre anterior to the femoral condyles resulting in a step-off.
  • Interpretation – When the posterior cruciate ligament is torn, the tibia is subluxated posteriorly due to the effect of gravity.
  • Validity-

Godfrey’s test

  • Patient position – Supine.
  • Joint position – Hip flexed to 90° and knee flexed to 90°. Stabilise the foot in neutral rotation. Ask the patient to extend the knee.
  • Procedure – Observe the position of the tibia in relation to the femoral condyles. Normally the tibial tuberosity lies one centimetre anterior to the femoral condyles resulting in a step-off.
  • Interpretation – When the posterior cruciate ligament is torn, the tibia is subluxated posteriorly due to the effect of gravity. The active contraction of the quadriceps leads to the reduction of gravity-induced posterior subluxation of tibial condyles.

Quadriceps active test

  • Knee flexed to 150 ask the patient to contract the quadriceps keeping the knee in flexion.

Actively resisted extension test

  • Keep the knee in 150 flexions. Ask the patient to extend the knee against resistance.

Patellar reflex reduction test

  • Keep the knee in 300 flexions. Elicit patellar tendon reflex. Active quadriceps contraction leads to correction of posterior sag.

McIntosh’s Pivot shift test

  • Patient position – Supine
  • Joint position – Knee extended.
  • Procedure – Examiner lifts up the patient’s leg with the knee in extension by holding at the ankle with one hand. Apply an internal rotation force. On the other hand, support the limb with the palm over the posterolateral aspect of the knee close to the fibular head. Apply a strong valgus force and flex the knee.
  • Interpretation – Pivot shift is anterior subluxation of lateral tibial condyle when the knee is extended and the reduction of subluxation when the knee is flexed. Internal rotation exaggerates the subluxation and the valgus force prevents easy reduction of subluxation. When the knee is flexed with valgus force initially the lateral tibial condyle remains subdued and suddenly gets reduced beyond 30-degree flexion with a demonstrable thud. When the knee is flexed the iliotibial band passes posterior to the centre of rotation of the knee exerting a posterior pull reducing the anterior subluxation of the lateral tibial condyle.

Noye’s flexion rotation drawer test

Noyes glide pivot shift test

  • Pivot shift test is done with axial compression and without internal rotation.

Hughston’s jerk test

  • Pivot shift demonstrated from flexion to extension. It demonstrates the subluxation of the lateral tibial condyle anteriorly during extension. It is done with valgus stress and internal rotation while the knee is moved from flexion to extension.

Losee’s test

Slocum’s Anterolateral Rotary Instability (ALRI) Test /Larson’s test

  • Patient position – patient lies in the lateral position with the affected limb up. The pelvis is tilted slightly posteriorly. The affected limb rests with only the heel in contact with the examination couch with the knee in extension. This will exert internal rotation stress on the knee leading to anterior subluxation of the lateral condyle of the tibia.
  • Joint position – Knee in extension.\
  • Procedure – Lift up the limb by holding the ankle with one hand to apply valgus stress on the knee. Keep the other hand on the joint line. Flex the knee.
  • Interpretation – If there is rotatory instability due to ACL deficiency, the knee can be felt to reduce at about 400 of flexion.

Reverse pivot shift test

  • Patient position – Supine
  • Joint position – Knee flexed.
  • Procedure – Examiner lifts up the patient’s leg with the knee in flexion by holding at the ankle with one hand. Apply an external rotation force. On the other hand, support the limb with the palm over the lateral aspect of the knee. Apply a strong valgus force and extend the knee.
  • Interpretation – Reverse pivot shift is posterior subluxation of lateral tibial condyle when the knee is flexed and the reduction of subluxation when the knee is extended. External rotation exaggerates the subluxation and the valgus force prevents easy reduction of subluxation. When the knee is extended with valgus force, initially the lateral tibial condyle remains subdued and then suddenly gets reduced with extension with a demonstrable thud.

Tests for posterolateral corner injuries

Tibial external rotation test (Dial test)

  • Patient position- Prone.
  • Knee tested in 30-degree flexion and 90-degree flexion
  • Procedure- Hold the foot and externally rotate the knee on both sides. Compare the amount of external rotation present on both sides.
  • Interpretation- If the amount of external rotation on the affected side exceeds the other side by more than 10 degrees then there is PLC injury.

External rotation recurvatum test

  • Patient position – Supine.
  • Joint position – Knee in full extension
  • Procedure – Examiner stands at the foot end of the examination couch. The limb is lifted up by holding the big toe which hill exert varus-external rotation-extension stress on the knee. Assess the amount of hyperextension, external rotation and varus that is present on both limbs.
  • Interpretation – In patients with PLC injury, the affected knee goes into excessive varus hyperextension and external rotation in comparison to the opposite side.

Posterolateral external rotation drawer test

  • Patient position – Supine.
  • The hip flexed to 45 degrees and the knee is flexed to 90 degrees.
  • Externally rotate the foot and fix it by sitting over it while the hip flexed to 45 degrees and the knee is flexed to 90 degrees. Do a posterior drawer test. Repeat at 30-degree flexion of the knee. Look for posterior subluxation of lateral tibial condyle.\Interpretation- If there is posterior subluxation of lateral tibial condyle when the test was done at 300 knee flexion and is absent at 900 flexions, then there is isolated PLC injury.

Posteromedial rotational instability test

Motion

Assessment of effusion

The absence of normal grooves around the patella may indicate a patellar intra-articular effusion. There are two ways to confirm the effusion. The knee is extended fully before the examination begins. This first way is the patellar tap. It is to squeeze the fluid between the patella and the femur by pressing at the medial patella using a non-dominant hand. Then, using the dominant hand to press on the patella vertically. If the patella is ballotable, then patellar intra-articular effusion is present. Another way is the milking of the patella. First, the effusion is milked at the medial border of the patella from the inferior to superior aspect. Then, using another hand, the effusion is milked at the lateral border of the patella from superior to inferior aspect. If the effusion is present, a bulge will be appearing at the medial border of the patella because the effusion is milked back to the medial patella.[rx]

Assessment of range of motion

Both the active and passive range of motion should be assessed. The normal knee extension is between 0 to 10 degrees. The normal knee flexion is between 130 to 150 degrees. Any pain, abnormal movement, or crepitus of the patella should be noted. If there is pain or crepitus during active extension of the knee, while the patella is being compressed against the patellofemoral groove, patellofemoral pain syndrome or chondromalacia patellae should be suspected. Pain with active range of motion but no pain during passive range of motion is suggestive of inflammation of the tendon. Pain during active and passive range of motion is suggestive of pathology in the knee joint.[rx]

Assessment of collateral ligaments

Valgus stress test can be performed with the examined knee in 25 degrees flexion to determine the integrity of the medial collateral ligament. Similarly, varus stress test can be performed to access the integrity of the lateral collateral ligament. The degree of collateral ligament sprain can also be assessed during the valgus and varus tests. In a first degree tear, the ligament has less than 5 mm laxity with a definite resistance when the knee is pulled. In a second degree sprain, there is laxity when the knee is tested at 25 degrees of flexion, but no laxity at extension with a definite resistance when the knee is pulled. In a third-degree tear, there will be 10 mm laxity with no definite resistance either with knee with full extension or flexion.[rx]

Assessment of anterior cruciate ligament

The anterior drawer and Lachman tests can be used to access the integrity of the anterior cruciate ligament. In the anterior drawer test, the person being examined should lie down on their back (supine position) with the knee in 90 degrees flexion. The foot is secured on the bed with the examiner sitting on the foot. The tibia is then pulled forward by using both hands. If the anterior movement of the affected knee is greater than the unaffected knee, then the anterior drawer test is positive. The Lachman test is more sensitive than the anterior drawer test. For the Lachman test, the person lies down in a supine position with the knee flexed at 20 degrees and the heel touching the bed. The tibia is then pulled forward. If there are 6 to 8 millimetres of laxity, with no definitive resistance when the knee is pulled, then the test is positive thus raising concern for a torn anterior cruciate ligament. A large collection of blood in the knee can be associated with bony fractures and cruciate ligament tear.[rx]

Assessment of posterior cruciate ligament

Posterior drawer test and tibial sag tests can determine the integrity of the posterior cruciate ligament. Similar to the anterior drawer test, the knee should be flexed 90 degrees and the tibia is pushed backwards. If the tibia can be pushed posteriorly, then the posterior drawer test is positive. In the tibial sag test, both knees are flexed at 90 degrees with the person in the supine position and bilateral feet touching the bed. Bilateral knees are then watched for the posterior displacement of the tibia. If the affected tibia slowly displaced posteriorly, the posterior cruciate ligament is affected.[rx]

Assessment of meniscus

Those with meniscal injuries may report symptoms such as clicking, catching, or locking of knees. Apart from joint line tenderness, there are three other methods of accessing meniscus tear: the McMurray test, the Thessaly test, and the Apley grind test. In the McMurray test, the person should lie down in a supine position with the knee should in 90 degrees flexion. the examiner put one hand with the thumb and the index finger on the medial and lateral joint lines respectively. Another hand is used to control the heel. To test the medial meniscus, the hand at the heel applies a valgus force and externally rotate the leg while extending the knee. To test for the lateral meniscus, the varus force, internal rotation are applied to the leg while extending the knee. Any clicking, popping, or catching at the respective joint line indicates the corresponding meniscal tear.[rx]

In the Apley compression test, the person lie down in a prone position with the knee flexed at 90 degrees. One hand is used to stabilise the hip and another hand grasp the foot and apply a downward compression force while external and internal rotates the leg. Pain during compression indicates meniscal tear. Examination for anterior cruciate ligament tear should be done for those with meniscal tear because these two conditions often occur together.[rx]

References

Lipoprotein – Types and Functions

lipoprotein is a biochemical assembly whose primary function is to transport hydrophobic lipid (also known as fat) molecules in water, as in blood plasma or other extracellular fluids. They consist of a Triglyceride and Cholesterol center, surrounded by a phospholipid outer shell, with the hydrophilic portions oriented outward toward the surrounding water and lipophilic portions oriented inward toward the lipid center. A special kind of protein, called apolipoprotein, is embedded in the outer shell, both stabilizing the complex and giving it a functional identity that determines its fate.

Lipoproteins are complex particles that have a central hydrophobic core of non-polar lipids, primarily cholesterol esters, and triglycerides. This hydrophobic core is surrounded by a hydrophilic membrane consisting of phospholipids, free cholesterol, and apolipoproteins. Plasma lipoproteins are divided into seven classes based on size, lipid composition, and apolipoproteins.

Lipoprotein any member of a group of substances containing both lipid (fat) and protein. They occur in both soluble complexes as in egg yolk and mammalian blood plasma and insoluble ones, as in cell membranes. Lipoproteins in blood plasma have been intensively studied because they are the mode of transport for cholesterol through the bloodstream and lymphatic fluid.

Types of Lipoprotein

  • Chylomicrons – These are large triglyceride-rich particles made by the intestine, which are involved in the transport of dietary triglycerides and cholesterol to peripheral tissues and the liver. These particles contain apolipoproteins A-I, A-II, A-IV, A-V, B-48, C-II, C-III, and E. Apo B-48 is the core structural protein and each chylomicron particle contains one Apo B-48 molecule. The size of chylomicrons varies depending on the amount of fat ingested. A high-fat meal leads to the formation of large chylomicron particles due to the increased amount of triglyceride being transported whereas in the fasting state the chylomicron particles are small carrying decreased quantities of triglyceride.
  • Chylomicron remnants – The removal of triglyceride from chylomicrons by peripheral tissues results in smaller particles called chylomicron remnants. Compared to chylomicrons these particles are enriched in cholesterol and are pro-atherogenic.
  • Very low-density lipoproteins (VLDL) – These particles are produced by the liver and are triglyceride-rich. They contain apolipoprotein B-100, C-I, C-II, C-III, and E. Apo B-100 is the core structural protein and each VLDL particle contains one Apo B-100 molecule. Similar to chylomicrons the size of the VLDL particles can vary depending on the quantity of triglyceride carried in the particle. When triglyceride production in the liver is increased, the secreted VLDL particles are large. However, VLDL particles are smaller than chylomicrons.
  • Intermediate density lipoproteins (IDL; VLDL remnants) – The removal of triglycerides from VLDL by muscle and adipose tissue results in the formation of IDL particles which are enriched in cholesterol. These particles contain apolipoprotein B-100 and E. These IDL particles are pro-atherogenic.
  • Low-density lipoproteins (LDL) – These particles are derived from VLDL and IDL particles and they are even further enriched in cholesterol. LDL carries the majority of the cholesterol that is in the circulation. The predominant apolipoprotein is B-100 and each LDL particle contains one Apo B-100 molecule. LDL consists of a spectrum of particles varying in size and density. An abundance of small dense LDL particles are seen in association with hypertriglyceridemia, low HDL levels, obesity, type 2 diabetes (i.e. patients with metabolic syndrome), and infectious and inflammatory states. These small dense LDL particles are considered to be more pro-atherogenic than large LDL particles for a number of reasons. Small dense LDL particles have a decreased affinity for the LDL receptor resulting in a prolonged retention time in the circulation. Additionally, they more easily enter the arterial wall and bind more avidly to intra-arterial proteoglycans, which traps them in the arterial wall. Finally, small dense LDL particles are more susceptible to oxidation, which could result in an enhanced uptake by macrophages.
  • High-density lipoproteins (HDL) – These particles play an important role in reverse cholesterol transport from peripheral tissues to the liver, which is one potential mechanism by which HDL may be anti-atherogenic. In addition, HDL particles have anti-oxidant, anti-inflammatory, anti-thrombotic, and anti-apoptotic properties, which may also contribute to their ability to inhibit atherosclerosis. HDL particles are enriched in cholesterol and phospholipids. Apolipoproteins A-I, A-II, A-IV, C-I, C-II, C-III, and E are associated with these particles. Apo A-I is the core structural protein and each HDL particle may contain multiple Apo A-I molecules. HDL particles are very heterogeneous and can be classified based on density, size, charge, or apolipoprotein composition.

 Lipoprotein

Lipoprotein Density (g/ml) Size (nm) Major Lipids Major Apoproteins
Chylomicrons <0.930 75-1200 Triglycerides Apo B-48, Apo C, Apo E, Apo A-I, A-II, A-IV
Chylomicron Remnants 0.930- 1.006 30-80 Triglycerides Cholesterol Apo B-48, Apo E
VLDL 0.930- 1.006 30-80 Triglycerides Apo B-100, Apo E, Apo C
IDL 1.006- 1.019 25-35 Triglycerides Cholesterol Apo B-100, Apo E, Apo C
LDL 1.019- 1.063 18- 25 Cholesterol Apo B-100
HDL 1.063- 1.210 5- 12 Cholesterol Phospholipids Apo A-I, Apo A-II, Apo C, Apo E
Lp (a) 1.055- 1.085 ~30 Cholesterol Apo B-100, Apo (a)

Basic Characteristics of Lipoproteins

Types of Lipoprotein Density (g/mL) Primary Components Diameter (µm)
Chylomicrons &lt;0.95 Dietary triacylglycerols (90%) and cholesterol 75–1200
Very-low-density lipoprotein 0.95–1.006 Endogenous triacylglycerols and cholesterol 30–80
Intermediate-density lipoproteins 1.006–1.019 Triacylglycerols and cholesterol 25
Low-density lipoproteins 1.019–1.063 Cholesterol 18–25
High-density lipoproteins 1.063–1.210 Phospholipid and protein 5–12

Functions of Lipoprotein

Lipids are one of the four main biological molecules of the human body, along with carbohydrates, proteins, and nucleic acids.

  • Lipids are essential components of life on a cellular level, as they are involved in multiple processes such as storing energy, serving as chemical messengers, and forming cell membranes, and transporting fat-soluble vitamins such as VitaminE.
  • For lipids to carry out these roles in the cell, however, they must travel to their destination cells after being absorbed in the gastrointestinal tract. Without lipoproteins, this transport would not be possible, as the hydrophilic environment of the blood is not compatible with the hydrophobic nature of lipids like cholesterol.
  • Therefore, lipoproteins play an integral role in the ability of the human body to utilize lipids, and the metabolism of these lipoproteins has a direct effect on the level of lipids in the serum and on the subsequent processes that involve lipids within the cell.
  • The handling of lipoprotein particles in the body is referred to as lipoprotein particle metabolism. It is divided into two pathways, exogenous and endogenous, depending in large part on whether the lipoprotein particles in question are composed chiefly of dietary (exogenous) lipids or whether they originated in the liver (endogenous), through de novo synthesis of triacylglycerols.
  • The hepatocytes are the main platform for the handling of triacylglycerols and cholesterol; the liver can also store certain amounts of glycogen and triacylglycerols. While adipocytes are the main storage cells for triacylglycerols, they do not produce any lipoproteins.
  • Bile emulsifies fats contained in the chyme, then pancreatic lipase cleaves triacylglycerol molecules into two fatty acids and one 2-monoacylglycerol. Enterocytes readily absorb the small molecules from the chymus. Inside of the enterocytes, fatty acids and monoacylglycerides are transformed again into triacylglycerides. Then these lipids are assembled with apolipoprotein B-48 into nascent chylomicrons. These particles are then secreted into the lacteals in a process that depends heavily on apolipoprotein B-48. As they circulate through the lymphatic vessels, nascent chylomicrons bypass the liver circulation and are drained via the thoracic duct into the bloodstream.
  • In the bloodstream, nascent chylomicron particles interact with HDL particles, resulting in HDL donation of apolipoprotein C-II and apolipoprotein E to the nascent chylomicron. The chylomicron at this stage is then considered mature. Via apolipoprotein C-II, mature chylomicrons activate lipoprotein lipase (LPL), an enzyme on endothelial cells lining the blood vessels. LPL catalyzes the hydrolysis of triacylglycerol that ultimately releases glycerol and fatty acids from the chylomicrons. Glycerol and fatty acids can then be absorbed in peripheral tissues, especially adipose and muscle, for energy and storage.

APOLIPOPROTEINS

Apolipoproteins have four major functions including 1) serving a structural role, 2) acting as ligands for lipoprotein receptors, 3) guiding the formation of lipoproteins, and 4) serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins (Table 3). Apolipoproteins thus play a crucial role in lipoprotein metabolism.

  • Apolipoprotein A-I – Apo A-I is synthesized in the liver and intestine and is the major structural protein of HDL accounting for approximately 70% of HDL protein. It also plays a role in the interaction of HDL with ATP-binding cassette protein A1 (ABCA1), ABCG1, and class B, type I scavenger receptor (SR-B1). Apo A-I is an activator of lecithin: cholesterol acyltransferase (LCAT), an enzyme that converts free cholesterol into cholesteryl ester.
  • Apolipoprotein A-II – Apo A-II is synthesized in the liver and is the second most abundant protein on HDL accounting for approximately 20% of HDL protein.
  • Apolipoprotein A-IV (2) – Apo A-IV is synthesized in the intestine during fat absorption. Apo A-IV is associated with chylomicrons and high-density lipoproteins but is also found in the lipoprotein-free fraction. Its precise role in lipoprotein metabolism remains to be determined but studies have suggested a role for Apo A-IV in regulating food intake.
  • Apolipoprotein A-V (3) – Apo A-V is synthesized in the liver and associates with triglyceride-rich lipoproteins. It is an activator of LPL mediated lipolysis and thereby plays an important role in the metabolism of triglyceride-rich lipoproteins.
  • Apolipoprotein B-48 – Apo B-48 is synthesized in the intestine and is the major structural protein of chylomicrons and chylomicron remnants. There is a single molecule of apo B-48 per chylomicron particle. There is a single apolipoprotein B gene that is expressed in both the liver and intestine. The intestine expresses a protein that is approximately ½ the size of the liver due to mRNA editing. The aerobic-1 editing complex is expressed in the intestine and edits a specific cytidine to a uracil in the apo B mRNA in the intestine creating a stop codon that results in the cessation of protein translation and a shorter Apo B (Apo B-48). Notably, Apo B-48 is not recognized by the LDL receptor.
  • Apolipoprotein B-100 – Apo B-100 is synthesized in the liver and is the major structural component of VLDL, IDL, and LDL. There is a single molecule of Apo B-100 per VLDL, IDL, and LDL particle. Apo B-100 is a ligand for the LDL receptor and therefore plays an important role in the clearance of lipoprotein particles.
  • Apolipoprotein C – The C apolipoproteins are synthesized primarily in the liver and freely exchange between lipoprotein particles and therefore are found in association with chylomicrons, VLDL, and HDL.
  • Apo C-II – is a co-factor for lipoprotein lipase (LPL) and thus stimulates triglyceride hydrolysis (4). Loss of function mutations in Apo C-II results in marked hypertriglyceridemia due to a failure to metabolize triglyceride-rich lipoproteins.
  • Apo C-III is an inhibitor of LPL (5) – Additionally, Apo C-III inhibits the interaction of triglyceride-rich lipoproteins with their receptors. Recent studies have shown that loss of function mutations in Apo C-III lead to decreases in serum triglyceride levels and a reduced risk of cardiovascular disease. Interestingly, inhibition of Apo C-III expression results in a decrease in serum triglyceride levels even in patients deficient in lipoprotein lipase indicating that the ability of Apo C-III to modulate serum triglyceride levels is not dependent solely on regulating lipoprotein lipase activity.
  • Apolipoprotein E (6) – Apolipoprotein E is synthesized in many tissues but the liver and intestine are the primary sources of circulating Apo E. Apo E exchanges between lipoprotein particles and is associated with chylomicrons, chylomicron remnants, VLDL, IDL, and a subgroup of HDL particles. There are three common genetic variants of Apo E (Apo E2, E3, and E4). ApoE2 differs from the most common isoform, Apo E3, by a single amino acid substitution where cysteine substitutes for arginine at residue 158. Apo E4 differs from Apo E3 at residue 112, where arginine substitutes for cysteine. Apo E3 and E4 are ligands for the LDL receptor while Apo E2 is poorly recognized by the LDL receptor. Patients who are homozygous for Apo E2 can develop familial dysbetalipoproteinemia. Apo E4 is associated with an increased risk of Alzheimer’s disease and an increased risk of atherosclerosis.
  • Apolipoprotein (a) (7) – Apo (a) is synthesized in the liver. This protein is a homolog of plasminogen and its molecular weight varies from 300,000 to 800,000. It is attached to Apo B-100 via a disulfide bond. High levels of Apo (a) are associated with an increased risk of atherosclerosis. Apo (a) is an inhibitor of fibrinolysis and can also enhance the uptake of lipoproteins by macrophages, both of which could increase the risk of atherosclerosis. The physiologic function of Apo (a) is unknown. Interestingly this apolipoprotein is found in primates but not in other species.

Apolipoproteins

Apolipoprotein MW Primary Source Lipoprotein Association Function
Apo A-I 28,000 Liver, Intestine HDL, chylomicrons Structural protein for HDL, Activates LCAT
Apo A-II 17,000 Liver HDL, chylomicrons Structural protein for HDL, Activates hepatic lipase
Apo A-IV 45,000 Intestine HDL, chylomicrons Unknown
Apo A-V 39,000 Liver VLDL, chylomicrons, HDL Promotes LPL mediated TG lipolysis
Apo B-48 241,000 Intestine Chylomicrons Structural protein for chylomicrons
Apo B-100 512,000 Liver VLDL, IDL, LDL, Lp (a) A structural protein, Ligand for LDL receptor
Apo C-I 6,600 Liver Chylomicrons, VLDL, HDL Activates LCAT
Apo C-II 8,800 Liver Chylomicrons, VLDL, HDL Co-factor for LPL
Apo C-II 8,800 Liver Chylomicrons, VLDL, HDL Inhibits LPL and uptake of lipoproteins
Apo E 34,000 Liver Chylomicron remnants, IDL, HDL Ligand for LDL receptor
Apo (a) 250,000- 800,00 Liver Lp (a) Inhibits plasminogen activation

LIPOPROTEIN RECEPTORS AND LIPID TRANSPORTERS

There are several receptors and transporters that play a crucial role in lipoprotein metabolism.

  • LDL receptor (8) – The LDL receptor is present in the liver and most other tissues. It recognizes Apo B-100 and Apo E and hence mediates the uptake of LDL, chylomicron remnants, and IDL, which occurs via endocytosis. After internalization, the lipoprotein particle is degraded in lysosomes and the cholesterol is released. The delivery of cholesterol to the cell decreases the activity of HMGCoA reductase, a key enzyme in the biosynthesis of cholesterol, and the expression of LDL receptors. LDL receptors in the liver play a major role in determining plasma LDL levels (a low number of receptors is associated with high plasma LDL levels while a high number of hepatic LDL receptors is associated with low plasma LDL levels). The number of LDL receptors is regulated by the cholesterol content of the cell. When cellular cholesterol levels are decreased the transcription factor SREBP is transported from the endoplasmic reticulum to the Golgi where proteases cleave and activate SREBP, which then migrates to the nucleus and stimulates the expression of LDL receptors (Figure 4). Conversely, when cellular cholesterol levels are high SREBP remains in the endoplasmic reticulum in an inactive form and the expression of LDL receptors is low.
  • LDL receptor-related protein (LRP) (10) – LRP is a member of the LDL receptor family. It is expressed in multiple tissues including the liver. LRP recognizes Apo E and mediates the uptake of chylomicron remnants and IDL.
  • Class B scavenger receptor B1 (SR-B1) (11) – SR-B1 is expressed in the liver, adrenal glands, ovaries, testes, macrophages, and other cells. In the liver and steroid producing cells, it mediates the selective uptake of cholesterol esters from HDL particles. In macrophages and other cells, it facilitates the efflux of cholesterol from the cell to HDL particles.
  • ATP-binding cassette transporter A1 (ABCA1) (12) – ABCA1 is expressed in many cells including hepatocytes, enterocytes, and macrophages. It mediates the transport of cholesterol and phospholipids from the cell to lipid poor HDL particles (pre-beta-HDL).
  • ATP-binding cassette transporter G1 (ABCG1) (13) – ABCG1 is expressed in many different cell types and mediates the efflux of cholesterol from the cell to HDL particles.
  • ATP-binding cassette transporter G5 and G8 (ABCG5/ABCG8) (14) – ABCG5 and ABCG8 are expressed in the liver and intestine and form a heterodimer. In the intestine, these transporters mediate the movement of plant sterols and cholesterol from inside the enterocyte into the intestinal lumen thereby decreasing their absorption and limiting the uptake of dietary plant sterols. In the liver, these transporters play a role in the movement of cholesterol and plant sterols into the bile facilitating the excretion of plant sterols.
  • Niemann-Pick C1-Like 1 (NPC1L1) (14) – NPC1L1 is expressed in the intestine and mediates the uptake of cholesterol and plant sterols from the intestinal lumen into the enterocyte.

ENZYMES AND TRANSFER PROTEINS INVOLVED IN LIPOPROTEIN METABOLISM

There are several enzymes and transfer proteins that play a key role in lipoprotein metabolism.

  • Lipoprotein lipase (LPL) (15) – LPL is synthesized in muscle, heart, and adipose tissue, then secreted and attached to the endothelium of the adjacent blood capillaries. This enzyme hydrolyzes the triglycerides carried in chylomicrons and VLDL to fatty acids, which can be taken up by cells. The catabolism of triglycerides results in the conversion of chylomicrons into chylomicron remnants and VLDL into IDL. This enzyme requires Apo C-II as a cofactor. Apo A-V also plays a key role in the activation of this enzyme. In contrast, Apo C-III and Apo A-II inhibit the activity of LPL. Insulin stimulates LPL expression and LPL activity is reduced in patients with poorly controlled diabetes, which can impair the metabolism of triglyceride-rich lipoproteins leading to hypertriglyceridemia.
  • Hepatic lipase (16) – Hepatic lipase is localized to the sinusoidal surface of liver cells. It mediates the hydrolysis of triglycerides and phospholipids in IDL and LDL leading to smaller particles (IDL is converted to LDL; LDL is converted from large LDL to small LDL). It also mediates the hydrolysis of triglycerides and phospholipids in HDL resulting in smaller HDL particles.
  • Endothelial lipase (17) – This lipase plays a major role in hydrolyzing the phospholipids in HDL.
  • Lecithin – cholesterol acyltransferase (LCAT) (18) LCAT is made in the liver. In the plasma, it catalyzes the synthesis of cholesterol esters in HDL by facilitating the transfer of fatty acid from position 2 of lecithin to cholesterol. This allows for the transfer of the cholesterol from the surface of the HDL particle (free cholesterol) to the core of the HDL particle (cholesterol ester), which facilitates the continued uptake of free cholesterol by HDL particles by reducing the concentration of cholesterol on the surface of HDL.
  • Cholesteryl ester transfer protein (CETP) (19) – This protein is synthesized in the liver and in the plasma mediates the transfer of cholesterol esters from HDL to VLDL, chylomicrons, and LDL and the transfer of triglycerides from VLDL and chylomicrons to HDL. Inhibition of CETP activity leads to an increase in HDL cholesterol and a decrease in LDL cholesterol.

References

Elbow Arthrocentesis – Anatomy, Indications, Contraindications

Elbow arthrocentesis is a procedure performed to aspirate the contents of a joint cavity to evaluate and treat elbow effusion. Arthrocentesis is considered a minor surgical procedure. However, there is always the chance, as with introducing any needle through the skin, for infection, injury to nerves, vessels, tendons, or other connective tissue. Therefore, this procedure should only be performed by health care providers trained in arthrocentesis with a strong understanding of elbow anatomy. Arthrocentesis is commonly used to evaluate the underlying etiology of joint effusion, including infectious, inflammatory, and hemorrhagic causes. Aspiration of the joint space and removal of the contents reduces the fluid pressure in the joint capsule and reduces pain. Additionally, access to the joint space provides the opportunity to inject therapeutic agents in the setting of pain or degenerative joint disease. Of the etiologies above, the most important to diagnose properly is septic arthritis, as cultures are crucial to prompt and adequate treatment.

Anatomy and Physiology

  • Osseous – The distal humerus, radial head, and olecranon comprise the elbow joint.  The olecranon process articulates with the trochlea of the humeral condyle forming a hinge joint for flexion and extension.  The radial head is held in place with the annular ligament arising from the proximal ulna and articulates with the ulna and the distal humerus.  The joint is encapsulated and contains the articular surfaces of the structures mentioned above. This space contains synovial fluid and is the target of elbow aspiration.
  • Muscular Compartments – The biceps crosses the elbow anteriorly, and the triceps crosses the elbow posteriorly, facilitating flexion and extension, respectively.  The flexor carpi radialis, palmaris longus, humeroulnar head of flexor digitorum superficials, and the humeral head of the flexor carpi ulnaris contribute to the flexor compartment and supination of the wrist originating at the medial epicondyle.  They primarily receive innervation via the median nerve.  The wrist extensors and supinators, including extensor carpi radialis brevis, extensor digitorum, and extensor digiti minimi, all originate on the lateral epicondyle and are innervated by the radial nerve.
  • Vasculature – Blood supply to the elbow is via extensive anastomoses originating from the brachial and radial arteries
  • Positioning – The patient should have their elbow bent to 90 degrees with their hand pronated (palm down); this exposes the approach trajectory by rolling the head of the radius out of the way. The aiming point for needle insertion is the juncture of the lateral humeral condyle, radial head, and olecranon process. These three landmarks form the anconeus triangle, and the insertion point is located centrally.  The needle is then inserted into the sulcus directed medial and perpendicular to the radius toward the distal end of the antecubital fossa.

Ultrasound guidance for the evaluation of fluid collection and needle guidance is recommended.

Indications of Elbow Arthrocentesis

  • Elbow arthrocentesis is performed to aspirate effusions for two reasons, both diagnosis and therapeutic relief of pain caused by fluid pressure.
  • Diagnostically the primary etiologies of concern are septic arthritis, hemarthrosis, and inflammation. Of these, a suspected septic joint and crystalline arthropathy are the two most common indications.
  • Additionally, arthrocentesis may help to evaluate the therapeutic response for septic arthritis or unexplained arthritis with synovial effusion.
  • Although not the topic of this discussion, access to the joint space may also be used to inject therapeutic agents and to challenge the joint with fluid for evaluation of joint capsule integrity if any overlying laceration is present.

Contraindications of Elbow Arthrocentesis

The only absolute contraindication to arthrocentesis is overlying cellulitis, which may lead to the seeding of the joint with bacteria. Relative contraindications include coagulopathy, joint prosthesis, acute fracture, and adjacent osteomyelitis. Prosthetic joints warrant discussion with orthopedic surgery before tapping, as many surgeons believe a prosthetic joint should only undergo tapping in the operative theater.

Equipment

  • Iodine solution or chlorhexidine
  • Sterile gloves and drape
  • Sterile gauze
  • Sterile fenestrated drapes
  • Lure-Lok syringes including one 5cc and another 5 to 20cc syringe
  • 20G and 27G needle
  • 1% Lidocaine or 0.5% bupivacaine
  • Collection tubes including a hematology tube, sterile tube, heparinized tube
  • Ultrasound with a sterile cover, if available

Personnel

This procedure can take place without an assistant; however, an assistant may make certain situations, including an anxious patient or unforeseen technical difficulties, easier.

Preparation

There are no stat indications for elbow arthrocentesis; thus, additional time can help improve a first-attempt success rate and reduce associated risks. Ensure all necessary equipment is available and works appropriately, correctly identify landmarks, and adhere to a sterile technique.

Technique

Position your patient with the elbow bent 90 degrees and pronated palm down. This position rolls the radial head to open the joint space. Use an ultrasound if available to localize fluid collection and direct the needle. Mark the approach by identifying the insertion site inferior to the lateral humeral epicondyle, anterior to the olecranon, and superior/posterior to the radial head (anconeus triangle). Use a skin pen to mark or pressure to indent the surface of the skin. Now clean the area with a wide margin using chlorhexidine or iodine solution. Gown, glove, and then drape in a sterile fashion. Raise a bleb of 1% lidocaine using a sterile technique at the site of insertion. Once anesthetized, an 18 to 22 gauge needle 1.5 inches long is attached to a 5 to 10mL syringe and advanced into the joint space while retracting to watch for blood return. Once the joint space is accessed, synovial fluid, blood, or infectious material may be aspirated. With the needle held in place, multiple syringes may be used to aspirate all the contents of the joint. If inflammatory etiology is suspected, a glucocorticoid may be injected before leaving the joint space to prevent relapse of effusion. The needle is then withdrawn, a bandage is applied, and the collected fluid is sent to the lab. Studies should include fluid gram stain and culture, cell count with differential, protein, glucose, and polarized light microscopy for crystalline arthropathies.

Other Considerations – Joint aspiration is safe within the therapeutic range of anticoagulation with warfarin or properly dosed DOC.  Considerations for the anticoagulated patient includes using a smaller needle size.Ultrasonography may be used in a sterile fashion to guide the needle if a dry tap occurs, and septic arthritis is suspected.Shaving is of no benefit.

Complications

Even though complications with arthrocentesis are rare, the clinician should take the time to inform the patient of potential complications arising from arthrocentesis. There are two major categories to take into consideration; infectious complications and noninfectious complications. Of the complications, the most feared is septic arthritis.  The frequency of this complication lies somewhere between 1 in 2000 and 1 in 15000. It is best avoided by maintaining a sterile field, minimizing attempts, using single-dose vials, changing to a new needle after drawing up medication before injecting, and preventing the introduction of a needle through cellulitis. The other concerning infection is septic bursitis, which arises when the needle approach travels through a bursa, the olecranon bursa in the case of the elbow, on the way to the joint and is due to direct inoculation from skin flora. Noninfectious complications that arise include tendon rupture, vascular damage, and neurologic damage. All three complications directly result from trauma secondary to the penetrating needle and are more common when injecting glucocorticoids than aspirating. These complications are mediated by carefully planning the approach and identifying the proper anatomical location for insertion and needle travel.  Bleeding management is with tamponade. The patient should also be informed there may be a recurrence of joint effusion until the resolution of the underlying etiology.

References

Sequestered Intervertebral Disc – Causes, Symptoms, Treatment

Sequestered intervertebral disc fragments have the potential to migrate both intramurally and extramurally within the spinal canal. There are no particular clinical features allowing for a clear differentiation between patients with atypical disc herniations and those with tumors []. Free disc fragments were previously only identified during surgery but are still frequently misinterpreted as neoplastic masses, even after the introduction of magnetic resonance imaging (MRI) []. This is because the imaging characteristics of sequestered disc fragments may mimic known characteristics of extramedullary (intra- and extradural) lesions, including neoplasms and other benign epidural lesions (such as synovial cysts, hematomas, and abscesses), further complicating preoperative diagnosis based on imaging findings [, ].

A sequestrated disc, also referred to as a free disc fragment, corresponds to extruded disc material that has no continuity with the parent disc and is displaced away from the site of extrusion. By definition, it corresponds to a subtype of disc extrusion.

The term “migrated” disc refers only to position and not to the continuity of disc substance. So, this term can be used when referring either to extruded discs that still have continuity or those without, i.e. sequestrated (e.g. disc extrusion migrated caudally, sequestrated disc migrated cranially).

Causes of Sequestered intervertebral disc

  • Disc herniation and sequestrated disc – are associated terms, being nucleus pulposus herniation a possible evolution from a degenerative disc. Disc degeneration is usually associated with the loss of proteoglycans. Multiple factors influence the degenerative process such as genetic, mechanical, and behavioral.
  • Mechanical load – is important in maintaining a healthy IVD by generating signals to cells that regulate proper matrix homeostasis. On the other hand, prolonged exposure to hypo- or hyper-loading correlates with disc degeneration /sequestrated disc induction.
  • Repetitive trauma – such as poor posture, poor ergonomics, or repetitive heavy work can lead to a sequestrated disc. These long term injuries are often also associated with poor muscle strength, obesity, and other factors such as smoking.
  • An Injury caused – by sudden forces or load on the disc such as a car accident or an awkward heavy lift. This sudden increase in pressure on the disc can cause damage and tears to the annulus that causes a bulging disc.
  • Spinal Degeneration – While some degeneration is a normal part of the aging process, poor spinal function and posture will dramatically speed up disc degeneration with a bulging disc.
  • People who have led a sedentary lifestyle or those who smoke – increase the chances for bulging discs sequestrated disc.
  • Continuous strain on the disc from injury or heavy lifting – and strain can wear them down throughout the years.
  • Weakened back muscles – can accelerate the process and may lead to a sudden herniation of the weakened disc. Although sequestrated disc occur over time, herniated discs may occur quickly by trauma.
  • Bad posture – including improper body positioning during sleep, sitting, standing, or exercise are all risk factors that may contribute to the development of a bulging disc.
  • Obesity
  • High contact sports or activities – are also risk factors.
  • Runners who fail to use shoes that provide orthopedic support – may also develop bulging discs.
  • Activities that place stress and strain on the spine – can lead to the weakening of the discs.
  • Road, traffic accident

Symptoms of Sequestered intervertebral disc

If a  sequestrated disc has not yet reached the stage of herniation, a patient may have little to no pain involved. A sequestrated disc may have no pain at all because it has not reached a certain severity level, and this can make it difficult to identify the bulging disc symptoms before the condition becomes more severe.

Most commonly, the sequestrated disc creates pressure points on nearby nerves which create a variety of sensations. Evidence of a bulging disc may range from mild tingling and numbness to moderate or severe pain, depending on the severity.

  • Un tolerable pain – patients are unable to walk totally. It may be a loss of motor function and sensory.
  • Tingling or pain in the fingers, hands, arms, neck, or shoulders – This could indicate a bulging disc in the cervical area.
  • Pain in the feet, thighs, lower spine, and buttocks – This is the most common symptom and could indicate an issue in the lumbar region.
  • Difficulty walking or feeling of impairment while lifting or holding things.
  • Loss of Bladder or Bowel Function – There are some bulging disc cases where professional care is essential. In some cases, such as when you lose bowel or bladder control, it is deemed an emergency, and you may require immediate surgery. These bulges usually are very significant and affect your nerve control involving your bladder or bowels. You should go straight to your nearest emergency department in these instances.
  • Weakness in your limb muscles – is a significant concern. If you experience arm, hand, leg, or foot weakness, please seek prompt medical assessment.
  • The reduced or altered sensation – is your next priority. Mild disc bulges can reduce your ability to feel things touching you, e.g. numbness or pins and needles. If you experience any of the above symptoms, you should seek professional assistance.
  • Referred Pain – Pain in your limbs, e.g. legs (sciatica) or arms (brachialgia) is usually a more significant injury than when experiencing only spinal pain. We recommend that you seek the professional advice of your trusted spinal care practitioner.
  • Spinal Pain – Interestingly, if you are only experiencing spinal pain, bulging discs are generally mild injuries and the most likely to rehabilitate quickly. Please adhere to low disc pressure postures and exercise accordingly. If in doubt, please seek professional advice.
  • Intermittent or continuous back pain. This may be made worse by movement, coughing, sneezing, or standing for long periods of time.
  • Spasm of the back muscles
  • Sciatica. Pain that starts near the back or buttock and travels down the leg to the calf or into the foot.
  • Muscle weakness in the legs
  • Numbness in the leg or foot
  • Decreased reflexes at the knee or ankle
  • Changes in bladder or bowel function

Associate clinical feature is

Approximate area of “saddle anesthesia” seen from behind (yellow highlight)

These symptoms require immediate medical evaluation as they may be a sign of a potentially life-threatening condition.

Diagnosis of the Sequestered intervertebral disc

History

Proper understanding of anatomical zones and vertebral levels is essential to interpret the clinical manifestations secondary to a sequestrated disc. Wiltse proposed these anatomical zones, based on the following landmarks: medial border of the articular facet, lateral, upper, and medial borders of the pedicles, coronal and sagittal planes at the center of the disc. On the axial plane, these landmarks determine the central zone, the subarticular zone (lateral recess), foraminal, and extraforaminal zones. On the sagittal plane, the levels are termed as follows: The supra pedicular level, the pedicular level, the intravesicular level, and the disc level. The correct knowledge of anatomy and the relationship between nerve roots and disc herniation allows the proper understanding of common clinical findings associated with this problem.

We summarize the anatomy, motor function, sensitive distribution, and reflex of the most commons nerve roots involved in cervical and lumbosacral nucleus pulposus herniation:

Cervical

  • C5 nerve root – Exits between C4 and C5 foramina, innervates deltoids and biceps (with C6), sensory distribution: lateral arm (axillary nerve) and is assessed with biceps reflex.
  • C6 nerve root – Exits between C5 and C6 foramina, innervates biceps (with C5) and wrist extensors, sensory distribution: lateral forearm (musculocutaneous nerve), assessed with brachioradialis reflex.
  • C7 nerve root – Exits between C6 and C7 foramina, innervates triceps, wrist flexors, and finger extensors, sensory distribution: middle finger, assessed with triceps reflex.
  • C8 nerve root – Exits between C7 and T1 foramina, innervates interosseus muscles and finger flexors, sensory distribution: ring and little fingers and distal half of the forearm (ulnar side), no reflex.

Lumbosacral

  • L1 nerve root – Exits between L1 and L2 foramina, innervates iliopsoas muscle, sensory distribution: upper third thigh, assessed with the cremasteric reflex (male).
  • L2 nerve root – Exits between L2 and L3 foramina, innervates iliopsoas muscle, hip adductor, and quadriceps, sensory distribution: middle third thigh, no reflex.
  • L3 nerve root – Exits between L3 and L4 foramina, innervates iliopsoas muscle, hip adductor, and quadriceps, sensory distribution: lower third thigh, no reflex.
  • L4 nerve root – Exits between L4 and L5 foramina, innervates quadriceps and tibialis anterior, sensory distribution: anterior knee, medial side of the leg, assessed with patellar reflex.
  • L5 nerve root – Exits between L5 and S1 foramina, innervates extensor hallucis longus, extensor digitorum longus, and Brevis, and gluteus medius, sensory distribution: anterior leg, lateral leg, and dorsum of the foot, no reflex.
  • S1 Nerve – back, radiating into buttock, lateral or posterior thigh, posterior calf, lateral or plantar foot; sensory loss on the posterior calf, lateral or plantar aspect of foot;  weakness on hip extension, knee flexion, plantar flexion of the foot; Achilles tendon; Medial buttock, perineal, and perianal region; weakness may be minimal, with urinary and fecal incontinence as well as sexual dysfunction.
  • S2-S4 Nerves – sacral or buttock pain radiating into the posterior aspect of the leg or the perineum; sensory deficit on the medial buttock, perineal, and perianal region; absent bulbocavernosus, anal wink reflex.

Cervical and the thoracic sequestrated disc can also exhibit symptoms of myelopathy such as spasticity, clumsiness, wide-based gate, and weakness, on physical examination hyperreflexia is the most important sign. The Lhermitte sign is the presence of an electric shock-like sensation towards the back and lower extremities, especially by flexing the neck. Bowel and bladder dysfunction may indicate a poor prognosis.

Physical Examination

A physical exam for diagnosing disc pain may include one or more of the following tests:

  • Palpation – Palpating (feeling by hand) certain structures can help identify the pain source. For example, worsened pain when pressure is applied to the spine may indicate sensitivity caused by a sequestrated disc.
  • Movement tests – Tests that assess the spine’s range of motion may include bending the neck or torso forward, backward, or to the side. Additionally, if raising one leg in front of the body worsens leg pain, it can indicate a lumbar herniated disc (straight leg raise test).
  • Muscle strength – A neurological exam may be conducted to assess muscle strength and determine if a nerve root is compressed by a herniated disc/sequestrated disc. A muscle strength test may include holding the arms or legs out to the side or front of the body to check for tremors, muscle atrophy, or other abnormal movements.
  • Reflex test – Nerve root irritation can dampen reflexes in the arms or legs. A reflex test involves tapping specific areas with a reflex hammer. If there is little or no reaction, it may indicate a compressed nerve root in the spine.
  • The straight leg raise test – With the patient lying supine, the examiner slowly elevates the patient’s led at an increasing angle, while keeping the leg straight at the knee joint. The test is positive if it reproduces the patient’s typical pain and paresthesia.
  • The contralateral (crossed) straight leg raise test – As in the straight leg raise test, the patient is lying supine, and the examiner elevates the asymptomatic leg. The test is positive if the maneuver reproduces the patient’s typical pain and paresthesia. The test has a specificity higher than 90%.

Lab Test

  • A medical history – in which you answer questions about your health, symptoms, and activity.
  • Erythrocyte sedimentation rate and C-reactive protein – are inflammatory markers, and they are requested if suspicious for a chronic inflammatory condition or infectious cause as the etiology. A complete blood count is useful when suspecting infection or malignancy.
  • A physical exam to assess your strength – reflexes, sensation, stability, alignment, and motion. You may also need blood tests.
  • Laboratory testing – may include white blood cell (WBC) count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).
  • Elevated ESR – could indicate infection, malignancy, chronic disease, inflammation, trauma, or tissue ischemia.
  • Elevated CRP – levels are associated with infection.

Imaging

  • X-rays – X-ray is the initial workup study when there is a strong suspicion of a specific cause of cervical or back pain (fracture, infection, tumor) or in the presence of red flags (fever, age more than 50, recent trauma, pain at night or rest, unexplained weight loss, progressive motor or sensory deficit, saddle anesthesia, history of cancer or osteoporosis, failure to improve after six weeks of conservative treatment). Anteroposterior and lateral x-ray is helpful to assess fracture, bony deformity, decreased intervertebral height, osteophytes, spondylolisthesis, and facet joint osteoarthritis.
  • Magnetic Resonance Imaging (MRI) scan – MRI is the recommended diagnostic imaging in cases of severe or progressive neurologic deficits, suspicion of an underlying condition such as infection, fracture, cauda equina syndrome, spinal cord compression. In cases of radiculopathy, most of the cases improve with conservative treatment and MRI is indicated in those cases with significant pain or neurologic deficits.
  • A myelogram – is a specialized X-ray where dye is injected into the spinal canal through a spinal tap. An X-ray fluoroscope then records the images formed by the dye. The dye used in a myelogram shows up white on the X-ray, allowing the doctor to view the spinal cord and canal, a bulging disc in detail. Myelograms can show a nerve being pinched and a bulging disc by a herniated disc, bony overgrowth, spinal cord tumors, and abscesses. A CT scan may follow this test.
  • Computed Tomography (CT) scan – is a noninvasive test that uses an X-ray beam and a computer to make 2-dimensional images of your spine. It may or may not be performed with a dye (contrast agent) injected into your bloodstream. This test is especially useful for confirming which bulging disc is damaged. CT scan is not usually requested in nucleus pulposus herniation. However, it can be helpful in some cases when there is a suspicion of calcified disc herniation (thoracic disc herniation has a 30 to 70% rate of calcification) which is more challenging especially when surgery is a consideration.
  • Electromyography (EMG) & Nerve Conduction Studies (NCS) – EMG tests measure the electrical activity of your muscles. Small needles are placed in your muscles, and the results are recorded on a special machine. NCS is similar, but it measures how well your nerves pass an electrical signal from one end of the nerve to another. These tests can detect nerve damage and muscle weakness and a bulging disc.
  • Discogram – A discogram may be recommended to confirm which bulging disc is painful if surgical treatment is considered. In this test, the radiographic dye is injected into the disc to recreate disc pain from the dye’s added pressure.

In the presence of low back pain without symptoms of radiculopathy, there is no need to request studies as most of the patients improve in a couple of weeks, a 4-week follow-up is a usual timeframe.

Treatment of Sequestered intervertebral disc

There is no conservative treatment. It is a medical emergency condition. So the first choice of surgery as soon as possible.

Surgery

  • Microdiscectomy – for a sequestrated disc, a minimally-invasive procedure in which the sequestrated disc portion of the disc is removed.
  • Artificial disc replacement – for degenerative disc disease and herniated discs is a minimally invasive procedure that replaces a damaged disc with a specialized implant that mimics the normal function of the disc, maintaining mobility.
  • Spinal fusion – fusion for degenerative disc disease, in which the disc space is fused together to remove motion at the spinal segment. Spinal fusion involves setting up a bone graft, as well as possible implanted instruments, to facilitate bone growth across the facet joints. Fusion occurs after the surgery.
  • Open Back Surgery – Traditionally, bulging discs are treated with an open back procedure, meaning the surgeon makes a large incision into the skin and cuts muscle and surrounding tissue to gain access to the problematic disc. This traditional surgical option is invasive, requires overnight hospitalization, general anesthesia, and requires a lengthy recovery coupled with strong pain medication.
  • Endoscopic Surgery – Fortunately, you have a second option with endoscopic spine surgery. Thanks to the advancement of surgical technology at bulged disc surgery can be performed using endoscopic procedures, meaning the surgeon makes a small incision to insert special surgical tools. During an endoscopic sequestrated disc operation, the surgeon uses a tiny camera to visualize and gain access to your damaged disc. This minimally invasive new approach offers shorter recovery, easier rehabilitation, and a much higher success rate than open back or neck surgery. A local anesthetic is all that is usually required.

Some patients will not benefit from conservative treatment and will require surgery to decompress the nerve involved. Classical surgical indications are motor deficit, cauda equina syndrome, and persistent pain after conservative treatment.

In cervical sequestrated disc, there is no evidence of effectiveness for conservative treatment compared with surgery. Different randomized controlled trials (RTC) have compared conservative versus surgical treatment in the sequestrated disc, observing faster pain relief and recovery in the early surgery groups, however, similar outcomes in the long term (one or two years) were found. In another trial, carefully selected patients who underwent surgery for lumbar disc herniation achieved greater improvement compared to nonoperative treated patients at eight years follow up .

References

Aortic Aneurysm – Causes, Symptoms, Treatment

An aortic aneurysm is the abnormal dilation of a segment of the aorta. Abdominal aortic aneurysm is the most common aortic aneurysm, occurring frequently in the infrarenal area. Degenerative aortic disorders are the prevalent etiology, affecting patients > 60 years of age. Most aneurysms are asymptomatic, but can cause compression of surrounding structures or rupture, which is a life-threatening emergency. Diagnosis is often made by ultrasound. As aneurysmal rupture carries a high mortality rate, surveillance is recommended for asymptomatic cases to monitor aortic diameter. Elective surgery (the majority via endovascular aortic repair) is an effective way to reduce complications and aneurysm-related death. This surgery is performed based on aortic size, underlying condition, and associated symptoms.

  • Abdominal aortic aneurysm (AAA): infradiaphragmatic dilation of the aorta (to an aortic diameter of ≥ 3 cm)
  • Types:
    • True aneurysm: dilation of the aorta involving all 3 layers (intima, media, adventitia)
      • Fusiform-shaped: bulges on all sides of the aorta (more common)
      • Saccular-shaped: bulges on 1 side
    • Pseudoaneurysm:
      • Dilation caused by a disruption of the aortic wall
      • Extravasated blood contained by periarterial connective tissue, not by all wall layers
      • Extravascular hematoma communicates with the intravascular space.
  • Location:
    • Suprarenal: involves visceral arteries; below the chest
    • Pararenal: involves origin of the renal arteries
    • Juxtarenal:
      • No aneurysm in origin of renal arteries but aneurysm starts just beyond renal arteries
      • No normal aortic segment between renal arteries and aneurysm
    • Infrarenal (most common):
      • Below renal arteries
      • There is a normal aortic segment between renal arteries and aneurysm.

Epidemiology

  • AAAs: more common than thoracic aortic aneurysms (TAAs)
  • In the United States:
    • More than 50% of patients with ruptured AAA die before reaching the hospital.
    • Over the past 30 years, AAA-related mortality has decreased, possibly due to:
      • Disease screening
      • Decline in smoking
      • Use of endovascular aortic repair

Etiology

  • Degenerative disorders:
    • Most common cause of AAA
    • Risk factors:
      • Age (> 60) and male sex
      • Smoking
      • Atherosclerosis (more common in AAA)
      • Hypertension
      • Caucasian race
    • Decreased risk noted in: females, non-Caucasians, and patients with diabetes
  • Genetic or developmental disorders:
    • Marfan’s syndrome
    • Turner’s syndrome
    • Ehlers-Danlos syndrome
    • Loeys-Dietz syndrome
    • Polycystic kidney disease
  • Family history of AAA and presence of other arterial aneurysms (popliteal, femoral, intracranial)
  • Vasculitis:
    • Giant cell arteritis
    • Behcet’s disease
    • Takayasu’s arteritis
    • HLA-B27–associated spondyloarthropathies
  • Infection:
    • Syphilis (tertiary)
    • Tuberculosis
    • Mycotic (Salmonella, staphylococcal, streptococcal, fungal infection)
  • Trauma: includes prior aortic procedure

 

Pathophysiology

Contributing factors

  • Embryology:
    • Embryologic origin can affect the response of aorta to cytokines and growth factors.
    • Abdominal aorta: derived from mesoderm
  • Genetics:
    • 20% from familial predisposition
  • Biomechanics, structure, and growth of artery:
    • Wall thickness of aorta decreases from the thoracic area to the distal aorta
    • Abdominal aorta:
      • Lower elastin, collagen content
      • Has avascular media (poor nutrition delivery)
      • Grows by ↑ thickness of lamellar units
      • Fewer lamellar units = more tension per lamellar unit
      • ↑ pulse pressures and more wall shear stress:
        • Noted in distal aorta, especially infrarenal aorta (most common location of aortic aneurysm)
  • Atherosclerosis:
    • AAA is associated with severe atherosclerosis.
    • High likelihood of progression of fatty streak to atheroma (compared with TAA)
  • Inflammation affects both TAA and AAA:
    • Predominantly T cells and macrophages
    • In AAA, both pro- and anti-inflammatory cytokines noted
  • Proteolysis by matrix metalloproteinases (MMPs):
    • ↑ breakdown of extracellular matrix
    • MMP-9 proportional to aneurysm diameter
    • MMP-2: ↑ growth of aneurysm

Pathogenesis

  • Regular vascular remodeling (synthesis, degradation, and repair) of extracellular matrix (ECM) components maintain the functional and structural integrity of the artery.
  • Above factors, in combination with age and environment (i.e. smoking, trauma) → result in breakdown of ECM → arterial medial degeneration → weakened vascular wall → dilation
  • The dilation + rapid expansion of aorta: ↑ risk of rupture or aortic dissection
  • Widening of the vessel disrupts laminar blood flow → turbulence + inflammation → possible thrombus formation within the vessel (with risk of embolism)

 

Clinical Presentation

Symptoms

  • Commonly asymptomatic
  • Depending on size and location:
    • Compression or erosion of surrounding structures: pain in the abdomen, lower back/flank (most common manifestations)
    • Rupture typically into retroperitoneum: sudden severe flank or back pain
    • Distal abdominal aneurysm compression and/or rupture: pelvic, groin or thigh, lower extremity pain
    • Thromboembolic events: claudication (limb ischemia), painful pulseless extremity (embolism)
    • Aortoduodenal fistula: upper gastrointestinal bleeding
    • Aortic infection: fever, weight loss, vague abdominal pain
    • Inflammatory aneurysm: patients are younger; abdominal and/or back pain

Signs

  • AAA often found incidentally in imaging studies
  • AAA rupture:
    • Life-threatening emergency!
    • Hypotension, tachycardia
  • Pulsatile abdominal mass (in 62% of ruptured AAAs)
  • Abdominal tenderness, abdominal bruit on examination
  • Ecchymosis (sign of retroperitoneal hematoma and blood extravasation into subcutaneous tissues)
    • Flank (Grey-Turner sign)
    • Proximal thigh (Fox’s sign)
    • Periumbilical (Cullen’s sign)
    • Scrotum (Bryant’s sign)
  • Reduced femoral and pedal pulses in thromboembolism

 

Diagnosis

History

  • Risk factors (hypertension, smoking, hypercholesterolemia)
  • Family history of aortic pathology
  • Known history of aneurysm in other areas (intracranial, iliac, femoral, popliteal aneurysms)
  • Prior aortic dissection
  • Other conditions: Marfan’s syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, and other connective tissue diseases
  • Prior aortic procedure

Diagnostic tests

  • Abdominal ultrasound:
    • Used for screening, diagnosis, and serial measurements
    • Determines the location and size of aneurysm
    • Screening:
      • Best initial step for asymptomatic patients
      • 1-time ultrasound is:
        • Recommended in men aged 65–75 years who have smoked
        • Suggested in women and men aged 65–75 years with family history of AAA or AAA rupture
    • Symptomatic patients: can be used bedside in unstable patients
    • Diagnosis of aneurysm: > 3 cm outer aortic diameter
    • Limited in detecting rupture, leakage, and other vessel involvement
    • Affected by body habitus and bowel gas
  • Abdominal computed tomography (CT) with contrast:
    • For stable symptomatic patients and planning operative repair
    • Defines extent of aneurysm, leakage, rupture, vessel involvement
    • Signs of impending rupture:
      • Hyperattenuating crescent sign (93% specificity)
      • Thrombus fissuration
      • Aortic blebs from surface of aorta
      • Irregular aortic wall
      • Draped aorta sign (rupture sealed by vertebral body)
    • Signs of rupture:
      • Intra- and/or retroperitoneal hematoma
      • Periaortic stranding
      • Indistinct aortic wall
  • Magnetic resonance imaging (MRI):
    • No radiation or dye (may be used for patients with contrast allergy)
    • Limited availability and higher cost
  • Arteriography:
    • Cannot accurately measure aortic diameter
    • Used intraoperatively (endovascular repair)

 

Management

Non-surgical management

  • Reduce cardiovascular risk:
    • Smoking cessation (most effective nonsurgical intervention to reduce aneurysm-related complications and death)
    • Exercise:
      • Avoid heavy lifting.
      • Avoid activities that lead to Valsalva (↑ blood pressure).
    • Hypertension control:
      • Antihypertensives given to reach recommended blood pressure goals
      • Unlike TAA, no specific medication recommended to limit AAA expansion
    • Lipid control with statins (target LDL < 70 mg/dL)
  • Avoid fluoroquinolones (may ↑ risk of dissection or rupture)
  • Surveillance: Asymptomatic AAA < 5.5 cm, periodic evaluation and aneurysm diameter surveillance

Table: Management of asymptomatic patients by AAA size

AAA management of asymptomatic patients (ultrasound) AAA size
Rescreen after 10 years ≥ 2.5 cm but < 3 cm
Imaging every 3 years 3–3.9 cm
Imaging every 12 months 4–4.9 cm
Imaging every 6 months 5–5.4 cm
Consider elective repair ≥ 5.5 cm

Consider repair if 5 cm in women; expansion of < 0.5 cm/6 months or > 1 cm/1 year; associated femoral, iliac, popliteal aneurysm, or PAD requiring revascularization

Surgical management

Indications for operative repair

  • AAA rupture: emergency repair
  • Elective repair: most effective way of preventing rupture and aneurysm-related death
    • Symptomatic AAA
    • Rapidly expanding (> 0.5 cm/6 months or > 1 cm/1 year)
    • Asymptomatic AAA:  when diameter ≥ 5.5 cm  (5 cm in women: higher rate of rupture)
    • AAA with coexisting iliac, femoral, or popliteal artery aneurysm
    • AAA associated with symptomatic peripheral arterial disease (PAD) undergoing revascularization

Operative options

  • Open surgical repair: 
    • Midline transperitoneal or retroperitoneal incision
    • Diseased aorta replaced with tube or prosthetic graft
    • Indicated for younger patients, low perioperative risk, or those who have contraindications for endovascular aortic repair (EVAR)
    • Higher perioperative mortality but long-term durability
    • Surveillance: CT angiography 5 years later, look for aortic dilation or pseudoaneurysm
  • EVAR:
    • In the United States: 80% of AAA surgical repair
    • Access through iliac or femoral arteries and endograft placed within AAA lumen
    • Requires anatomic suitability (site and structure of aneurysm and access vessels)
    • Decreased operative mortality but higher rate of re-intervention
    • Surveillance:
      • CT angiography 1 month and 1 year post-operatively, then duplex ultrasonography/CT annually if with uncomplicated surgery
      • Look for endoleak, sac enlargement, migration of stents, and device integrity

 

Differential Diagnosis

  • Ruptured viscus: a condition in which gastrointestinal wall integrity is lost with subsequent leakage of enteric contents into the peritoneal cavity, resulting in peritonitis. A ruptured viscus is life-threatening and requires surgical management.
  • Mesenteric ischemia: a rare, life-threatening syndrome caused by inadequate blood flow through the mesenteric vessels resulting in ischemia and gangrene of the bowel wall. Mesenteric ischemia can be acute or chronic. Acute mesenteric ischemia is a surgical emergency, while the chronic condition requires risk factor modification, as it is related to vascular disease.
  • Strangulated hernia: Hernias are protrusions of abdominal content (peritoneum, visceral fat, and/or viscera) through a congenital or acquired defect in the abdominal wall. Strangulation involves the constriction of hernial contents leading to bowel ischemia and requires emergency surgery to avoid bowel loss, perforation, and sepsis.
  • Acute cholecystitis: a condition characterized by inflammation of the gallbladder, most often due to obstruction of the cystic duct by a gallstone. Management includes IV fluids, pain control, and IV antibiotics for secondary infection. Complicated cholecystitis and progressive symptoms are indications for emergency cholecystectomy.
  • Acute pancreatitis: an inflammation of the pancreas that typically causes epigastric pain that radiates to the back. This condition is often treated with aggressive fluid resuscitation, bowel rest, and pain control. Surgery is indicated if the condition is associated with gallstones.
  • Diverticular abscess: a group of various intestinal conditions characterized by abnormal outpouchings of the colonic mucosa (diverticula). Over time, these diverticula may accumulate intestinal content, become infected, swell, and develop into an abscess. Intravenous antibiotics are the recommended treatment, with percutaneous drainage needed for large abscess or failed medical treatment.

Hearing Loss – Causes, Symptoms, Diagnosis, Treatment

Hearing loss is an extremely common medical condition, progressing in incidence and severity with age. The affected population is also vast, varying between neonates to elderly patients, and is nearly omnipresent in the 70+ age group. The diagnosis and management require a multi-disciplinary team that includes the general practitioner, otolaryngologist, speech therapist, audiologist, and social worker. To correctly address hearing loss, understanding the nature of hearing loss, and the equipment that is needed to improve auditory reception is crucial. In terms of children’s hearing loss, pediatricians need to be integrated into their care to ensure the normal hearing and language development of the child.

Hearing loss is a partial or total inability to hear.[rx] Hearing loss may be present at birth or acquired at any time afterward.[rx][rx] Hearing loss may occur in one or both ears.[rx] In children, hearing problems can affect the ability to learn spoken language, and in adults, it can create difficulties with social interaction and at work.[rx] Hearing loss can be temporary or permanent. Hearing loss related to age usually affects both ears and is due to cochlear hair cell loss.[rx] In some people, particularly older people, hearing loss can result in loneliness.[rx] Deaf people usually have little to no hearing.[rx]

Types of Hearing Loss

  • Sudden sensorineural hearing loss (SSHL) – presumed to be of viral origin, is an otologic emergency that is medically treated with corticosteroids.
  • Sensorineural hearing loss – can occur from head trauma or abrupt changes in air pressure (e.g., airplane descent), which can cause inner ear fluid compartment rupture or leakage, which can be toxic to the inner ear. There has been a variable success with emergency surgery when this happens.
  • Bilateral progressive hearing loss – over several months, also diagnosed as autoimmune inner ear disease, is managed medically with long-term corticosteroids and sometimes with drug therapy. Autoimmune inner ear disease is when the body’s immune system misdirects its defenses against the inner ear structures to cause damage in this part of the body.
  • Fluctuating sensorineural hearing loss – may be from an unknown cause or associated with Ménière’s disease. Symptoms of Meniere’s disease are hearing loss, tinnitus (ringing in the ears), and vertigo. Ménière’s disease may be treated medically with a low-sodium diet, diuretics, and corticosteroids. If the vertigo is not medically controlled, then various surgical procedures are used to eliminate vertigo.
  • Sensorineural hearing loss from disease – in the central nervous system may respond to medical management for the specific disease affecting the nervous system. For example, hearing loss secondary to multiple sclerosis may be reversed with treatment for multiple sclerosis.
  • Irreversible sensorineural hearing loss – the most common form of hearing loss, maybe managed with hearing aids. When hearing aids are not enough, this type of hearing loss can be surgically treated with cochlear implants.
There are four levels of deafness or hearing impairment. These are
  • Mild deafness or mild hearing impairment – The person can only detect sounds between 25 and 29 decibels (dB). They may find it hard to understand the words other people are saying, especially if there is a lot of background noise.
  • Moderate deafness or moderate hearing impairment – The person can only detect sounds between 40 and 69 dB. Following a conversation using hearing alone is very difficult without using a hearing aid.
  • Severe deafness – The person only hears sounds above 70 to 89 dB. A severely deaf person must either lip-read or use sign language in order to communicate, even if they have a hearing aid.
  • Profound deafness – Anybody who cannot hear a sound below 90dB has profound deafness. Some people with profound deafness cannot hear anything at all, at any decibel level. Communication is carried out using sign language, lip-reading, or reading and writing.

Causes of Hearing Loss

The normal hearing function involves sound waves arriving at the auricle, passing through the external auditory canal (EAC), causing a vibration of the tympanic membrane . Vibration then gets transmitted via the ossicles (malleus, incus, stapes) to the cochlea. Subsequently, hair cells inside the cochlea stimulate the eighth cranial nerve that transfers the stimuli to the brain. Processing of crude sounds occurs in the higher cortices of the brain and this includes the comprehension of language.

Hearing loss can be conductive, sensorineural, or mixed. Conductive hearing loss takes place with disruption of the transmission of the sound waves to the cochlea. The most common causes include abnormal formation of the auricle or helix, cerumen impaction, ear canal foreign bodies, otitis externa, dysfunction or fixation of the ossicular chain, and middle ear effusion. Cholesteatoma, a benign though locally-destructive trapping of squamous debris arising from the tympanic membrane, as well as other benign or malignant tumors, can result in conductive hearing loss.

Sensorineural hearing loss (SNHL) usually results from problematic transmission of the stimuli at or after the cochlea. This loss could be related to hair cell dysfunction or a disorder of the eighth nerve itself. The main difference between the two kinds of hearing loss, apart from the pathophysiological features, is that patients with conductive hearing loss perceive the sounds diminished, while SNHL patients may perceive the sounds diminished and distorted.

Hearing loss that involves problematic transmission before and after the cochlea is called mixed hearing loss.

There are multiple reasons for hearing impairment. In the pediatric population, genetic causes are the most common, accounting for more than 50% of hearing loss. Genetic causes involve various syndromes that have hearing loss as one of their features; however, there is an entire entity of non-syndromic genetic hearing loss, wherein patients suffer hearing loss while the rest of their function is normal. Mutations, autosomal differences, as well as unknown genetic diversity, relates to this type of hearing loss. Prenatal causes can also relate to hearing loss in infants. These include exposure to various bacterial or viral infections as well as different teratogens. Perinatal causes are less common, predominantly related to prematurity, low APGAR score, neonatal jaundice, and sepsis. Postnatal causes such as meningococcal infections and mumps can also cause hearing loss as a late complication, as well as head injuries or chronic or recurrent otitis media.

Age-related hearing loss involves a gradual reduction of hearing capacity of the individual and poor speech discrimination scores, most noticeable initially in noisy environments, which is likely related to age-related degeneration of the cochlea in various sites, particularly the hair cells. Otosclerosis and cholesteatomas are leading causes of conductive hearing loss. Another entity that can occur in the adult population is sudden sensorineural hearing loss. This condition is very specific, with a sudden or rapid onset of hearing loss in one ear. This is often preceded by a viral upper respiratory infection, and virally-mediated inflammatory markers are the presumed cause.

Hearing loss can be broadly characterized as congenital or acquired in the pediatric population.

Congenital causes

Congenital causes may lead to hearing loss being present or acquired soon after birth. Hearing loss can be caused by hereditary and non-hereditary genetic factors or by certain complications during pregnancy and childbirth, including:

  • maternal rubella, syphilis, or certain other infections during pregnancy;
  • low birth weight;
  • birth asphyxia (a lack of oxygen at the time of birth);
  • inappropriate use of particular drugs during pregnancy, such as aminoglycosides, cytotoxic drugs, antimalarial drugs, and diuretics;
  • severe jaundice in the neonatal period, which can damage the hearing nerve in a newborn infant.

Acquired causes

Acquired causes may lead to hearing loss at any age, such as:

  • infectious diseases including meningitis, measles and mumps;
  • chronic ear infections;
  • collection of fluid in the ear (otitis media);
  • use of certain medicines, such as those used in the treatment of neonatal infections, malaria, drug-resistant tuberculosis, and cancers;
  • injury to the head or ear;
  • excessive noise, including occupational noise such as that from machinery and explosions;
  • recreational exposure to loud sounds such as that from use of personal audio devices at high volumes and for prolonged periods of time and regular attendance at concerts, nightclubs, bars and sporting events;
  • ageing, in particular due to degeneration of sensory cells; and
  • wax or foreign bodies blocking the ear canal.

Among children, chronic otitis media is a common cause of hearing loss.

High-risk factors in neonates
  • Damage to the inner ear – Aging and exposure to loud noise may cause wear and tear on the hairs or nerve cells in the cochlea that send sound signals to the brain. When these hairs or nerve cells are damaged or missing, electrical signals aren’t transmitted as efficiently, and hearing loss occurs. Higher pitched tones may become muffled to you. It may become difficult for you to pick out words against background noise.
  • The gradual buildup of earwax – Earwax can block the ear canal and prevent conduction of sound waves. Earwax removal can help restore your hearing.
  • Ear infection and abnormal bone growths or tumors – In the outer or middle ear, any of these can cause hearing loss.
  • Ruptured eardrum (tympanic membrane perforation) – Loud blasts of noise, sudden changes in pressure, poking your eardrum with an object and infection can cause your eardrum to rupture and affect your hearing.
  • Congenital infections
  • Family history
  • Craniofacial anomalies
  • Hyperbilirubinemia
  • Birth weight 1500 g
  • Low Apgar
  • Bacterial meningitis
  • Need to prolonged intubation
  • chickenpox
  • cytomegalovirus
  • mumps
  • meningitis
  • sickle cell disease
  • syphilis
  • lyme disease
  • diabetes
  • hypothyroidism
  • arthritis
  • some cancers
  • teenagers exposed to second-hand smoke

Symptoms of Hearing Loss

Signs and symptoms of hearing loss may include:

  • Muffling of speech and other sounds
  • Difficulty understanding words, especially against background noise or in a crowd
  • Trouble hearing consonants
  • Frequently asking others to speak more slowly, clearly and loudly
  • Needing to turn up the volume of the television or radio
  • Withdrawal from conversations
  • Avoidance of some social settings
  • difficulty using the telephone
  • loss of sound localization
  • difficulty understanding speech, especially of children and women whose voices are of a higher frequency.
  • difficulty understanding speech in the presence of background noise (cocktail party effect)
  • sounds or speech sounding dull, muffled or attenuated
  • need for increased volume on television, radio, music and other audio sources
  • pain or pressure in the ears
  • a blocked feeling
  • hyperacusis, heightened sensitivity with accompanying auditory pain to certain intensities and frequencies of sound, sometimes defined as “auditory recruitment”
  • tinnitus, ringing, buzzing, hissing or other sounds in the ear when no external sound is present
  • vertigo and disequilibrium
  • trypanophobia, also known as Euphonia, abnormal hearing of one’s own voice and respiratory sounds, usually as a result of a patulous (a constantly open) eustachian tube or dehiscent superior semicircular canals
  • disturbances of facial movement (indicating a possible tumor or stroke) or in persons with Bell’s Palsy

Hearing impairment in infants

The following signs may indicate a hearing problem:

  • Before the age of 4 months, the baby does not turn their head toward a noise.
  • By the age of 12 months, the baby still has not uttered a single word.
  • The infant does not appear to be startled by a loud noise.
  • The infant responds to you when they can see you, but respond far less or do not respond at all when you are out of sight and call out their name.
  • The infant only seems to be aware of certain sounds.

Hearing impairment in toddlers and children

These signs might become more evident in slightly older children:

  • The child is behind others the same age in oral communication.
  • The child keeps saying “What?” or “Pardon?”
  • The child talks in a very loud voice, and tends to produce louder-than-normal noises.
  • When the child speaks, their utterances are not clear.

Signs of hearing loss in 1 ear

It’s not always easy to tell if you’ve lost hearing in 1 ear, as you may still be able to hear with your other ear.

Signs of a hearing problem in 1 ear include:

  • your hearing is worse when sound comes from 1 side
  • all sounds seem generally quieter than usual
  • finding it hard to tell where sound is coming from
  • difficulty ignoring background noise or telling different sounds apart
  • finding speech unclear
  • difficulty hearing in noisy places or over long distances

Hearing loss in 1 ear is often caused by sound temporarily being unable to pass through the ear – for example, because of earwax or an ear infection.

Signs of hearing loss in children

Your child may have a problem with their hearing if they:

  • are slow to learn to talk, or are n’t clear when they speak
  • do not reply when you call them
  • talk very loudly
  • ask you to repeat yourself or respond inappropriately to questions
  • turn up the volume of the TV very high

Hearing loss in children can be caused by a build-up of fluid in the ear (glue ear), which tends to get better over time and can be treated.

Signs of hearing loss in babies

Babies have a hearing check in the first few weeks after birth, but speak to your health visitor or see a GP if you think they might have difficulty hearing.

They may have a problem with their hearing if they:

  • are not startled by loud noises
  • seem to hear some sounds but not others
  • notice you when they see you, but not when you call their name
  • do not turn towards voices by 4 months of age
  • have not started to say any recognizable words by around 15 months

Diagnosis of Hearing Loss

History and Physical

History in pediatric cases is critical for early diagnosis of hearing loss. This history involves questions regarding the prenatal history of the child, their delivery, and the first days of life as well as the post-natal history up until the moment of the symptom presentation, as well as a family history of hearing loss. A child with hearing loss may present with non-reaction to sounds, behavioral problems, speech issues, language delay, or even school failure, as well as mispronouncing words. Family history, especially if there is a member with early hearing loss, also has great value in suspecting hearing loss.

Adult history acquisition is more straightforward and involves questions regarding the onset of symptoms, the severity, the presence of vertigo, neurological symptoms, infections, and other conditions that could be related to hearing loss. Past medical history, as well as family history, along with work and noise exposure, are also important. In this way, there is a differentiation between the causes of hearing loss, and the clinician can proceed to the appropriate investigations.

Physical examination involves a full otolaryngology examination, with otoscopy bilaterally (including pneumatic otoscopy) to rule out any obvious conductive hearing loss. Foreign bodies, cerumen, infections, tympanic membrane perforations, as well as middle ear effusion, need to be ruled out in the first instance. Subsequently, identification of dysmorphic and other physical findings is essential, especially in young children and infants. These can include facial abnormalities or asymmetry, ear, neck and skin anomalies, other organ dysfunction, or even balance irregularities. As a result, a comprehensive inspection, otoscopy, and neurological examination are crucial to reach the correct diagnosis. Weber and Rinne tests are easy, fast, and globally useful to differentiate between SNHL and conductive hearing loss and may aid in interpreting the formal audiogram.

Evaluation

An accurate hearing evaluation is possible for the population of all ages, though there are specific limitations that are age- or cognition-related regarding formal audiometric evaluation that may complicate the picture. According to the American Academy of Pediatrics as well as the Joint Committee on Infant Hearing, all infants should undergo a hearing evaluation to rule out any hearing impairment at birth, or by the age of one month. Additionally, all newborns and infants with hearing loss need to get a comprehensive evaluation that focuses on medical and birth history as well as a family history for the previous three generations according to the American College of Medical Genetics and Genomics.

Hearing loss evaluation can differ according to the age of the child. BAER (brainstem audio-evoked response) test is the method for early diagnosis of hearing loss in newborns and infants. Otoacoustic emissions are also an option in newborns, and it is an easy, inexpensive technique, but they are less reliable than BAER tests. Finally, audiometry works with older children, aged 4 to 5 and older, who can respond to sound stimuli according to instructions. There are age-specific audiometric tests that can be performed. Young, pre-lingual, children can be conditioned to respond to play stimuli that can assess whether they can hear. This method of testing is not ear-specific, and can only confirm they have at least one ear that can hear at a given test level. This is important because as long as there is one ear that hears at a normal level, normal language development can be expected. Tympanograms and audiograms are of value in adults and children, but provide information only regarding the mobility of the tympanic membrane.

General screening test

A doctor may ask the patient to cover one ear and describe how well they hear words spoken at different volumes, as well as checking sensitivity to other sounds. If the doctor suspects a hearing problem, they will probably be referred to either an ear, nose, and throat (ENT) specialist or an audiologist.

Further tests will be carried out, including:
  • A tuning fork test – This is also known as the Rinne test. A tuning fork is a metal instrument with two prongs that produces a sound when it is struck. Simple tuning fork tests may help the doctor detect whether there is any hearing loss, and where the problem is. A tuning fork is vibrated and placed against the mastoid bone behind the ear. The patient is asked to indicate when they no longer hear any sound. The fork, which is still vibrating, is then placed 1 to 2 centimeters (cm) from the auditory canal. The patient is asked again whether they can hear the fork.
  • Audiometer test – The patient wears earphones, and sounds are directed into one ear at a time. A range of sounds is presented to the patient at various tones. The patient has to signal each time a sound is heard. Each tone is presented at various volumes, so that the audiologist can determine at which point the sound at that tone is no longer detected. The same test is carried out with words. The audiologist presents words at various tones and decibel levels to determine where the ability to hear stops.
  • Bone oscillator test – This is used to find out how well vibrations pass through the ossicles. A bone oscillator is placed against the mastoid. The aim is to gauge the function of the nerve that carries these signals to the brain.
  • App-based hearing tests – Mobile apps are available that you can use by yourself on your tablet to screen for moderate hearing loss.
  • Tuning fork tests – Tuning forks are two-pronged, metal instruments that produce sounds when struck. Simple tests with tuning forks can help your doctor detect hearing loss. This evaluation may also reveal where in your ear the damage has occurred.
  • Audiometer tests – During these more-thorough tests conducted by an audiologist, you wear earphones and hear sounds and words directed to each ear. Each tone is repeated at faint levels to find the quietest sound you can hear.
Routine screening of children

The American Academy of Pediatrics (AAP) recommends that children have their hearing tests at the following times:

  • when they start school
  • at 6, 8, and 10 years of age
  • at least once when they are in middle school
  • once during high school
Testing newborns

The otoacoustic emissions (OAE) test involves inserting a small probe into the outer ear; it is usually done while the baby is asleep. The probe emits sounds and checks for “echo” sounds bouncing back from the ear. If there is no echo, the baby might not necessarily have a hearing problem, but doctors will need to carry out further tests to make sure and to find out why

Treatment of Hearing Loss

Management of conductive hearing loss focuses on the treatment of the underlying disease. Conservative methods such as removal of the foreign body, micro-suction of the cerumen or discharge in the ear canal are necessary if the ear canal is blocked . With regards to otitis media, myringotomy to release the middle ear fluid will allow the sound wave to reach the cochlea, while ventilation tubes are useful if the otitis media is persistent, causing hearing loss. However, evidence shows that hearing loss can represent a post-operative complication due to tympanosclerosis, though this is very rare. Finally, if the hearing loss is due to cholesteatoma, this requires surgical removal with results in hearing restoration dependent upon the degree of destruction of the middle ear structures. Chronic or refractory, inoperable, conductive hearing loss can be treated with bone-conduction hearing aids or via a BAHA, a bone-implanted conduction aid, with excellent results.

Conservative treatment of sensorineural hearing involves the use of assistive listening devices and amplification. Hearing aids are devices designed to improve audition up to 40 to 60 dB with good results. They require individualized fittings and venting plans and can be very expensive.  The overall results are very good. Surgical treatment is provided to infants diagnosed with SNHL, as they undergo cochlear implantation under the age of 6 months. The intervention requires an ear, nose, and throat specialist, and long-term monitoring is essential to ensure normal linguistic and social development of the child. Similarly, refractory, severe SNHL in adults can be treated with cochlear implantation. This will destroy any remnant native hearing, replacing it with the device, so this must be done judiciously. Excellent outcomes have been achieved routinely with this procedure in severe SNHL.

Examples of hearing aids include

  • Behind-the-ear (BTE) hearing aids – These consist of a dome called an earmold and a case, with a connection linking one to the other. The case sits behind the outer ear, with the connection to the dome coming down the front of the ear. The sound from the device is either electrically or acoustically routed to the ear. BTE hearing aids tend to last longer than other devices, as the electrical components are located outside the ear, meaning that there is less moisture and earwax damage These devices are more popular with children who need a sturdy and easy-to-use device.
  • In-the-canal (ITC) hearing aids – These fill the outer part of the ear canal and can be seen. Soft ear inserts, usually made of silicone, are used to position the loudspeaker inside the ear. These devices fit most patients straight away and have better sound quality.
  • Completely in the canal (CIC) hearing aids – These are tiny, discreet devices but not recommended for people with severe hearing loss.
  • Bone conduction hearing aids – These assist people with conductive hearing loss, as well as those unable to wear conventional type hearing aids. The vibrating part of the device is held against the mastoid with a headband. The vibrations go through the mastoid bone, to the cochlea. These devices can be painful or uncomfortable if worn for too long.

Cochlear implants

If the eardrum and middle ear are functioning correctly, a person may benefit from a cochlear implant. This thin electrode is inserted into the cochlea. It stimulates electricity through a tiny microprocessor placed under the skin behind the ear. A cochlear implant is inserted to help patients whose hearing impairment is caused by hair cell damage in the cochlea. The implants usually improve speech comprehension. The latest cochlear implants have new technology that helps patients enjoy music, understand speech better even with background noise, and use their processors while they are swimming.

On the outside, a cochlear implant consists of

  • A microphone: This gathers sound from the environment.
  • A speech processor: This prioritizes the sounds that matter more to the patient, such as speech. The electrical sound signals are split into channels and sent through a very thin wire to the transmitter.
  • A transmitter: This is a coil secured with a magnet. It is located behind the outer ear and transmits the processed sound signals to the internally implanted device.

On the inside

  • A surgeon secures a receiver and stimulator in the bone beneath the skin. The signals are converted into electrical impulses and sent through internal wires to the electrodes.
  • Up to 22 electrodes are wound through the cochlea. The impulses are sent to the nerves in the lower passages of the cochlea and then directly to the brain. The number of electrodes depends on the manufacturers of the implant.

Children will usually have cochlear implants in both ears, while adults tend to have just one.

Sign language and lip-reading

Sign language can help communication between people who are no longer able to hear. Some people with hearing impairment may have speech problems, as well as difficulties in understanding speech from other people. A high percentage of people with hearing impairment can learn other ways of communicating. Lip reading and sign language can replace or complement oral communication. There is a range of sign languages that are, in some cases, wildly different to one another.

Lip-reading

Also known as speechreading, lip reading is a method for understanding spoken language by watching the speaker’s lip, facial and tongue movements, as well as extrapolating from the data provided by the context and any residual hearing the patient might have. People who became hearing impaired after they learned to speak can pick up lip reading rapidly; this is not the case for those who are born hearing-impaired.

Sign language

This is a language that uses signs made with the hands, facial expressions, and body postures, but no sounds. It is used mainly by those who are deaf. There are several different types of sign languages. British Sign Language (BSL) is very different from American Sign Language (ASL). For instance, BSL uses a two-handed alphabet, whereas American sign language uses a one-handed alphabet. Some countries use the sign language introduced by missionaries from far away. Norwegian sign language, for example, is used in Madagascar. Sign language is completely different from the spoken form, word order, and grammar in BSL is not the same as it is in spoken English. ASL is more grammatically similar to spoken Japanese than spoken English.

Prevention

Overall, it is suggested that half of all cases of hearing loss can be prevented through public health measures.

In children under 15 years of age, 60% of hearing loss is attributable to preventable causes. This figure is higher in low- and middle-income countries (75%) as compared to high-income countries (49%). Overall, preventable causes of childhood hearing loss include:

  • Infections such as mumps, measles, rubella, meningitis, cytomegalovirus infections, and chronic otitis media (31%).
  • Complications at the time of birth, such as birth asphyxia, low birth weight, prematurity, and jaundice (17%).
  • Use of ototoxic medicines in expecting mothers and babies (4%).
  • Others (8%)

Some simple strategies for prevention of hearing loss include

  • immunizing children against childhood diseases, including measles, meningitis, rubella and mumps;
  • immunizing adolescent girls and women of reproductive age against rubella before pregnancy;
  • preventing cytomegalovirus infections in expectant mothers through good hygiene; screening for and treating syphilis and other infections in pregnant women;
  • strengthening maternal and child health programs, including the promotion of safe childbirth;
  • following healthy ear care practices;
  • reducing exposure (both occupational and recreational) to loud sounds by raising awareness about the risks; developing and enforcing relevant legislation; and encouraging individuals to use personal protective devices such as earplugs and noise-canceling earphones and headphones.
  • screening of children for otitis media, followed by appropriate medical or surgical interventions;
  • avoiding the use of particular drugs which may be harmful to hearing, unless prescribed and monitored by a qualified physician;
  • referring infants at high risks, such as those with a family history of deafness or those born with low birth weight, birth asphyxia, jaundice, or meningitis, for early assessment of hearing, to ensure prompt diagnosis and appropriate management, as required;
  • implementing the WHO-ITU global standard for personal audio systems and devices. This can be done by governments and manufacturers of smartphones and MP3 players. If adhered to, the standard could help prevent hearing loss due to listening practices that are harmful to hearing; and
  • educating young people and the population in general on hearing loss, its causes, prevention, and identification.

The following measures may help protect your hearing

  • TV, radio, music players, and toys – Do not set the volume too high. Children are especially sensitive to the damaging effects of loud music. Noisy toys can put children’s hearing at risk.
  • Headphones – Focus on isolating the sounds you want to hear and blocking out as much environmental sound as is possible, instead of drowning it out with high volume.
  • Occupational health – If you work in a noisy environment, such as discos, nightclubs, and pubs, wear earplugs or earmuffs.
  • Leisure venues – If you go to pop concerts, motor racing, drag racing, and other noisy events, wear earplugs.
  • Cotton swabs – Do not prod them into adult or infant ears. The same applies to Q-tips or tissues.

Staging

According to the American National Standards Institute, hearing loss ranking is as follows:

  • Slight hearing loss: 16 to 25 dB
  • Mild hearing loss: 26 to 40 dB
  • Moderate hearing loss: 41 to 55 dB
  • Severe hearing loss: 71 to 90 dB
  • Profound: over 90 dB

Complications

Complications of hearing loss in children involve speech delay and failure to thrive in school. Any child with a speech delay requires a formal hearing evaluation, as this is the most common cause.

Adult patients, who are frequently elderly, can easily become isolated and depressed if their hearing loss is not addressed.

WHO response

WHO assists Members States in developing programs for ear and hearing care that are integrated into the primary health-care system of the country. WHO’s work includes:

  • providing technical support to the Member States in the development and implementation of national plans for hearing care;
  • providing technical resources and guidance for training of health-care workers on hearing care;
  • developing and disseminating recommendations to address the major preventable causes of hearing loss;
  • undertaking advocacy to raise awareness about the prevalence, causes, and impact of hearing loss as well as opportunities for prevention, identification, and management;
  • developing and disseminating evidence-based tools for effective advocacy;
  • observing and promoting World Hearing Day as an annual advocacy event;
  • building partnerships to develop strong hearing care programmes, including initiatives for affordable hearing aids, cochlear implants and services;
  • collating data on deafness and hearing loss to demonstrate the scale and the impact of the problem;
  • launching and promoting the WHO-ITU global standard for personal audio systems and devices;
  • promoting safe listening to reduce the risk of recreational noise-induced hearing loss through the WHO Make Listening Safe initiative;
  • raising awareness on safe listening to reduce the risk of recreational noise-induced hearing loss through the WHO Make Listening Safe initiative;
  • promoting the social inclusion of people with disabilities, including people with hearing loss and deafness, for example, through community-based rehabilitation networks and programs.
  • launching and hosting the World Hearing Forum, which is a global advocacy alliance of all stakeholders in the field of hearing.
  • In 2017, the 70th World Health Assembly adopted a resolution on the prevention of deafness and hearing loss. This resolution calls upon the Member States to integrate strategies for ear and hearing care within the framework of their primary health care systems, under the umbrella of universal health coverage. It also requests WHO to undertake a number of actions for the promotion of ear and hearing care at the global level, including many of those noted above.

References

Enlarge Spleen – Causes, Symptoms, Treatment

Enlarge Spleen/Splenomegaly is defined as enlargement of the spleen measured by weight or size. The spleen plays a significant role in hematopoiesis and immunosurveillance. The major functions of the spleen include clearance of senescent and abnormal erythrocytes and their remnants, opsonized platelets and white blood cells and removal of microorganisms and antigens. The spleen also serves as a secondary lymphoid organ and is the site for maturation and storage of T and B lymphocytes, playing an important role in the synthesis of immunoglobulin G (IgG) by mature B-lymphocytes upon interaction with the T-lymphocytes.  The spleen also synthesizes the immune system peptides properdin and tuftsin. Approximately one-third of circulating platelets are stored in the spleen. The normal position of the spleen is within the peritoneal cavity in the left upper quadrant adjacent to ribs 9 through 12. The normal-sized spleen abuts the stomach, colon, and left kidney.

The size and weight of spleen may vary and correlates with weight, height, and sex of an individual, with larger spleen size seen in men compared to women, and in heavier or taller individuals. A normally sized spleen measures up to 12 cm in craniocaudal length.  A length of 12 cm to 20 cm indicates splenomegaly, and a length greater than 20 cm is definitive of massive splenomegaly. The normal weight of the adult spleen is 70 g to 200 g; a spleen weight of 400 g to 500 g indicates splenomegaly and a spleen weight greater than 1000 g is definitive of massive splenomegaly. The normal-sized spleen is usually not palpable in adults. However, it may be palpable due to variations in body habitus and chest wall anatomy. Splenomegaly may be diagnosed clinically or radiographically using ultrasound, CT imaging, or MRI.  Splenomegaly may be a transient condition due to acute illness or may be due to serious underlying acute or chronic pathology.

Splenomegaly is an enlargement of the spleen.[rx] The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of hypersplenism which include: some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes, or platelets in any combination; a compensatory proliferative response in the bone marrow; and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput-medusae, is an important sign of portal hypertension.[rx]

Types of Enlarge Spleen

Splenomegaly can be classified based on its pathophysiologic mechanism:

  • Congestive  by pooled blood (e.g., portal hypertension)
  • Infiltrative  by invasion by cells foreign to the splenic environment (e.g., metastases, myeloid neoplasms, lipid storage diseases)
  • Immune  by an increase in immunologic activity and subsequent hyperplasia (e.g., endocarditis, sarcoidosis, rheumatoid arthritis)
  • Neoplastic  when resident immune cells originate a neoplasm (e.g., lymphoma).

The standard system for classifying splenomegaly on radiography is:[rx][rx]

  • Normal (not splenomegaly) – the largest dimension is less than 11 cm
  • Moderate splenomegaly – the largest dimension is between 11–20 cm
  • Severe splenomegaly – the largest dimension is greater than 20 cm

Causes of Enlarge Spleen

There are several potential causes of splenomegaly.

  • Liver disease (cirrhosis, hepatitis): Parenchymal liver disease causes increased vascular pressure leading to an increase in spleen size.
  • Hematologic malignancies (lymphomas, leukemias, myeloproliferative disorders): Neoplastic cells cause infiltration of the spleen leading to splenomegaly.
  • Venous thrombosis (portal or hepatic vein thrombosis): This leads to an increase in vascular pressure leading to splenomegaly.
  • Splenic congestion (venous thrombosis, portal hypertension, congestive heart failure).
  • Cytopenias (Immune thrombocytopenic purpura, autoimmune hemolytic anemia, immune-mediated neutropenia, Felty syndrome): Immune-mediated destruction of red blood cells, white blood cells or platelets lead to functional splenomegaly.
  • Splenic sequestration (pediatric sickle cell disease, hemolytic anemias, thalassemias).
  • Acute or chronic infection (bacterial endocarditis, infectious mononucleosis, HIV, malaria, tuberculosis, histiocytosis, abscess).
  • Connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis, Adult-onset Still’s disease, and some familial autoinflammatory syndromes).
  • Infiltrative disorders (sarcoidosis, amyloidosis, glycogen storage diseases).
  • Splenic sequestration (pediatric sickle cell, hemolytic anemias, thalassemias).
  • Focal lesions (hemangiomas, abscess, cysts, metastasis).
  • malaria
  • Hodgkin’s disease
  • leukemia
  • heart failure
  • cirrhosis
  • tumors in the spleen or from other organs that have spread to the spleen
  • viral, bacterial, or parasitic infections
  • inflammatory diseases, such as lupus or rheumatoid arthritis
  • sickle cell disease

The mechanism underlying splenic enlargement varies based on the etiology. In the case of acute infectious illness, the spleen performs increased work in clearing antigens and producing antibodies and increases the number of reticuloendothelial cells contained within the spleen. These increased immune functions may result in splenic hyperplasia. In the case of liver disease and congestion, underlying illness causes increased venous pressure causing congestive splenomegaly. Extramedullary hematopoiesis exhibited in myeloproliferative disorders can lead to splenic enlargement (infiltrative splenomegaly).

The possible causes of moderate splenomegaly (spleen <1000 g) are many and include

Splenomegaly grouped on the basis of the pathogenic mechanism
Increased function Abnormal blood flow Infiltration
Removal of defective RBCs

  • spherocytosis
  • thalassemia
  • hemoglobinopathies
  • nutritional anemias
  • early sickle cell anemia

Immune hyperplasia

Response to infection (viral, bacterial, fungal, parasitic)

  • mononucleosis, AIDS,[15] viral hepatitis
  • subacute bacterial endocarditis, bacterial sepsis
  • splenic abscess, typhoid fever
  • brucellosis, leptospirosis, tuberculosis
  • histoplasmosis
  • malaria, leishmaniasis, trypanosomiasis
  • ehrlichiosis.

Disordered immunoregulation

  • rheumatoid arthritis, including cases of Felty’s syndrome
  • systemic lupus erythematosus
  • serum sickness
  • familial hemophagocytic lymphohistiocytosis
  • autoimmune hemolytic anemia
  • autoimmune lymphoproliferative syndrome, an autosomal dominant disorder
  • sarcoidosis
  • drug reactions

Extramedullary hematopoiesis

  • myelofibrosis
  • marrow infiltration by tumors, leukemias
  • marrow damage by radiation, toxins
Organ Failure

  • cirrhosis

Vascular

  • hepatic vein obstruction
  • portal vein obstruction
  • Budd–Chiari syndrome
  • splenic vein obstruction

Infections

  • hepatic schistosomiasis
  • hepatic echinococcosis
Metabolic diseases

  • Gaucher disease
  • Niemann–Pick disease
  • alpha-mannosidosis
  • Hurler syndrome and other mucopolysaccharidoses[17]
  • amyloidosis
  • Tangier disease

Benign and malignant “infiltrations”

  • leukemias (acute, chronic, lymphoid, and myeloid)
  • lymphomas (Hodgkins and non-Hodgkin’s)
  • myeloproliferative disease
  • metastatic tumors (commonly melanoma)
  • histiocytosis X
  • hemangioma, lymphangioma
  • splenic cysts
  • hamartomas
  • eosinophilic granuloma
  • littoral cell angioma[rx][rx][rx]

Normal spleen (in green)

The causes of massive splenomegaly (spleen >1000 g) are

  • chronic myelogenous leukemia
  • myelofibrosis
  • malaria
  • Inflammatory diseases such as sarcoidosis, lupus, and rheumatoid arthritis
  • Trauma, such as an injury during contact sports
  • Cancer that has spread (metastasized) to the spleen
  • A cyst, a noncancerous fluid-filled sac
    A large abscess, a pus-filled cavity usually caused by a bacterial infection
  • Infiltrative diseases such as Gaucher disease, amyloidosis, or glycogen storage diseases splenic marginal zone lymphoma

Symptoms of Enlarge Spleen

An enlarged spleen may be caused by

  • No symptoms in some cases
  • Pain or fullness in the left upper abdomen that may spread to the left shoulder
  • Feeling full without eating or after eating only a small amount from the enlarged spleen pressing on your stomach
  • pressure or pain in the left upper part of your abdomen (near the stomach),
  • feeling full without eating a large meal,
  • or pain your left shoulder blade or shoulder area when taking a deep breath.
  • Anemia
  • Fatigue
  • Frequent infections
  • Easy bleeding

Diagnosis of Enlarged Spleen

History and Physical

The most common physical symptom associated with splenomegaly is vague abdominal discomfort. Patients may complain of pain in the left upper abdomen or referred pain in the left shoulder. Abdominal bloating, distended abdomen, anorexia, and/or early satiety may also occur. More commonly, patients will present with symptoms due to the underlying illness causing splenomegaly. Constitutional symptoms such as weakness, weight loss, and night sweats suggest malignant illness. Patients with splenomegaly due to acute infection may present with fever, rigors, generalized malaise, or focal infectious symptoms. Patients with underlying liver disease may present with symptoms related to cirrhosis or hepatitis. Symptoms of anemia (lightheadedness, dyspnea, or exertion), easy bruising, bleeding, or petechiae may indicate splenomegaly due to the underlying hemolytic process.

Physical examination of the spleen is performed with the patient in supine and right lateral decubitus position with neck, hips, and knees flexed. This positioning relaxes abdominal wall musculature and rotates the spleen more anteriorly. Light fingertip pressure is applied below the left costal margin during deep inspiration. The examiner may feel the rounded edge of the spleen pass underneath the fingertips at maximum inspiration. The exam is abnormal if the spleen is palpated more than 2 cm below the costal margin. In massive splenomegaly, the spleen may be palpated deep into the abdomen, crossing the midline of the abdomen and may even extend into the pelvis. Studies have shown that normal sized spleens may be palpable in approximately 3% of adults.

Patients may have an abnormally palpable spleen with or without exam findings of contributing underlying illness. Patients with splenomegaly due to acute infection may have exam findings consistent with infectious mononucleosis, endocarditis, or malaria. Exam findings of petechiae, abnormal mucosal bleeding, or pallor may accompany hematologic diseases. Jaundice, hepatomegaly, ascites, or spider angiomata may be present in patients with liver disease.  Patients with rheumatologic diseases may present with joint tenderness, swelling, rash, or an abnormal lung exam.

Evaluation

A combination of serum testing and imaging studies may definitively diagnose splenomegaly and the underlying cause. Derangement in the complete blood (cell) counts and morphology including WBC, RBC, and platelets will vary based on the underlying disease state. Abnormalities in liver function tests, lipase, rheumatologic panels, and disease-specific infectious testing aid in the diagnosis of causative disease. Hypersplenism may present with leukopenia, anemia, and thrombocytopenia.

Investigations

Investigations for splenomegaly should be targeted to the most likely underlying cause and include:

  • Blood tests – FBC/blood film/U+E/LFTs/LDH/autoimmune screen/blood culturesHIV test
  • CXR – looking for bihilar lymphadenopathy which may suggest an underlying lymphoproliferative process or infection. Malaria film if recent foreign travel to a malaria-endemic area Echo if infective endocarditis is suspected
  • CT thorax abdop Elvis  – if underlying malignancy suspected. Bone marrow aspirate and trephine if an underlying hematological process is likely
  • Lymph node biopsy – Imaging may be used to diagnose splenomegaly and elucidate its underlying cause. The spleen has a similar attenuation as the liver when measured on CT imaging. In addition to diagnosing splenomegaly (a splenic measurement of greater than 10 cm in craniocaudal length), abdominal CT may detect splenic abscess, mass lesions, vascular abnormalities, cysts, inflammatory changes, traumatic injury, intra-abdominal lymphadenopathy, or liver abnormalities.
  • Sonography in trauma (FAST) exam – uses ultrasound to assess for the presence of fluid where it should not be in trauma evaluation. A FAST exam looks at four windows: pericardial window, Morrison’s pouch (right upper quadrant between liver and right kidney), left upper quadrant (between the spleen and left kidney), and the suprapubic region to look at the bladder and pelvis. The exam is considered positive with fluid in any of these spaces, and combination with hemodynamic instability is an indication for exploratory laparotomy. With positive fluid in the pericardial window, a pericardiocentesis is an appropriate followup.
  • Computed tomography (CT) – are beneficial tools to visualize and characterize the spleen. Both modalities function to measure the spleen and identify physical abnormalities. While not necessary, the use of contrast can aid in tracing blood flow and help identify any leaks or pathologic fluid collection.
  • Ultrasound – is a useful imaging modality in measuring the spleen and spares the patient radiation from CT imaging. Normal spleen size measured via ultrasound is less than 13 cm superior to the inferior axis, 6 cm to 7 cm in medial to lateral axis and 5 cm to 6 cm in anterior to the posterior plane.
  • MRI, PET scans – liver-spleen colloid scanning, and splenectomy and splenic biopsy may be indicated in certain cases.

Treatment of Enlarge Spleen

Treatment of splenomegaly is targeted at treating the underlying disease and protecting the patient from complications of splenomegaly itself.  Patients with splenomegaly from any cause are at increased risk of splenic rupture, and increased attention must be made to protect the patient from abdominal trauma. Treatment ranges from abdominal injury avoidance in the young healthy patient with splenomegaly due to infectious mononucleosis, to splenectomy of a massively enlarged spleen in a patient with hairy cell leukemia. Likewise, the prognosis is largely dependent on the underlying disease state.

  • Splenic sequestration – is seen in sickle cell anemia is often managed with blood transfusions/exchange transfusions. Sometimes splenectomy is required for ITP. Low dose radiation therapy can also shrink the spleen size in patients with primary myelofibrosis.
  • Patients who undergo splenectomy – are at increased risk of infections secondary to encapsulated organisms such as Haemophilus InfluenzaeStreptococcus pneumonia, and Neisseria meningitides. Vaccinations against these organisms are highly recommended in patients who have undergone splenectomy. Careful attention must be paid to post-splenectomy patients presenting with febrile illnesses as they may require more aggressive, empiric antibiotic therapy.
  • If the splenomegaly underlies hypersplenism – splenectomy is indicated and will correct the hypersplenism. However, the underlying cause of hypersplenism will most likely remain; consequently, a thorough diagnostic workup is still indicated, as, leukemia, lymphoma and other serious disorders can cause hypersplenism and splenomegaly. After splenectomy, however, patients have an increased risk for infectious diseases.
  • Infective endocarditis suspected – TTE (transthoracic) +/- TOE (transoesophageal) for vegetations, at least 3 different sets of blood cultures from different sites at the different time should be sent and discuss with cardiology and microbiology for appropriate treatment

Patients undergoing splenectomy should be vaccinated against Haemophilus influenzaeStreptococcus pneumoniae, and Meningococcus. They should also receive annual influenza vaccinations. Long-term prophylactic antibiotics may be given in certain cases.

Differential Diagnosis

There are several potential causes of splenomegaly, and careful and thorough evaluation is often needed to find the underlying cause of splenomegaly.

These include:

  • Cirrhosis
  • Hepatitis
  • Rheumatoid arthritis
  • Felty syndrome
  • Systemic lupus erythematosus
  • Lymphoma
  • Sickle cell anemia

Liver disease (cirrhosis, hepatitis) is one of the most common causes and history of liver disease, abnormal physical exam findings and elevated liver enzymes in addition to abnormal liver imaging can help diagnose liver diseases.

Hematologic malignancies and metastasis shall be especially considered in patients with constitutional symptoms and weight loss. Abnormal peripheral blood smear and biopsy can assist in diagnosing malignancies.

Autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) frequently are associates with splenomegaly. In RA, the presence of splenomegaly in addition to neutropenia is termed Felty syndrome.

Acute and chronic infections including viral, bacterial, fungal, and mycobacterial infections can all cause splenomegaly and shall be carefully ruled out.

Cytopenias and diseases causing splenic sequestration can be ruled out by complete blood counts, peripheral blood smear and hemoglobin electrophoresis.

Infiltrative disorders such as glycogen storage diseases are a rare cause of splenomegaly and shall be considered if other more common causes are ruled out in patients with other clinical features consistent with these glycogen storage diseases.

References

Splenomegaly – Causes, Symptoms, Treatment

Splenomegaly is defined as enlargement of the spleen measured by weight or size. The spleen plays a significant role in hematopoiesis and immunosurveillance. The major functions of the spleen include clearance of senescent and abnormal erythrocytes and their remnants, opsonized platelets and white blood cells and removal of microorganisms and antigens. The spleen also serves as a secondary lymphoid organ and is the site for maturation and storage of T and B lymphocytes, playing an important role in the synthesis of immunoglobulin G (IgG) by mature B-lymphocytes upon interaction with the T-lymphocytes.  The spleen also synthesizes the immune system peptides properdin and tuftsin. Approximately one-third of circulating platelets are stored in the spleen. The normal position of the spleen is within the peritoneal cavity in the left upper quadrant adjacent to ribs 9 through 12. The normal-sized spleen abuts the stomach, colon, and left kidney.

The size and weight of spleen may vary and correlates with weight, height, and sex of an individual, with larger spleen size seen in men compared to women, and in heavier or taller individuals. A normally sized spleen measures up to 12 cm in craniocaudal length.  A length of 12 cm to 20 cm indicates splenomegaly, and a length greater than 20 cm is definitive of massive splenomegaly. The normal weight of the adult spleen is 70 g to 200 g; a spleen weight of 400 g to 500 g indicates splenomegaly and a spleen weight greater than 1000 g is definitive of massive splenomegaly. The normal-sized spleen is usually not palpable in adults. However, it may be palpable due to variations in body habitus and chest wall anatomy. Splenomegaly may be diagnosed clinically or radiographically using ultrasound, CT imaging, or MRI.  Splenomegaly may be a transient condition due to acute illness or may be due to serious underlying acute or chronic pathology.

Splenomegaly is an enlargement of the spleen.[rx] The spleen usually lies in the left upper quadrant (LUQ) of the human abdomen. Splenomegaly is one of the four cardinal signs of hypersplenism which include: some reduction in the number of circulating blood cells affecting granulocytes, erythrocytes, or platelets in any combination; a compensatory proliferative response in the bone marrow; and the potential for correction of these abnormalities by splenectomy. Splenomegaly is usually associated with increased workload (such as in hemolytic anemias), which suggests that it is a response to hyperfunction. It is therefore not surprising that splenomegaly is associated with any disease process that involves abnormal red blood cells being destroyed in the spleen. Other common causes include congestion due to portal hypertension and infiltration by leukemias and lymphomas. Thus, the finding of an enlarged spleen, along with caput-medusae, is an important sign of portal hypertension.[rx]

Types of Splenomegaly

Splenomegaly can be classified based on its pathophysiologic mechanism:

  • Congestive  by pooled blood (e.g., portal hypertension)
  • Infiltrative  by invasion by cells foreign to the splenic environment (e.g., metastases, myeloid neoplasms, lipid storage diseases)
  • Immune  by an increase in immunologic activity and subsequent hyperplasia (e.g., endocarditis, sarcoidosis, rheumatoid arthritis)
  • Neoplastic  when resident immune cells originate a neoplasm (e.g., lymphoma).

The standard system for classifying splenomegaly on radiography is:[rx][rx]

  • Normal (not splenomegaly) – the largest dimension is less than 11 cm
  • Moderate splenomegaly – the largest dimension is between 11–20 cm
  • Severe splenomegaly – the largest dimension is greater than 20 cm

Causes of Splenomegaly

There are several potential causes of splenomegaly.

  • Liver disease (cirrhosis, hepatitis): Parenchymal liver disease causes increased vascular pressure leading to an increase in spleen size.
  • Hematologic malignancies (lymphomas, leukemias, myeloproliferative disorders): Neoplastic cells cause infiltration of the spleen leading to splenomegaly.
  • Venous thrombosis (portal or hepatic vein thrombosis): This leads to an increase in vascular pressure leading to splenomegaly.
  • Splenic congestion (venous thrombosis, portal hypertension, congestive heart failure).
  • Cytopenias (Immune thrombocytopenic purpura, autoimmune hemolytic anemia, immune-mediated neutropenia, Felty syndrome): Immune-mediated destruction of red blood cells, white blood cells or platelets lead to functional splenomegaly.
  • Splenic sequestration (pediatric sickle cell disease, hemolytic anemias, thalassemias).
  • Acute or chronic infection (bacterial endocarditis, infectious mononucleosis, HIV, malaria, tuberculosis, histiocytosis, abscess).
  • Connective tissue diseases (systemic lupus erythematosus, rheumatoid arthritis, Adult-onset Still’s disease, and some familial autoinflammatory syndromes).
  • Infiltrative disorders (sarcoidosis, amyloidosis, glycogen storage diseases).
  • Splenic sequestration (pediatric sickle cell, hemolytic anemias, thalassemias).
  • Focal lesions (hemangiomas, abscess, cysts, metastasis).
  • malaria
  • Hodgkin’s disease
  • leukemia
  • heart failure
  • cirrhosis
  • tumors in the spleen or from other organs that have spread to the spleen
  • viral, bacterial, or parasitic infections
  • inflammatory diseases, such as lupus or rheumatoid arthritis
  • sickle cell disease

The mechanism underlying splenic enlargement varies based on the etiology. In the case of acute infectious illness, the spleen performs increased work in clearing antigens and producing antibodies and increases the number of reticuloendothelial cells contained within the spleen. These increased immune functions may result in splenic hyperplasia. In the case of liver disease and congestion, underlying illness causes increased venous pressure causing congestive splenomegaly. Extramedullary hematopoiesis exhibited in myeloproliferative disorders can lead to splenic enlargement (infiltrative splenomegaly).

The possible causes of moderate splenomegaly (spleen <1000 g) are many and include

Splenomegaly grouped on the basis of the pathogenic mechanism
Increased function Abnormal blood flow Infiltration
Removal of defective RBCs

  • spherocytosis
  • thalassemia
  • hemoglobinopathies
  • nutritional anemias
  • early sickle cell anemia

Immune hyperplasia

Response to infection (viral, bacterial, fungal, parasitic)

  • mononucleosis, AIDS,[15] viral hepatitis
  • subacute bacterial endocarditis, bacterial sepsis
  • splenic abscess, typhoid fever
  • brucellosis, leptospirosis, tuberculosis
  • histoplasmosis
  • malaria, leishmaniasis, trypanosomiasis
  • ehrlichiosis.

Disordered immunoregulation

  • rheumatoid arthritis, including cases of Felty’s syndrome
  • systemic lupus erythematosus
  • serum sickness
  • familial hemophagocytic lymphohistiocytosis
  • autoimmune hemolytic anemia
  • autoimmune lymphoproliferative syndrome, an autosomal dominant disorder
  • sarcoidosis
  • drug reactions

Extramedullary hematopoiesis

  • myelofibrosis
  • marrow infiltration by tumors, leukemias
  • marrow damage by radiation, toxins
Organ Failure

  • cirrhosis

Vascular

  • hepatic vein obstruction
  • portal vein obstruction
  • Budd–Chiari syndrome
  • splenic vein obstruction

Infections

  • hepatic schistosomiasis
  • hepatic echinococcosis
Metabolic diseases

  • Gaucher disease
  • Niemann–Pick disease
  • alpha-mannosidosis
  • Hurler syndrome and other mucopolysaccharidoses[17]
  • amyloidosis
  • Tangier disease

Benign and malignant “infiltrations”

  • leukemias (acute, chronic, lymphoid, and myeloid)
  • lymphomas (Hodgkins and non-Hodgkin’s)
  • myeloproliferative disease
  • metastatic tumors (commonly melanoma)
  • histiocytosis X
  • hemangioma, lymphangioma
  • splenic cysts
  • hamartomas
  • eosinophilic granuloma
  • littoral cell angioma[rx][rx][rx]

Normal spleen (in green)

The causes of massive splenomegaly (spleen >1000 g) are

  • chronic myelogenous leukemia
  • myelofibrosis
  • malaria
  • Inflammatory diseases such as sarcoidosis, lupus, and rheumatoid arthritis
  • Trauma, such as an injury during contact sports
  • Cancer that has spread (metastasized) to the spleen
  • A cyst, a noncancerous fluid-filled sac
    A large abscess, a pus-filled cavity usually caused by a bacterial infection
  • Infiltrative diseases such as Gaucher disease, amyloidosis, or glycogen storage diseases splenic marginal zone lymphoma

Symptoms of Splenomegaly

An enlarged spleen may be caused by

  • No symptoms in some cases
  • Pain or fullness in the left upper abdomen that may spread to the left shoulder
  • Feeling full without eating or after eating only a small amount from the enlarged spleen pressing on your stomach
  • pressure or pain in the left upper part of your abdomen (near the stomach),
  • feeling full without eating a large meal,
  • or pain your left shoulder blade or shoulder area when taking a deep breath.
  • Anemia
  • Fatigue
  • Frequent infections
  • Easy bleeding

Diagnosis of Splenomegaly

History and Physical

The most common physical symptom associated with splenomegaly is vague abdominal discomfort. Patients may complain of pain in the left upper abdomen or referred pain in the left shoulder. Abdominal bloating, distended abdomen, anorexia, and/or early satiety may also occur. More commonly, patients will present with symptoms due to the underlying illness causing splenomegaly. Constitutional symptoms such as weakness, weight loss, and night sweats suggest malignant illness. Patients with splenomegaly due to acute infection may present with fever, rigors, generalized malaise, or focal infectious symptoms. Patients with underlying liver disease may present with symptoms related to cirrhosis or hepatitis. Symptoms of anemia (lightheadedness, dyspnea, or exertion), easy bruising, bleeding, or petechiae may indicate splenomegaly due to the underlying hemolytic process.

Physical examination of the spleen is performed with the patient in supine and right lateral decubitus position with neck, hips, and knees flexed. This positioning relaxes abdominal wall musculature and rotates the spleen more anteriorly. Light fingertip pressure is applied below the left costal margin during deep inspiration. The examiner may feel the rounded edge of the spleen pass underneath the fingertips at maximum inspiration. The exam is abnormal if the spleen is palpated more than 2 cm below the costal margin. In massive splenomegaly, the spleen may be palpated deep into the abdomen, crossing the midline of the abdomen and may even extend into the pelvis. Studies have shown that normal sized spleens may be palpable in approximately 3% of adults.

Patients may have an abnormally palpable spleen with or without exam findings of contributing underlying illness. Patients with splenomegaly due to acute infection may have exam findings consistent with infectious mononucleosis, endocarditis, or malaria. Exam findings of petechiae, abnormal mucosal bleeding, or pallor may accompany hematologic diseases. Jaundice, hepatomegaly, ascites, or spider angiomata may be present in patients with liver disease.  Patients with rheumatologic diseases may present with joint tenderness, swelling, rash, or an abnormal lung exam.

Evaluation

A combination of serum testing and imaging studies may definitively diagnose splenomegaly and the underlying cause. Derangement in the complete blood (cell) counts and morphology including WBC, RBC, and platelets will vary based on the underlying disease state. Abnormalities in liver function tests, lipase, rheumatologic panels, and disease-specific infectious testing aid in the diagnosis of causative disease. Hypersplenism may present with leukopenia, anemia, and thrombocytopenia.

Investigations

Investigations for splenomegaly should be targeted to the most likely underlying cause and include:

  • Blood tests – FBC/blood film/U+E/LFTs/LDH/autoimmune screen/blood culturesHIV test
  • CXR – looking for bihilar lymphadenopathy which may suggest an underlying lymphoproliferative process or infection. Malaria film if recent foreign travel to a malaria-endemic area Echo if infective endocarditis is suspected
  • CT thorax abdop Elvis  – if underlying malignancy suspected. Bone marrow aspirate and trephine if an underlying hematological process is likely
  • Lymph node biopsy – Imaging may be used to diagnose splenomegaly and elucidate its underlying cause. The spleen has a similar attenuation as the liver when measured on CT imaging. In addition to diagnosing splenomegaly (a splenic measurement of greater than 10 cm in craniocaudal length), abdominal CT may detect splenic abscess, mass lesions, vascular abnormalities, cysts, inflammatory changes, traumatic injury, intra-abdominal lymphadenopathy, or liver abnormalities.
  • Sonography in trauma (FAST) exam – uses ultrasound to assess for the presence of fluid where it should not be in trauma evaluation. A FAST exam looks at four windows: pericardial window, Morrison’s pouch (right upper quadrant between liver and right kidney), left upper quadrant (between the spleen and left kidney), and the suprapubic region to look at the bladder and pelvis. The exam is considered positive with fluid in any of these spaces, and combination with hemodynamic instability is an indication for exploratory laparotomy. With positive fluid in the pericardial window, a pericardiocentesis is an appropriate followup.
  • Computed tomography (CT) – are beneficial tools to visualize and characterize the spleen. Both modalities function to measure the spleen and identify physical abnormalities. While not necessary, the use of contrast can aid in tracing blood flow and help identify any leaks or pathologic fluid collection.
  • Ultrasound – is a useful imaging modality in measuring the spleen and spares the patient radiation from CT imaging. Normal spleen size measured via ultrasound is less than 13 cm superior to the inferior axis, 6 cm to 7 cm in medial to lateral axis and 5 cm to 6 cm in anterior to the posterior plane.
  • MRI, PET scans – liver-spleen colloid scanning, and splenectomy and splenic biopsy may be indicated in certain cases.

Treatment of Splenomegaly

Treatment of splenomegaly is targeted at treating the underlying disease and protecting the patient from complications of splenomegaly itself.  Patients with splenomegaly from any cause are at increased risk of splenic rupture, and increased attention must be made to protect the patient from abdominal trauma. Treatment ranges from abdominal injury avoidance in the young healthy patient with splenomegaly due to infectious mononucleosis, to splenectomy of a massively enlarged spleen in a patient with hairy cell leukemia. Likewise, the prognosis is largely dependent on the underlying disease state.

  • Splenic sequestration – is seen in sickle cell anemia is often managed with blood transfusions/exchange transfusions. Sometimes splenectomy is required for ITP. Low dose radiation therapy can also shrink the spleen size in patients with primary myelofibrosis.
  • Patients who undergo splenectomy – are at increased risk of infections secondary to encapsulated organisms such as Haemophilus InfluenzaeStreptococcus pneumonia, and Neisseria meningitides. Vaccinations against these organisms are highly recommended in patients who have undergone splenectomy. Careful attention must be paid to post-splenectomy patients presenting with febrile illnesses as they may require more aggressive, empiric antibiotic therapy.
  • If the splenomegaly underlies hypersplenism – splenectomy is indicated and will correct the hypersplenism. However, the underlying cause of hypersplenism will most likely remain; consequently, a thorough diagnostic workup is still indicated, as, leukemia, lymphoma and other serious disorders can cause hypersplenism and splenomegaly. After splenectomy, however, patients have an increased risk for infectious diseases.
  • Infective endocarditis suspected – TTE (transthoracic) +/- TOE (transoesophageal) for vegetations, at least 3 different sets of blood cultures from different sites at the different time should be sent and discuss with cardiology and microbiology for appropriate treatment

Patients undergoing splenectomy should be vaccinated against Haemophilus influenzaeStreptococcus pneumoniae, and Meningococcus. They should also receive annual influenza vaccinations. Long-term prophylactic antibiotics may be given in certain cases.

Differential Diagnosis

There are several potential causes of splenomegaly, and careful and thorough evaluation is often needed to find the underlying cause of splenomegaly.

These include:

  • Cirrhosis
  • Hepatitis
  • Rheumatoid arthritis
  • Felty syndrome
  • Systemic lupus erythematosus
  • Lymphoma
  • Sickle cell anemia

Liver disease (cirrhosis, hepatitis) is one of the most common causes and history of liver disease, abnormal physical exam findings and elevated liver enzymes in addition to abnormal liver imaging can help diagnose liver diseases.

Hematologic malignancies and metastasis shall be especially considered in patients with constitutional symptoms and weight loss. Abnormal peripheral blood smear and biopsy can assist in diagnosing malignancies.

Autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) frequently are associates with splenomegaly. In RA, the presence of splenomegaly in addition to neutropenia is termed Felty syndrome.

Acute and chronic infections including viral, bacterial, fungal, and mycobacterial infections can all cause splenomegaly and shall be carefully ruled out.

Cytopenias and diseases causing splenic sequestration can be ruled out by complete blood counts, peripheral blood smear and hemoglobin electrophoresis.

Infiltrative disorders such as glycogen storage diseases are a rare cause of splenomegaly and shall be considered if other more common causes are ruled out in patients with other clinical features consistent with these glycogen storage diseases.

References

Treatment of Ischial Bursitis

Treatment of Ischial Bursitis/Ischial bursitis also is known as ischiogluteal bursitis or weaver’s bottom is a condition where the bursa that lies between the ischial tuberosity and the gluteus maximus muscle becomes inflamed. This bursa is present physiologically in order to reduce the amount of frictional force generated between the gluteal muscle and the ischial tuberosity that otherwise might become damaged or irritated by this contact. This inflammation of the bursa is most commonly caused by prolonged pressure on the ischium, as occurs in sitting for extended periods of time or from the repeated movement of the Gluteus Maximus muscle in such activities as bicycling. These activities cause an inflammatory reaction that results in swelling and tenderness over the lower buttock and upper posterior thigh. Many other differential diagnoses have common presentations such as sciatica and tendonitis of hamstring muscles.

Ischial bursitis or ischiogluteal bursitis is the inflammation of the ischiogluteal bursa due to excessive or inappropriate physical exercise, prolonged sitting, running, repetitive jumping, and kicking. Since ischial bursitis is a rare, infrequently recognized pathology and is difficult to differentiate from the soft tissue disease and tumors (both malignant and benign), herein exemplified is a case with ischiogluteal bursitis whereby the role of magnetic resonance imaging (MRI) in the prompt diagnosis has been highlighted.

Pathophysiology of Ischial Bursitis

Bursa comes in a variety of forms: adventitious, subcutaneous, submuscular, and synovial. An ischial bursa is synovial, meaning it is composed of a fatty connective tissue capsule filled with synovial fluid. When infection or irritation occurs, cells of the synovia proliferate, resulting in increased production of synovial fluid. Inflammatory mediators such as cyclooxygenase, cytokines, and metalloproteases mediate this process. The result is a thick fluid-filled cavity with high amounts of fibrin, resulting in the formation of granulation tissue. Over time, this tissue will gradually interfere with the normal motion and activity of the surrounding tissues whether they are muscle, bone, or tendon.

Types of Ischial Bursitis

An ischial bursa is located between the hamstring muscle and the ischial tuberosity of the pelvis in the buttock area. This area bears the weight of the body when sitting. The hip joint is one of the largest joints in the body. It is composed of one osseous (contains bone) joint. The hip is built for weight-bearing and movement in several different planes. The stability of the hip joint comes from the capsule, ligaments, muscle and a cartilaginous tissue called the labrum. There are four bursae surrounding the hip joint. A bursa is a fluid-filled sack that reduces friction between tendons, and between tendons and bone. The most commonly injured bursa is the trochanteric bursa. The four major bursae of the hip are:

  • Trochanteric Bursa – located on the outside of the hip between the greater trochanter of the femur (leg bone) and the gluteal muscles
  • Ischial Bursa – located between the hamstring muscle and the ischial tuberosity of the pelvis in the buttock area. This area bears the weight of the body when sitting.
  • Iliopsoas Bursa – located in the groin area between the large psoas muscle and femur bone
  • Gluteal Medius Bursa – located between the gluteus medius muscle and the greater trochanter. It is near the trochanteric bursa.

Causes of Ischial Bursitis

  • Muscle Tightness – Tightness in the leg muscles and ischial bursitis itself increases the friction on ischial bursitis. Visit the knee stretches section for simple tests to see if your muscles are tight
  • Muscle Weakness – Weakness in the buttock muscles (glutes) puts more strain on ischial bursitis increasing your chances of developing ischial bursitis.
  • A direct blow to the ischial bursa from falling on the outside of the hip or on the buttocks can produce inflammation and irritation.
  • A fall onto the hip or ischial bursa.
  • Constant pressure on the ischial bursa from lying on that side.
  • Repeated stress or friction injury as the tendon rubs over the ischial bursa during activity. The weakness of the muscles over the ischial bursa.
  • Complications from rheumatoid arthritis, osteoarthritis or gout.
  • Infection of the ischial bursa.
  • The tightness of the structures of the hip like the psoas hip flexor, iliotibial band, and hamstrings.
  • The ischial bursa can become swollen as a response to other hip conditions.
  • Flat Feet – If you have flat feet (dropped foot arches) it slightly changes the angle of the leg, putting more friction through Ischial bursitis
  • Excessive long-distance or hill running – Overuse can also lead to ischial bursitis due to repetitive friction. Hill running puts even more tension through ischial bursitis.
  • Running on a sloped surface –  Lots of running surfaces e.g. roads and running tracks are slightly banked. The foot position on the lower leg causes ischial bursitis to be stretched
  • The sudden increase in activity – Someone who rapidly increases their training is at risk of developing due to the sudden increase in friction at the hip
  • Leg Length Discrepancy – If one leg is slightly shorter than the other it puts more strain on the hip.
  • Bowlegs – The curved nature of bow legs means there is a larger than normal space between the knees. This puts an extra stretch on the bursa

Symptoms of Ischial Bursitis

  • Pain, tenderness, swelling, warmth, or redness  may travel up or down the thigh or leg
  • Initially, pain at the beginning of an exercise that lessens once warmed up; eventually, pain throughout the activity, worsening as the activity continues; may cause the athlete to stop in the middle of training or competing
  • Pain that is worse when running down hills or stairs, on banked tracks, or next to the curb on the street
  • Pain that is felt most when the foot of the affected leg hits the ground
  • Possibly, crepitation (a crackling sound) when the tendon or bursa is moved or touched
  • Stabbing or stinging pain along the outside of the knee
  • A feeling of the snapping over the knee as it bends and straightens
  • Swelling near the outside of your knee
  • Occasionally, tightness and pain at the outside of the hip
  • Continuous pain following activity, particularly with walking, climbing, or descending stairs, or moving from a sitting to a standing position
  • Pain that is worse when running down hills or stairs.
  • Pain that is felt most when the foot of the affected leg hits the ground.
  • Possibly, a crackling sound when the bursa is moved or touched.

Diagnosis of Ischial Bursitis

A thorough subjective and objective examination from a physiotherapist may be sufficient to diagnose ischiogluteal bursitis. Further investigations such as an Ultrasound, X-ray, CT or MRI scan are often required to assist with diagnosis and assess the severity of the condition.

Treatments of Ischial Bursitis

Treatment of ischial bursitis is relatively symptom driven. Primary treatment is lifestyle modification by stopping the activity that caused bursitis in the first place, whether it was a physical activity or sitting for long periods of time on hard surfaces.

  • Rest – People with ischial bursitis may need to cut back on the intensity, duration and frequency of activity that leads to ischial bursitis pain (for example, reduce running or cycling mileage). People with moderate to severe ischial bursitis and pain may need to take time off from their sport and works. It can be frustrating and difficult for active people to cut back on their training schedules; however, rest is necessary for the injury to heal.
  • Ice – Apply ice to the affected area for 5-10 minutes at a time three to five times per day to help reduce inflammation. Make sure you wrap the ice in a thin towel to prevent an ice burn from occurring. You may need to ice the area every day for around 6-12 weeks.
  • Warm-up – Five to 10 minutes of gentle exercise and stretching can literally increase the body’s temperature, helping muscles become more elastic and responsive and reducing the chance of ischial bursitis or other injuries.
  • Change footwear – Switching out shoes and/or getting orthotic inserts can alter a person’s biomechanics and reduce the risk of ischial bursitis pain.
  • Massage – Much like the foam roller exercise, massage may help relieve tension and improve blood flow in-band thereby reducing pain.
  • Avoid Sitting on Hard Seats – Avoiding hard seats or stools is one of the best ways to reduce the pain from bursitis. If you do need to sit down for long periods, use a pillow or a doughnut cushion. Also sit upright and maintain a good posture while sitting.
  • Stretching – A doctor may recommend stretching or yoga to promote flexible muscles and other soft tissue.
  • Change running biomechanics – Runners may consider shortening their stride and running on soft, flat surfaces, such as tracks and even, grassy trails.
  • Change cycling biomechanics – Cyclists may consider adjusting saddle position and pedal clips. Even a small adjustment can alter the biomechanics of their pedaling and reduce ischial bursitis pain.
  • Ultrasound – Efforts to heal ischial bursitis and reduce pain may get a small boost from ultrasound and electrical muscle stimulation.
  • Iontophoresis – Doctors and physical therapists occasionally recommend iontophoresis, which uses a mild electrical current to administer an anti-inflammatory medicine (e.g. dexamethasone) through healthy skin and into the sore area. This treatment may be appropriate for people who can’t tolerate injections or want to avoid injections.
  • Frictional massage – It is recommended to use friction massage additional to the therapy on chronic bursitis because it affects the adhesions in chronic bursal problems. It breaks down scar tissue, increases extensibility and mobility of the structure, promotes normal orientation of collagen fibers, increases blood flow, reduces stress levels, and allows healing to take place. Friction massage is beneficial to the underlying structures. By using the Graston technique of friction massage the patient should be forewarned because it may initially aggravate a chronic subacute inflammation that is present. It is postulated that deep friction, especially with the Graston technique instruments, may initiate a new inflammatory cascade, which is necessary to reach the remodeling stage of the inflammatory process and result in healing of the area.

Medication

Longer-Term Treatment of Ischial Bursitis

  • Strengthening Exercises –  Strengthening the glutes, quads, and hamstrings improves how the hip and knee function which reduces the friction on bursitis. Visit the knee strengthening section for exercises that will help
  • Stretching Exercises – Stretching the quads, hamstrings, and ischial bursitis also helps reduce the friction at the knee. Visit the stretches section to see if tight muscles are likely contributing to your ischial bursitis
  • Gluteus stretch – Lie stretched out on your back with your head supported by a cushion. Bend one knee. With both hands around the knee, pull it slowly toward your chest and hold the position for 5 to 10 seconds. Slowly straighten your leg, and do the same with your other knee. Repeat 5 to 10 times.
  • Piriformis stretch –
  • Sit on the floor with both legs straight. Cross one leg over the other, with your foot along the knee. With the opposite hand, gently pull your bent knee across the middle of your body. Hold this position for 10 to 30 seconds. You should feel a stretch in the muscles of your outer thigh. Repeat with the other leg.
  • Taping – Taping can also be used to reduce the forces going through ischial bursitis – see you physical therapist/ sports injury specialist for more information
  • Massage – Deep tissue massage to the Iliotibial Band can reduce tightness, but it can be quite painful
  • Injections – If other treatments have failed, a cortisone injection can be given to help reduce pain and inflammation. However, it should always be accompanied by strengthening and stretching exercises to ensure the problem doesn’t return
  • Orthotics – Special insoles can be worn in your shoes to correct poor foot positions such as flat feet. See an orthopedist for a full assessment and advice

Physical Therapists

Common Physical Therapy interventions in the treatment of Hip Bursitis (Ischial Bursa) include:

  • Manual Therapeutic Technique (MTT) – hands-on care including soft tissue massage, stretching and joint mobilization by a physical therapist to regain mobility and range of motion of the knee. The use of mobilization techniques also helps to modulate pain.
  • Therapeutic Exercises (TE) – including stretching and strengthening exercises to regain range of motion and strengthen muscles of the knee to support, stabilize, and decrease the stresses placed on the ischial bursa and tendons of the hip joint.
  • Neuromuscular Reeducation (NMR) – to restore stability, retrain the lower extremity and improve movement techniques and mechanics (for example, running, kneeling, squatting and jumping) of the involved lower extremity to reduce stress on ischial bursa and tendons in daily activities.
  • Modalities including the use of ultrasound –  electrical stimulation, ice, cold laser, and others to decrease pain and inflammation of the ischial bursa.
  • A home program that includes strengthening, stretching and stabilization exercises and instructions to help the person perform daily tasks and advance to the next functional level.
  • In addition to the home program –  it is often necessary to initiate therapy in our office to directly treat the bursa.  Our office will usually use therapeutic ultrasound, electrical stimulation, transverse friction, cross friction or active release massage in addition to manual muscle and joint manipulation to treat this painful condition.  We will also employ correct stretching and strengthening exercises as well as Kinesio or KT Tape to help stabilize the region between treatment sessions.

References

Treatment of Ischial BursitisTes

What Is Appendicitis? Causes, Symptoms, Treatment

What Is Appendicitis?/Appendicitis is an inflammation of the appendix that may lead to an abscess, ileus, peritonitis, or death if untreated. Appendicitis is the most common abdominal surgical emergency. The current standard treatment of uncomplicated appendicitis is usually surgery, but there has been increasing evidence published on the use of antibiotics.

Appendicitis is inflammation of the vermiform appendix. This is a hollow organ located at the tip of the cecum, usually in the right lower quadrant of the abdomen. The appendix develops embryonically in the fifth week. During this time there is a movement of the midgut to the external umbilical cord with the eventual return to the abdomen and rotation of the cecum. This results in the usual retrocecal location of the appendix. It is most often a disease of acute presentation, usually within 24 hours, but it can also present as a more chronic condition. If there has been a perforation with a contained abscess, then the presenting symptoms can be more indolent. The exact function of the appendix has been a debated topic. Today it is accepted that this organ may have an immunoprotective function and acts as a lymphoid organ especially in the younger person. Other theories contend that the appendix acts as a storage vessel for “good” colonic bacteria. Still, others argue that it is a mear developmental remnant and has no real function.

Anatomy of Appendicitis

The vermiform appendix is a tubular structure attached to the base of the caecum at the confluence of the taeniae coli. It is approximately 8-10 cm long in adults and represents the underdeveloped distal end of the large caecum seen in other animals. In humans it is regarded as a vestigial organ, and acute inflammation of this structure is called acute appendicitis

  • Retrocaecal/retrocolic (75%)—Right loin pain is often present, with tenderness on examination. Muscular rigidity and tenderness to deep palpation are often absent because of protection from the overlying caecum. The psoas muscle may be irritated in this position, leading to hip flexion and exacerbation of the pain on hip extension (psoas stretch sign)
  • Subcaecal and pelvis (20%)—Suprapubic pain and urinary frequency may predominate. Diarrhea may be present as a result of irritation of the rectum. Abdominal tenderness may be lacking, but rectal or vaginal tenderness may be present on the right. Microscopic haematuria and leucocytes may be present on urine analysis
  • Pre-ileal and post-ileal (5%)—Signs and symptoms may be lacking. Vomiting may be more prominent, and diarrhea may result from irritation of the distal ileum

Direct and indirect (secondary) signs of acute appendicitis in graded-compression, real-time US, colour Doppler and contrast-enhanced US (CEUS; adopted according to references 7, 9, 20 and 21)

Causes of Appendicitis

A blockage in the lining of the appendix that results in infection is the likely cause of appendicitis. The bacteria multiply rapidly, causing the appendix to become inflamed, swollen and filled with pus. If not treated promptly, the appendix can rupture.

There are numerous issues that can cause appendix luminal blockage, including:

  • Appendicoliths or fecaliths, which are calcified fecal deposits, also known as “appendix stones” (this is more common in children than adults) (rx)
  • Intestinal worms or parasites, including pinworm (Enterobius vermicularis)
  • Irritation and ulcers in the gastrointestinal (GI) tract resulting from long-lasting disorders, such as Crohn’s disease or ulcerative colitis
  • Abdominal injury or trauma
  • Enlarged lymph tissue of the wall of the appendix, which is typically the result of infections in the GI tract
  • Benign or malignant tumors
  • Various foreign objects, such as stones, bullets, air gun pellets, and pins (rx)
  • Sometimes appendicitis is due to a viral, bacterial, or fungal infection that has spread to the appendix. (rx) Possible causes of infection include, but are not limited to:
  • E. coli, which are bacteria found in the environment, foods, and intestines of animals. Most strains of E. coli are harmless, but others can cause illness. (rx)
  • Pseudomonas bacteria, which are found in soil and water and moist areas such as sinks and toilets (rx)
  • Bacteroides, bacteria that already inhabit the digestive tract of humans (rx)
  • Adenovirus, a very common virus spread through contact or through the air that can cause cold-like symptoms as well as bladder and other infections. (rx)
  • Salmonella, a foodborne bacteria that typically causes gastrointestinal upset (diarrhea, nausea, and vomiting) but can have serious complications
  • Shigella bacteria, germs that are very contagious and typically result in diarrheal illness that usually lasts no more than a week. (rx)
  • Measles, a highly contagious virus spread through the air and contact. Vaccination protects most of the population, but there are outbreaks in which unvaccinated people are susceptible (rx)
  • The fungal infections mucormycosis (a rare but serious mold infection caused by environmental molds) (rx) and histoplasmosis; most people who breathe in these spores won’t get sick or will have mild symptoms, but infection can become severe in people with weakened immune systems (11

Appendicitis can have more than one cause, and in many cases, the cause is not clear. Possible causes include

  • Blockage of the opening inside the appendix
  • enlarged tissue in the wall of your appendix, caused by an infection in the gastrointestinal (GI) tract or elsewhere in your body
  • inflammatory bowel disease
  • stool, parasites, or growths that can clog your appendiceal lumen
  • trauma to your abdomen

Appendicitis can cause serious complications, such as:

  • A ruptured appendix – A rupture spreads infection throughout your abdomen (peritonitis). Possibly life-threatening, this condition requires immediate surgery to remove the appendix and clean your abdominal cavity.
  • A pocket of pus that forms in the abdomen – If your appendix bursts, you may develop a pocket of infection (abscess). In most cases, a surgeon drains the abscess by placing a tube through your abdominal wall into the abscess. The tube is left in place for two weeks, and you’re given antibiotics to clear the infection.


Symptoms of Appendicitis

Classically, appendicitis presents as an initial generalized or periumbilical abdominal pain that then localizes to the right lower quadrant. Initially, as the visceral afferent nerve fibers at T8 through T10 are stimulated, and this leads to vague centralized pain. As the appendix becomes more inflamed and the adjacent parietal peritoneum is irritated, the pain becomes more localized to the right lower quadrant. Pain may or may not be accompanied by any of the following symptoms:

  • Sudden pain that begins on the right side of the lower abdomen
  • Sudden pain that begins around your navel and often shifts to your lower right abdomen
  • Pain that worsens if you cough, walk or make other jarring movements
  • Nausea and vomiting
  • Loss of appetite
  • Low-grade fever that may worsen as the illness progresses
  • Constipation or diarrhea
  • Abdominal bloating
  • Anorexia
  • Nausea/vomiting
  • Fever (40% of patients)
  • Diarrhea
  • Generalize malaise
  • Urinary frequency or urgency
  • begins near your belly button and then moves lower and to your right
  • Gets worse in a matter of hours
  • Gets worse when you move around, take deep breaths, cough, or sneeze
  • Is severe and often described as different from any pain you’ve felt before
  • Occurs suddenly and may even wake you up if you’re sleeping
  • An inability to pass gas
  • A low-grade fever
  • Swelling in your abdomen
  • The feeling that having a bowel movement will relieve discomfort

Symptoms can be different for each person and can seem like the following conditions that also cause pain in the abdomen:

  • Abdominal adhesions
  • Constipation
  • Inflammatory bowel disease, which includes Crohn’s disease and ulcerative colitis, long-lasting disorders that cause irritation and ulcers in the GI tract
  • Intestinal obstruction
  • Pelvic inflammatory disease

As inflammation progresses, signs of peritoneal inflammation develop. Signs include:

  • Right lower quadrant guarding and rebound tenderness over McBurney’s point (1.5 to 2 inches from the anterior superior iliac spine on a straight line from the ASIS to the umbilicus)
  • Rovsing’s sign (right lower quadrant pain elicited by palpation of the left lower quadrant)
  • Dunphy’s sign (increased abdominal pain with coughing)

Other associated signs such as psoas sign (pain on external rotation or passive extension of the right hip suggesting retrocecal appendicitis) or obturator sign (pain on internal rotation of the right hip suggesting pelvic appendicitis) are rare.

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Real-time US signs of acute appendicitis
Direct signs Indirect signs
  • Non-compressibility of the appendix , Perforation: appendix might be compressible
  • Free fluid surrounding appendix
  • The diameter of the appendix > 6 mm
  • Local abscess formation
  • Single wall thickness of ≥ 3 mm
  • Increased echogenicity of local mesenteric fat
Target sign:

  • Hypoechoic fluid-filled lumen
  • Hyperechoic mucosa/submucosa
  • Hypoechoic muscular layer
  • Enlarged local mesenteric lymph nodes
Appendicolith: hyperechoic with posterior shadowing
  • Thickening of the peritoneum
  • Colour Doppler and the contrast-enhanced US:
  • Hypervascularity in the early stages of AA
  • Hypo- to avascularity in abscess and necrosis
  • Signs of secondary small bowel obstruction

 

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Diagnosis of Appendicitis

Clinical

  • Aure-Rozanova’s sign – Increased pain on palpation with a finger in right Petit triangle (can be a positive Shchetkin-Bloomberg’s).[rx]
  • Bartomier-Michelson’s sign – Increased pain on palpation at the right iliac region as the person being examined lies on his or her left side compared to when he/she lies on the back.[rx]
  • Dunphy’s sign – Increased pain in the right lower quadrant with coughing.[rx]
  • Hamburger sign -The patient refuses to eat (anorexia is 80% specific for appendicitis)[rx]
  • Kocher’s (Kosher’s) sign – From the person’s medical history, the start of pain in the umbilical region with a subsequent shift to the right iliac region.[rx]
  • Psoas sign – Place your hand just above the patient’s right knee and ask the patient to push up against your hand causing contraction of the psoas muscle which causes pain if the psoas muscle is inflamed, which could be due to appendicitis, or another source of inflammation.
  • Massouh sign – Developed in and popular in southwest England, the examiner performs a firm swish with his or her index and middle finger across the abdomen from the xiphoid process to the left and the right iliac fossa. A positive Massouh sign is a grimace of the person being examined upon a right-sided (and not left) sweep.[rx]
  • Obturator sign – Flex the patient’s right thigh at the hip with the knee flexed and rotate internally.  Increased pain at the right lower quadrant suggests inflammation of the internal obturator muscle from overlying appendicitis or abscess. The person being evaluated lies on her or his back with the hip and knee both flexed at ninety degrees. The examiner holds the person’s ankle with one hand and knee with the other hand. The examiner rotates the hip by moving the person’s ankle away from his or her body while allowing the knee to move only inward. A positive test is a pain with internal rotation of the hip.[rx]
  • Psoas sign, also known as Obraztsova’s sign –  is right lower-quadrant pain that is produced with either the passive extension of the right hip or by the active flexion of the person’s right hip while supine. The pain that is elicited is due to inflammation of the peritoneum overlying the iliopsoas muscles and inflammation of the psoas muscles themselves. Straightening out the leg causes pain because it stretches these muscles while flexing the hip activates the iliopsoas and causes pain.[rx]
  • Rovsing’s sign – Pain in the lower right abdominal quadrant with continuous deep palpation starting from the left iliac fossa upwards (counterclockwise along the colon). The thought is there will be increased pressure around the appendix by pushing bowel contents and air toward the ileocaecal valve provoking right-sided abdominal pain.[rx] .While standing on the patient’s right side, gradually do slow deep palpation of the left lower quadrant.  Increased pain on the right suggests right-sided peritoneal irritation.
  • Sitkovskiy (Rosenstein)’s a sign – Increased pain in the right iliac region as the person is being examined lies on his/her left side.[rx]

Investigation of acute appendicitis

  • Urine analysis—up to 40% can have abnormalities
  • Pregnancy test—to exclude pregnancy
  • Full blood count—neutrophil (> 75%) predominant leucocytosis is present in 80-90%
  • C reactive protein—raised concentration may be present, but its absence should not exclude a diagnosis of appendicitis
  • White Blood Cell Count (WBC) –Although an increase in peripheral WBC with a left shift may be the earliest marker of inflammation, its presence or absence is not significant enough to diagnose or exclude acute appendicitis. Many patients with gastroenteritis, mesenteric adenitis, pelvic inflammatory disease, and many other conditions have an elevated WBC. A normal WBC is also not uncommon in patients with appendicitis.
  • Urinalysis – Urinalysis is usually normal but may not be due to the inflamed appendix sitting on the ureter or bladder.

Differential diagnosis of acute appendicitis

Surgical

  • Intestinal obstruction
  • Intussusception
  • Acute cholecystitis
  • Perforated peptic ulcer
  • Mesenteric adenitis
  • Meckel’s diverticulitis
  • Colonic/appendicular diverticulitis
  • Pancreatitis
  • Rectus sheath hematoma

Urological

  • Right ureteric colic
  • Right pyelonephritis
  • Urinary tract infection

Gynecological

  • Ectopic pregnancy
  • Ruptured ovarian follicle
  • Torted ovarian cyst
  • Salpingitis/pelvic inflammatory disease

Medical

  • Gastroenteritis
  • Terminal ileitis
  • Diabetic ketoacidosis
  • Preherpetic pain on the right 10th and 11th dorsal nerves
  • Porphyria

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Imaging and diagnosis of acute appendicitis

Investigation Diagnostic criteria Evidence
Plain radiography None No role in the diagnosis of acute appendicitis,w6although in some cases a faecolith may be shown
Ultrasonography A peristaltic and non-compressible structure with diameter >6 mmw8 The sensitivity of 86%; specificity of 81%
Computed tomography scanning Abnormal appendix identified or calcified appendicolith seen in association with periappendiceal inflammation or diameter >6 mmw8 The sensitivity of 94% and specificity of 95% in the diagnosis of acute appendicitis
Magnetic resonance imaging Not confirmed Restricted to cases in which radiation and diagnostic difficulties preclude the use of other modalities (for example, pregnancy)

 

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Ultrasound (US)

  • The use of ultrasound is increasing, particularly in children in whom the risks of ionizing radiation are greatest. The advantages include decreased cost relative to other imaging modalities and lack of ionizing radiation exposure. However, it is operator-dependent.
  • The visualization of a thickened, non-compressible appendix greater than 6 mm in diameter is diagnostic. If the US is non-diagnostic, further imaging with CT or MRI, particularly in pregnancy, is required. In practice, a positive ultrasound can be used to reduce CT scan utilization. However, a negative or non-diagnostic result is not sufficient to rule out appendicitis. During childbearing age, it can be helpful to exclude a tubo-ovarian abscess.

CT Scan

  • CT of the abdomen and pelvis is considered the modality of choice for a definitive assessment of patients being evaluated for possible appendicitis. However, a major concern with CT scan is radiation exposure, particularly in children. Practitioners should, therefore, use these scans judiciously. Limited-range CT scans have been proposed in children to reduce the radiation dose. The following findings may be seen:
  • Dilated appendix greater than 6 mm with a thickened wall (greater than 2 mm)
  • Peri-appendiceal inflammation (peri-appendiceal fat stranding)
  • Appendicolith
  • Appendiceal or abscess
  • Free fluid

If the practitioner does not visualize the appendix, appendicitis is not ruled out.

MRI

  • MRI is a reliable modality which is particularly useful for pregnant women and children when ultrasound is inconclusive. Since intravenous (IV) gadolinium can cross the placenta, it should not be used during pregnancy. Also, patients with renal insufficiency should not receive IV gadolinium.

The following factors limit MRI use:

  • Higher cost
  • More time required to acquire images
  • Skilled radiologist required to interpret MRI
  • Not widely available

Also, MRI is not a test of choice for unstable patients and young children in whom sedation may be required. In recent years, the utility of rapid MRI without contrast agents or sedation has been assessed for a diagnosis of pediatric appendicitis.

Treatment of Appendicitis

If practitioners are evaluating the patient for appendicitis, they should also obtain an early surgical consultation.Intravenously administer the isotonic crystalloid fluid.

  • Antibiotic prophylaxis, which is coverage for gram-negative and gram-positive aerobic and anaerobic bacteria, and anaerobes (Bacteroides fragilis and Escherichia coli), is recommended. However, its administration should be timed in consultation with the surgical service to ensure that high antibiotic levels coincide with the operative procedure. Treat nonperforated appendicitis with cefoxitin or cefotetan.

In perforated appendicitis consider the following choices:

  • Carbapenem
  • Ticarcillin-clavulanate
  • Piperacillin-tazobactam
  • Ampicillin-sulbactam
  • Provide adequate analgesia
  • The primary treatment for appendicitis is surgery. Doctors should make operative decisions in con
  • Antibiotics are less effective if an appendicolith is present.[rx] Surgery is the standard management approach for acute appendicitis.[rx] The cost-effectiveness of surgery versus antibiotics is unclear.[rx]
  • Using antibiotics to prevent potential postoperative complications in emergency appendectomy procedures is recommended, and the antibiotics are effective when given to a person before, during, or after surgery.[rx]
  • Pain medications (such as morphine) do not appear to affect the accuracy of the clinical diagnosis of appendicitis and therefore should be given early in the patient’s care.[rx] Historically there were concerns among some general surgeons that analgesics would affect the clinical exam in children, and some recommended that they not be given until the surgeon was able to examine the person.[rx]

Surgery of Appendicitis

Health care professionals call the surgery to remove the appendix an appendectomy. A surgeon performs the surgery using one of the following methods:

  • Laparoscopic surgery – During laparoscopic surgery, surgeons use several smaller incisions and special surgical tools that they feed through the incisions to remove your appendix. Laparoscopic surgery leads to fewer complications, such as hospital-related infections, and has a shorter recovery time.
  • Laparotomy – Surgeons use laparotomy to remove the appendix through a single incision in the lower right area of your abdomen.

Surgery versus antibiotics

We found three systematic reviews (each with a search date of 2011). The three reviews reported many of the same RCTs, but in different combinations (see Further information on studies). Each review reported a synthesis of different outcome measures and came to different conclusions; therefore, we have reported all three reviews here to cover the full spectrum of evidence.

Treatment success

Surgery compared with antibiotics Appendicectomy may be more effective than antibiotics at reducing treatment failure including recurrence at up to 1 year, but maybe less effective at reducing some complications in adults with uncomplicated acute appendicitis. However, the evidence is weak and results varied by outcome measured (very low-quality evidence).

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Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favors
Treatment success
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Initial treatment failure (antibiotic: failure to achieve definite improvement without the need for surgery and hospital discharge without an operation; appendicectomy: failure to achieve pathologically confirmed appendicitis after surgery or another surgical indication for operation)
40/470 (9%) with appendicectomy
137/510 (27%) with antibiotics
OR 2.43
95% CI 0.94 to 6.33
P = 0.07
Significant heterogeneity: I² = 69%, P = 0.01
Heterogeneity not further explained
Not significant
Systematic review Adults with suspected acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Overall treatment failure (initial treatment failure plus anyone in the antibiotic group requiring appendicectomy because of recurrence) up to 1 year
40/470 (9%) with appendicectomy
205/510 (40%) with antibiotics
OR 6.72
95% CI 3.48 to 12.99
P <0.00001
Moderate effect size appendicectomy
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Overall complications (e.g., surgical site infection, organ space infection, small bowel obstruction, other)
60/510 (12%) with antibiotics
83/470 (18%) with appendicectomy
OR 0.54
95% CI 0.37 to 0.78
P = 0.001
Small effect size antibiotics
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
Mean cure (within 2 weeks [free of symptoms such as abdominal pain, fever, inflammatory parameters] and without major complication [including recurrence] within 1 year)
97% with appendicectomy
73% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 97% (95% CI 94% to 99%)
Antibiotics: 73% (95% CI 63% to 82%)
Mean cure rates were higher with appendicectomy, but the review did not report a between-group P value
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
No major complications (including the need for further [invasive] treatment or prolonged admission [e.g., abscesses, ileus, deep wound infection, recurrence, re-operation, secondary perforation])
97% with appendicectomy
83% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 97% (95% CI 93% to 99%)
Antibiotics: 83% (95% CI 72% to 91%)
Proportion of people with no major complications was higher with appendicectomy, but the review did not report a between-group P value
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
5 RCTs in this analysis
No minor complications (e.g., superficial wound infections, negative appendix at histology [no appendicitis], diarrhoea, urinary tract infection)
91% with appendicectomy
96% with antibiotics
Absolute numbers not reported
The review pooled data for each group and calculated 95% CI
Appendicectomy: 91% (95% CI 83% to 96%)
Antibiotics: 96% (95% CI 93% to 97%)
Proportion of people with no minor complications was higher with antibiotics, but the review did not report a between-group P value
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Complications (antibiotics: perforated or gangrenous appendix, peritonitis, or wound infection [in people who failed antibiotics and had appendicectomy subsequently]; appendicectomy: perforated appendicitis, peritonitis, or wound infection)
84/470 (18%) with antibiotics
108/430 (25%) with appendicectomy
RR 0.69
95% CI 0.54 to 0.89
P = 0.004
Small effect size antibiotics
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Risk of complicated appendiciti
54/470 (11%) with antibiotics
131/430 (31%) with appendicectomy
RR 0.46
95% CI 0.19 to 1.12
P = 0.09
Significant heterogeneity: I² = 82%, P <0.001
A sensitivity analysis removing 1 RCT with high crossover found a similar result, but there was still significant heterogeneity among groups (RR 0.58, 95% CI 0.18 to 1.90; I² = 74%)
Not significant

Mortality (from appendicitis)

Surgery compared with antibiotics We don’t know whether appendicectomy and antibiotics differ in effectiveness at reducing mortality from appendicitis in adults with uncomplicated acute appendicitis (very low-quality evidence).

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Mortality
Systematic review Adults with acute uncomplicated appendicitis(no abscess or phlegmon [rx]
5 RCTs in this analysis
Mortality 
with antibiotics
with appendicectomy

No data from the following reference on this outcome.

[/stextbox]

Length of hospital stay

Surgery compared with antibiotics We don’t know whether appendicectomy and antibiotics differ ineffectiveness at reducing the length of hospital stay in adults with uncomplicated acute appendicitis (rx).

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Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favors
Length of hospital stay
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
4 RCTs in this analysis
Duration of hospital stay days 
with antibiotics
with appendicectomy
Mean difference 0.66 days
95% CI 0.44 days to 0.87 days
P <0.0001
1 RCT in the review was not included in the analysis; the review reported this was based on visual inspection, but did not report any further reason for its exclusion
Effect size not calculated appendicectomy
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Length of primary hospital stay, days (antibiotics: days of admission for people treated with antibiotics and discharged with antibiotics; appendicectomy: days of admission for people treated with appendicectomy and discharged with further follow-up)
with antibiotics
with appendicectomy
Mean difference +0.20 days
95% CI –0.16 days to +0.87 days
P = 0.29
Not significant
Systematic review Adults with acute uncomplicated appendicitis[rx] (no abscess or phlegmon)
5 RCTs in this analysis
Length of hospital stay days 
with antibiotics
with appendicectomy
Mean difference +0.34 days
95% CI –0.06 days to +0.73 days
P = 0.09
Not significant

 

[/stextbox]

Return to normal activities

Surgery compared with antibiotics Antibiotics may be more effective than appendicectomy at reducing the duration of sick leave or disability in adults with uncomplicated acute appendicitis. However, results vary based on the analysis performed (rx).

[stextbox id=’custom’]

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Sick leave days
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings
2 RCTs in this analysis
Duration of sick leave days 
with antibiotics
with appendicectomy
Mean difference –0.69 days
95% CI –1.65 days to +0.27 days
Not significant
Systematic review Adults with acute uncomplicated appendicitis[rx] (no abscess or phlegmon)
3 RCTs in this analysis
Duration of sick leave or disability 
with antibiotics
with appendicectomy
Standard mean difference –0.19
95% CI –0.06 to –0.33
P = 0.005
Effect size not calculated antibiotics

Quality of life

No data from the following reference on this outcome.

Adverse effects

Ref (type) Population Outcome, Interventions Results and statistical analysis Effect size Favours
Adverse effects
Systematic review Mainly adults, mean age 28.2 years (range 13–75 years), suspected acute appendicitis based on disease history, clinical status, and laboratory findings Adverse effects 
with antibiotics
with appendicectomy
Systematic review Adults with a diagnosis of uncomplicated acute appendicitis Re-admissions with recurrence of symptoms 
with antibiotics
with appendicectomy
Significance not reported
Systematic review Adults with acute uncomplicated appendicitis (no abscess or phlegmon)
5 RCTs in this analysis
Recurrence of symptoms 
with antibiotics
with appendicectomy

 

[/stextbox]


References

What Is Appendicitis?


Crossed Hemiplegia; Causes, Symptoms, Treatment

Crossed Hemiplegia alternate hemiplegia. It affects the alter side of the body instated of the affected side. Hemiplegia Paralysis of one side of the face and the opposite side of the body? Hemiplegia is a neurological condition that affects paralysis is on one vertical half of the body. Its most obvious result is a varying degree of weakness and lack of control on one side of the body. It affects everyone differently but its most obvious result is a varying degree of weakness and lack of control in one side of the body. You may be reading this because your child or someone you know has hemiplegia.

Hemiplegia, paralysis of the muscles of the lower face, arm, and leg on one side of the body. The most common cause of hemiplegia is a stroke, which damages the corticospinal tracts in one hemisphere of the brain. The corticospinal tracts extend from the lower spinal cord to the cerebral cortex. They decussate, or cross, in the brainstem; therefore, damage to the right cerebral hemisphere results in paralysis of the left side of the body. Damage to the left hemisphere of a right-handed person may also result in aphasia. Other causes of hemiplegia include trauma, such as spinal cord injury; brain tumors; and brain infections.

Hemiplegia is a condition where half of the body is paralyzed due to damage to the parts of the brain responsible for movement. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke, etc.

Types of Hemiplegia

  • Alternate hemiplegia –  paralysis of one side of the face and the opposite side of the body.
  • Cerebral hemiplegia –  that due to a brain lesion.
  • Crossed hemiplegia – alternate hemiplegia. It affects the alter side of the body instated of the affected side.
  • Facial hemiplegia paralysis – of one side of the face.
  • Spastic hemiplegia – with spasticity of the affected muscles and increased tendon reflexes.
  • Spinal hemiplegia – due to a lesion of the spinal cord.

While hemiplegia is typically characterized as paralysis on one side of the body, there are multiple types of hemiplegia—some of which may be more limited in scope than others. A few different types of hemiplegia include:

  • Facial Hemiplegia – Also referred to as partial facial paralysis, this is a form of partial hemiplegia where the muscles on one side of the face are paralyzed. Often caused by a stroke or similar brain injury. This may or may not be associated with complete/incomplete hemiplegia in other areas of the body.
  • Cerebral Hemiplegia  – When hemiplegia is caused by cerebral palsy (or other conditions affecting the brain), it can be referred to as cerebral hemiplegia. Cerebral hemiplegia symptoms are often similar to other forms of hemiplegia but may vary in severity and duration depending on the condition causing the paralysis.
  • Spastic Hemiplegia – A variation of hemiplegia where the muscles on one side of the body are in a state of constant contraction. This type of hemiplegia may result in muscle pain, deformities in affected limbs (in extreme cases), and difficulty walking or maintaining motor control. Closely linked to cerebral palsy, and the severity (as well as the duration) of spastic hemiplegia symptoms may vary from case to case.
  • Spinal Hemiplegia – Often the result of an incomplete injury to the spinal cord or lesions on spinal nerves (especially at the C6 vertebra or higher). Spinal cord injury hemiplegia is often a long-term condition.

Causes of Crossed Hemiplegia

Though the arms, legs, and possibly torso are the regions of the body most obviously affected by hemiplegia, in most cases of hemiplegia these body regions are actually perfectly healthy. Instead, the problem resides in the brain, which is unable to produce, send, or interpret signals due to disease or trauma-related damage. Less frequently, hemiplegia results from damage to one side of the spinal cord, but these sorts of injuries more typically produce global problems, not just paralysis on one side of the body.

  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Strokes and transient ischemic attacks (better known as TIA or mini-strokes).
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Strokes and transient ischemic attacks (better known as TIA or mini-strokes).
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
Crossed Hemiplegia

Rx

Some common causes of hemiplegia include

Stroke is the commonest cause of hemiplegia. Insufficient blood supply to the brain leads to loss of brain functions. The stroke may be caused by:

  • A clot formed within the blood vessel blocking the blood supply -> a thrombus
  • A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation -> an emboli
  • A bleed from a blood vessel supplying the brain -> a hemorrhage
  • A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation. -> an emboli
  • A bleed from a blood vessel supplying the brain -> a hemorrhage
  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
  • Head injury
  • Diabetes
  • Brain tumor
  • Infections –> meningitis, encephalitis, meningitis, brain abscess
  • Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
  • Inflammation of the blood vessels -> vasculitis
  • Diseases affecting the nerves -> like Multiple Sclerosis; acute necrotizing myelitis.
  • Conditions presenting from birth -> cerebral palsy. Lack of blood supply damages nerve cells in the brain. Birth trauma, difficult labor, perinatal strokes in infants within 3 days of birth can all cause cerebral palsy.
  • Hereditary diseases –> leukodystrophies. This is a rare disorder affecting the myelin sheath which covers and protects nerve cells in the brain. The condition usually appears in infancy or childhood.
  • Vascular – cerebral hemorrhage
  • Neoplastic – glioma-meningioma
  • Demyelination – disseminated sclerosis, lesions to the internal capsule
  • Traumatic – cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • Congenitalcerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
  • Disseminated – multiple sclerosis
  • Psychological – parasomnia (nocturnal hemiplegia)
  • Severe headache
  • Impairment or loss of vision
  • Memory loss
  • Confusion
  • Loss of balance or co-ordination
  • Poor balance and dizziness
  • Sudden numbness, paralysis or weakness of an arm, leg or side of the face.
  • Slurred or abnormal speech
  • Loss of consciousness
  • Incontinence

Symptoms of Crossed Hemiplegia

What Is Hemiplegia?

Rx

The main symptom of hemiplegia is weakness or paralysis on one side of the child’s body. The condition can vary in severity and affects each child differently. It will only affect one side of the child’s body. General symptoms include

  • Total or partial loss of sensation on just one side.
  • Changes in cognition, mood, or perception.
  • Difficulty speaking.
  • Changes on the other side of the body, since those muscles, may begin to atrophy or become painful due to chronic muscle spasms.
  • Spastic attacks during which the muscles move without your conscious control.
  • Seizures.
  • Pusher syndrome – With this symptom, hemiplegics shift their weight to the paralyzed side of the body, resulting in significant loss of motor control.
  • Severe, throbbing pain, often on one side of your head
  • A pins-and-needles feeling, often moving from your hand up your arm
  • Numbness on one side of your body, which can include your arm, leg, and half of your face
  • Weakness or paralysis on one side of your body
  • Loss of balance and coordination
  • Dizziness or vertigo
  • Nausea and vomiting

You may also have problems with your senses, communication, and drowsiness

  • Seeing zigzag lines, double vision, or blind spots
  • Extreme sensitivity to light, sound, and smell
  • Language difficulties, such as mixing words or trouble remembering a word
  • Slurred speech
  • Confusion
  • Loss of consciousness or coma
  • Difficulty walking
  • Poor balance
  • Little or no use of one hand or leg
  • Speech problems
  • Visual problems
  • Behavioral problems
  • Learning difficulties
  • Epilepsy
  • Developmental delay, for example learning to walk later than other children

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Diagnosis of Crossed Hemiplegia

To diagnose a stroke doctor hemiplegia will usually make an assessment using several of the following

Treatment of Crossed Hemiplegia

Some potential hemiplegia exercises to consider include

  • Strength Training Exercises – Some strength training exercises can prove to be beneficial for hemiplegics. The training recommended may vary depending on the type of hemiplegia, but common exercises include knee rolling, single-leg dropouts, and single-leg bridges, among others. In some cerebral hemiplegia patients, this can help improve range of motion and functionality in the affected limbs—though this isn’t certain.
  • Muscle Stretches – Stretching specific muscle groups helps hemiplegics stave off some of the side effects of hemiplegia, such as joint/muscle pain from not moving limbs for too long and muscular atrophy. Spastic hemiplegics may need assistance in safely moving their contracted muscles without injury.
  • Seated Aerobics – Seated aerobics provide a relatively safe way to burn calories and improve health from virtually anywhere. This form of exercise is recommended for hemiplegics recovering from a spinal cord injury.
  • Water Aerobics – This hemiplegia exercise allows hemiplegics to relax their muscles and support the full weight of their bodies relatively easily as they stretch and work on their range of motion. Some rehabilitation programs use water aerobics as a chance to help people with paralysis to get out of the chair and experience some freedom of movement as they work muscles that are often neglected during in-chair exercises.
  • Muscle relaxant – that help to increase muscle strength. It can be done either by any drugs or manually applying heat and electromagnetic radiation.
  • Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
  • Support groups – family education, and advocacy by family support, friend circle, etc.
  • Psychotherapy – to help you deal with the psychological effects of the disease.
  • Exercise therapy – to help you remain healthy in spite of your disability.

Initial Treatment of Hemiplegia

Immediate treatment is aimed at limiting the size of the stroke and preventing further stroke. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischaemic stroke or by stopping the bleeding of a hemorrhagic stroke.  This will involve administering medications and may involve surgery in some cases.

Medications

Crossed Hemiplegia

RX

  • Thrombolytic therapy – These medications dissolve blood clots allowing blood flow to be re-established
  • Anticoagulants (eg: heparin) or aspirin These medications help to prevent blot clots from getting bigger and prevent new blood clots from forming
  • Antihypertensives  In cases of hemorrhagic stroke these medications may be prescribed to help lower high blood pressure
  • Medications– to reduce swelling in the brain and medications to treat underlying causes for the stroke eg: heart rhythm disorders may also be given.
  • Blood thinners – to reduce cardiovascular blockages and decrease the chances of future strokes.
  • Antibiotics usually delivered intravenously, to combat brain infections.
  • Muscle relaxant drugs – Tolperisone or eperisone hcl
  • Surgery to address secondary issues-particularly involuntary muscle contractions, spinal damage, or damage to the ligaments or tendons on the unaffected side of the body.
  • Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
  • Support groups – family education, and advocacy.
  • Psychotherapy to help you deal with the psychological effects of the disease.
  • Exercise therapy to help you remain healthy in spite of your disability.

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Treatment of Alternate Hemiplegia

Brain cells do not generally regenerate. Following a stroke, surviving brain cells can take over the function of areas that are dead or damaged, but only to a certain degree. The adaptive ability of the brain requires the relearning of various skills. As each person who suffers a stroke is affected differently, individual rehabilitation plans are developed in conjunction with the patient, family, and healthcare team. These aim to teach skills and maximize function so that the person can achieve maximum independence.

Physiotherapy

Treatment of hemiplegia requires coordination of several health professionals. A physiotherapist, occupational therapist, a physician, a surgeon and support from family, etc.

  • Treatment is focused – to find the causative factor and check its further progression. Secondly, after a few days, rehabilitation therapy helps to minimize disability.
  • Several medicines – are prescribed to control the primary cause such as antihypertensive, anti-thrombolytic agents to dissolve the clot, drugs to control cerebral edema, etc.
  • Intensive physical therapy – is begun after a few days. Activities such as walking, standing are done repeatedly under the guidance of a physiotherapist. It helps to improve the muscular functions which have become rigid. It is aimed to make the patient self-sufficient to perform his daily activities.
  • The patient is taught – to move his affected arm with his strong arm. With exercise, it is possible to maintain the flexibility of joints and it also prevents tightening and shortening of muscles. Speech therapy is simultaneously begun to improve communication and speaking skills.
  • Speech therapy – to improve communication
  • Occupational therapy to improve daily functions such as eating, cooking, toileting, and washing.
Recovery can take months and it may be several days or weeks after the stroke before doctors are able to give an accurate prediction for recovery.

Occupational therapy

  • Occupational therapy – Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening the hand, shoulder, and torso, and participating in activities of daily living (ADLs), such as eating and dressing.
  • Therapists – may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual – which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Rehabilitation & Therapy for Hemiplegia

1. Improving motor control

a. Neurofacilitatory Techniques

In Stroke Physical Therapy these therapeutic interventions use sensory stimuli (e.g. quick stretch, brushing, reflex stimulation, and associated reactions), which are based on neurological theories, to facilitate movement in patients following stroke. The following are the different approaches

  • Bobath Concept- Berta & Karel Bobath’s approach focuses to control responses from the damaged postural reflex mechanisms. Emphasis is placed on affected inputs facilitation and normal movement patterns (Bobath, 1990).
  • ii.Brunnstrom – Brunnstrom approach is one form of neurological exercise therapy in the rehabilitation of stroke patients. The relative effectiveness of Neuro-developmental treatment versus the Brunnstrom method was studied by Wagenaar and colleagues from the perspective of the functional recovery of stroke patients. The result of this study showed no clear differences in the effectiveness of the two methods within the framework of functional recovery.
  • iii.Rood – Emphasise the use of activities in developmental sequences, sensation stimulation, and muscle work classification. Cutaneous stimuli such as icing, tapping, and brushing are employed to facilitate activities.
  • iv. Proprioceptive neuromuscular facilitation (PNF) – Developed by Knott and Voss, they advocated the use of peripheral inputs as stretch and resisted movement to reinforce existing motor response. Total patterns of movement are used in the treatment and are followed in a developmental sequence.

b. Learning theory approach

  • i. Conductive education – In Stroke Physical Therapy, Conductive education is one of the methods in treating neurological conditions including hemiplegic patients. Cotton and Kinsman (1984) demonstrated a neuropsychological approach using the concept of CE for adult hemiplegia. The patient is taught how to guide his movements towards each task-part of the task by using his own speech – rhythmical intention.
  • ii. Motor relearning theory – Carr & Shepherd, both are Australian physiotherapists, developed this approach in 1980. It emphasizes the practice of functional tasks and the importance of relearning real-life activities for patients. Principles of learning and biomechanical analysis of movements and tasks are important. There is no evidence adequately supporting the superiority of one type of exercise approach over another. However, the aim of the therapeutic approach is to increase physical independence and to facilitate the motor control of skill acquisition and there is strong evidence to support the effect of rehabilitation in terms of improved functional independence and reduced mortality.

c. Functional electrical stimulation (FES) 

  • FES is a modality that applied a short burst of electrical current to the hemiplegic muscle or nerve. In Stroke Physical Therapy, FES has been demonstrated to be beneficial to restore motor control, spasticity, and reduction of hemiplegic shoulder pain and subluxation.  A recent meta-analysis of the randomized controlled trial study showed that FES improves motor strength. A study by Faghri has identified that FES can significantly improve arm function, electromyographic activity of posterior deltoid, the range of motion and reduction of severity of subluxation and pain of the hemiplegic shoulder.

d. Biofeedback

  • Biofeedback is a modality that facilitates the cognizant of electromyographic activity in selected muscle or awareness of joint position sense via visual or auditory cues. In Stroke Physical Therapy the result of studies in biofeedback is controversial. A meta-analysis of 8 randomized controlled trials of biofeedback therapy demonstrated that electromyographic biofeedback could improve motor function in stroke patients.
  • A conflicting meta-analysis study by showing that biofeedback was not efficacious in improving the range of motion in the ankle and shoulder in a stroke patient. Moreland conducted another meta-analysis that concluded that EMG biofeedback alone or with conventional therapy did not superior to conventional physical therapy in improving upper- extremity function in the adult stroke patient.

2. Hemiplegic shoulder management

Shoulder subluxation and pain of the affected arm is not uncommon in at least 30% of all patient after stroke, whereas subluxation is found in 80% of stroke patients. It is associated with the severity of the disability and is common in patients in rehabilitation settings. Suggested interventions are as follows:

  • a. Exercise – Active weight-bearing exercise can be used as a means of improving motor control of the affected arm; introducing and grading tactile, proprioceptive, and kinesthetic stimulation; and preventing edema and pain. In Stroke Physical Therapy, Upper extremity weight bearing can be used to lengthen or inhibit tight or spastic muscles while simultaneously facilitating muscles that are not active (Donatelli, 1991). According to Robert (1992), the amount of shoulder pain in hemiplegia was related most to loss of motion. He advocated that the provision of ROM exercise (caution to avoid improvement) as treatment as early as possible.
  • b. Functional electrical stimulation – Functional electrical stimulation (FES) is an increasingly popular treatment for hemiplegic stroke patients. It has been applied in stroke physical therapy for the treatment of shoulder subluxation spasticity and functionally, for the restoration of function in the upper and lower limb. In Stroke Physical Therapy, Electrical stimulation is effective in reducing pain and severity of subluxation, and possibly in facilitating recovery of arm function
  • c. Positioning & proper handling – In Stroke Physical Therapy, proper positioning and handling of the hemiplegic shoulder, whenever in bed, sitting and standing or during lifting, can prevent shoulder injury is recommended in the AHCPR & SIGN guidelines for stroke rehabilitation. In Stroke Physical Therapy, positioning can be therapeutic for tone control and neuro-facilitation of stroke patients (Davies, 1991). Braus et al 94 found shoulder hand syndrome reduced from 27% to 8% by the instruction to everyone including family on handling technique.
  • d. Neuro-facilitation
  • e. Passive limb physiotherapy – Maintenance of a full pain-free range of movement without traumatizing the joint and the structures can be carried out. In Stroke Physical Therapy, at no time should pain in or around the shoulder joint be produced during treatment.
  • f. Pain relief physiotherapy – Passive mobilization as described by Maitland can be useful in gaining relief of pain and range of movement. In Stroke Physical Therapy other treatment modalities such as thermal, electrical, cryotherapy, etc. can be applied for shoulder pains or musculoskeletal in nature.
  • g. Reciprocal pulley – The use of reciprocal pulley appears to increase the risk of developing shoulder pain in stroke patients. It is not related to the presence of subluxation or to muscle strength.
  • h. Sling – In Stroke Physical Therapy the use of a sling is controversial. No shoulder support will correct a glenohumeral joint subluxation. However, it may prevent the flaccid arm from hanging against the body during functional activities, thus decreasing shoulder joint pain. They also help to relieve downward traction on the shoulder capsule caused by the weight of the arm.

3. Limb physiotherapy

  • Limb physiotherapy/Stroke Physical Therapy includes passive, assisted-active and active range-of-motion exercise for the hemiplegic limbs. This can be effective management for the prevention of limb contractures and spasticity and is recommended within AHCPR. Self-assisted limb exercise is effective for reducing spasticity and shoulder protection. Adams and coworkers recommended passive full-range-of-motion exercise for a paralyzed limb for potential reduction of complication for stroke patients

4. Chest physiotherapy

  • In Stroke Physical Therapy, evidence shows that both cough and forced expiratory technique (FET) can eliminate induced radio aerosol particles in the lung field. Directed coughing and FET can be used as a technique for bronchial hygiene clearance in stroke patients.

5. Positioning

  • In Stroke, Physical Therapy consistent “reflex-inhibitory” patterns of posture in resting is encouraged to discourage physical complication of stroke and to improve recovery (Bobath, 1990).
  • Meanwhile, therapeutic positioning is a widely advocated strategy to discourage the development of abnormal tone, contractures, pain, and respiratory complications. It is an important element in maximizing the patient’s functional gains and quality of life.

6. Tone management

  • A goal of Stroke Physical Therapy interventions has been to “normalize tone to normalize movement.” Therapy modalities for reducing tone include stretching, prolonged stretching, passive manipulation by therapists, weight-bearing, ice, contraction of muscles antagonistic to spastic muscles, splinting, and casting.
  • Research on tone-reducing techniques has been hampered by the inadequacies of methods to measure spasticity and the uncertainty about the relationship between spasticity and volitional motor control.
  • The manual stretch of finger muscles, pressure splints, and dantrolene sodium do not produce apparent long-term improvement in motor control. Dorsal resting hand splints reduced spasticity more than volar splints, but the effect on motor control is uncertain while TENS stimulation showed improvement for chronic spasticity of lower extremities.

7. Sensory re-education

  • Bobath and other therapy approaches recommend the use of sensory stimulation to promote the sensory recovery of stroke patients.

8. Balance retraining

  • Re-establishment of balance function in patients following stroke has been advocated as an essential component in the practice of stroke physical therapy. Some studies of patients with hemiparesis revealed that these patients have a greater amount of postural sway, the asymmetry with greater weight on the non-paretic leg, and a decreased ability to move within a weight-bearing posture. Meanwhile, research has demonstrated moderate relationships between balance function and parameters such as gait speed, independence, wheelchair mobility, reaching, as well as dressing. Some tenable support on the effectiveness of treatment of disturbed balance can be found in studies comparing the effects of balance retraining plus physiotherapy treatment and physiotherapy treatment alone.

9. Fall prevention

  • In Stroke Physical Therapy, falls are one of the most frequent complications and the consequences of which are likely to have a negative effect on the rehabilitation process and its outcome.
  • According to the systematic review of the Cochrane Library, which evaluated the effectiveness of several fall prevention interventions in the elderly, there was significant protection against falling from interventions that targeted multiple, identified, risk factors in individual patients. The same is true for interventions which focused on behavioral interventions targeting environmental hazards plus other risk factors

10. Gait re-education

  • Recovery of independent mobility is an important goal for the immobile patient, and much therapy is devoted to gait-reeducation. Bobath assumes abnormal postural reflex activity is caused by dysfunction so gait training involved tone normalization and preparatory activity for gait activity.
  • In contrast, Carr and Shepherd advocate task-related training with methods to increase strength, coordination and flexible MS system to develop skill in walking while Treadmill training combined with the use of a suspension tube. Some patient’s body weight can effective in regaining walking ability when used as an adjunct to convention therapy 3 months after active training.

11. Functional Mobility Training

  • To handle the functional limitations of stroke patients, functional tasks are taught to them based on movement analysis principles. In Stroke Physical Therapy these tasks include bridging, rolling to sit to stand and vice versa, transfer skills, walking and staring, etc.
  • Published studies report that many patients improve during rehabilitation. The strongest evidence of benefit is from studies that have enrolled patients with chronic deficits or have included a no-treatment control group.
  • Meanwhile, early mobilization helps prevent compilations e.g. DVT, skin breakdown contracture and pneumonia. Evidence has shown better orthostatic tolerance and earlier ambulation.

12. Upper limb training

By 3 months poststroke, approximately 37% of the individuals continue to have decreased upper extremities (UE) function. Recovery of UE function lags behind that of the lower extremities because of the more complex motor skill required of the UE in daily life tasks. That means many individuals who have a stroke are at risk for a lowered quality of life. Many approaches to the physical rehabilitation of adults post-stroke exist that attempt to maximize motor skill recovery. However, the literature does not support the efficacy of any single approach. The followings are the current approaches to motor rehabilitation of the UE.

  • a. Facilitation models – They are the most common methods of intervention for the deficits in UE motor skills including Bobath, proprioceptive neuromuscular facilitation, Brunnstrom’s movement therapy, and Rood’s sensorimotor approach. There is some evidence that practice based on the facilitation models can result in improved motor control of UE. However, an intervention based on the facilitation models has not been effective in restoring the fine hand coordination required for the performance of actions.
  • b. Functional electric stimulation – In Stroke Physical Therapy, Functional electric stimulation (FES) can be effective in increasing the electric activity of muscles or increased active range of motion in individuals with stroke. Some evidence showed that FES may be more effective than facilitation approaches.
  • c. Electromyographic biofeedback – In Stroke Physical Therapy, biofeedback can contribute to improvements in motor control at the neuromuscular and movement levels. Some studies have shown improvements in the ability to perform actions during post-testing after biofeedback training. However, the ability to generalize these skills and incorporate them into daily life is not measured.
  • d. Constraint-induced therapy – Constraint-Induced (CI) therapy was designed to overcome the learned nonuse of the affected UE. In the most extreme form of CI therapy, individual post-stroke is prevented from using the less affected UE by keeping it in a splint and sling for at least 90% of their waking hours. Studies have found that the most extreme of CI therapy can effect rapid improvement in UE motor skill and that is retained for at least as long as 2 years. However, CI therapy currently is effective only in those with distal voluntary movement.

13. Mobility appliances and equipment

  • Small changes in an individual’s local ‘environment’ can greatly increase independence, use of a wheelchair or walking stick. However, little research has been done for these ‘treatments’. It is acknowledged that walking aids and mobility appliances may benefit selected patients.

14. Acupuncture 

  • The World Health Organisation (WHO) has listed acupuncture as a possible treatment for pariesis after stroke. Studies had sown its beneficial effects on stroke rehabilitation.
  • Hua had reported a significant difference in changes of neurological score between the acupuncture group and the control group after 4 weeks of treatment in an RCT and no adverse effects were observed in patients treated with acupuncture.

15. Vasomotor training 

  • Early stimulation of the muscle pump can reduce the venous stasis and enhance the general circulation of the body. It then hastens the recovery process.

16. Edema management

  • Use of intermittent pneumatic pump, elastic stocking or bandages and massage can facilitate the venous return of the oedematous limbs. Therefore, the elasticity and flexibility of the musculoskeletal system can be maintained and enhance the recovery process and prevent complications like pressure ulcers.

Homeopathic Medicines for Hemiplegia

Homeopathic medicines cannot cure hemiplegia. However, the medicines can be administered to improve the state of paralysis, improve blood circulation, help control loss of power, improve the power of muscles to come extent and improve the overall health of the patient.

Some common medicines for hemiplegia and such states of paralysis are:

  • Plumbum Metallicum – This medicine is sourced by processing and potentizing the metal lead. It helps the neuro-muscular system of the body. It is administered with the intention to improve some muscle power. Plumbum met, as it is called, may be indicated all kinds of paralysis such as hemiplegia, paraplegia, and quadriplegia. As said earlier, it cannot cure paralysis as such.
  • Causticum Similar to the above medicine, Causticum is also a friend to all paralysis patients. It is aimed at improving some muscle power and not cure it.
  • Nux vomicaThis herbal medicine helps in the early stages of hemiplegia and not after some months or years.
  • Lathyrus sativus – This is another example of a toxin transformed into medicine. It is safe, There are some spasticity and stiffness in some muscles, in the cases of hemiplegia, where Lathyrus may be called for.
  • GelsemiumThis plant remedy is useful for early cases of paralysis including hemiplegia. It is supposed to improve muscle strength in the cases of paralysis.

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Prevention

Reducing the number of controllable risk factors is the best way to prevent a stroke.  This can include:

  • Stopping smoking
  • Losing weight
  • Eating a balanced diet low in sodium and saturated and trans fat
  • Moderating alcohol intake (no more than 2 small drinks per day)
  • Exercising regularly in order to stay physically fit
  • Maintaining good control of existing medical conditions such as diabetes, high blood pressure and high cholesterol.

Referances

Crossed Hemiplegia

What Is Facial Hemiplegia? Diagnosis, Treatment

What Is Facial Hemiplegia?/Facial Hemiplegia also referred to as partial facial paralysis, this is a form of partial hemiplegia where the muscles on one side of the face are paralyzed. Often caused by a stroke or similar brain injury. This may or may not be associated with complete/incomplete hemiplegia in other areas of the body.

Hemiplegia is a neurological condition that affects paralysis is on one vertical half of the body. Its most obvious result is a varying degree of weakness and lack of control on one side of the body. It affects everyone differently but its most obvious result is a varying degree of weakness and lack of control in one side of the body. You may be reading this because your child or someone you know has hemiplegia.

Hemiplegia, paralysis of the muscles of the lower face, arm, and leg on one side of the body. The most common cause of hemiplegia is a stroke, which damages the corticospinal tracts in one hemisphere of the brain. The corticospinal tracts extend from the lower spinal cord to the cerebral cortex. They decussate, or cross, in the brainstem; therefore, damage to the right cerebral hemisphere results in paralysis of the left side of the body. Damage to the left hemisphere of a right-handed person may also result in aphasia. Other causes of hemiplegia include trauma, such as spinal cord injury; brain tumors; and brain infections.

Hemiplegia is a condition where half of the body is paralyzed due to damage to the parts of the brain responsible for movement. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke, etc.

Types of Hemiplegia

  • Alternate hemiplegia –  paralysis of one side of the face and the opposite side of the body.
  • Cerebral hemiplegia –  that due to a brain lesion.
  • Crossed hemiplegia – alternate hemiplegia. It affects the alter side of the body instated of the affected side.
  • Facial hemiplegia paralysis – of one side of the face.
  • Spastic hemiplegia – with spasticity of the affected muscles and increased tendon reflexes.
  • Spinal hemiplegia – due to a lesion of the spinal cord.

While hemiplegia is typically characterized as paralysis on one side of the body, there are multiple types of hemiplegia—some of which may be more limited in scope than others. A few different types of hemiplegia include:

  • Facial Hemiplegia – Also referred to as partial facial paralysis, this is a form of partial hemiplegia where the muscles on one side of the face are paralyzed. Often caused by a stroke or similar brain injury. This may or may not be associated with complete/incomplete hemiplegia in other areas of the body.
  • Cerebral Hemiplegia  – When hemiplegia is caused by cerebral palsy (or other conditions affecting the brain), it can be referred to as cerebral hemiplegia. Cerebral hemiplegia symptoms are often similar to other forms of hemiplegia but may vary in severity and duration depending on the condition causing the paralysis.
  • Spastic Hemiplegia – A variation of hemiplegia where the muscles on one side of the body are in a state of constant contraction. This type of hemiplegia may result in muscle pain, deformities in affected limbs (in extreme cases), and difficulty walking or maintaining motor control. Closely linked to cerebral palsy, and the severity (as well as the duration) of spastic hemiplegia symptoms may vary from case to case.
  • Spinal Hemiplegia – Often the result of an incomplete injury to the spinal cord or lesions on spinal nerves (especially at the C6 vertebra or higher). Spinal cord injury hemiplegia is often a long-term condition.

Causes of Facial Hemiplegia

Though the arms, legs, and possibly torso are the regions of the body most obviously affected by hemiplegia, in most cases of hemiplegia these body regions are actually perfectly healthy. Instead, the problem resides in the brain, which is unable to produce, send, or interpret signals due to disease or trauma-related damage. Less frequently, hemiplegia results from damage to one side of the spinal cord, but these sorts of injuries more typically produce global problems, not just paralysis on one side of the body.

  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Strokes and transient ischemic attacks (better known as TIA or mini-strokes).
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Strokes and transient ischemic attacks (better known as TIA or mini-strokes).
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
What Is Facial Hemiplegia?

Rx

Some common causes of hemiplegia include

Stroke is the commonest cause of hemiplegia. Insufficient blood supply to the brain leads to loss of brain functions. The stroke may be caused by:

  • A clot formed within the blood vessel blocking the blood supply -> a thrombus
  • A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation -> an emboli
  • A bleed from a blood vessel supplying the brain -> a hemorrhage
  • A thrombus breaks away from its site of origin and forms a block elsewhere in the circulation. -> an emboli
  • A bleed from a blood vessel supplying the brain -> a hemorrhage
  • Traumatic brain injuries to one side of the brain only. These may be caused by car accidents, falls, acts of violence, and other factors.
  • Cardiovascular problems, particularly aneurysms and hemorrhages in the brain.
  • Infections, particularly encephalitis and meningitis. Some serious infections, particularly sepsis and abscesses in the neck, may spread to the brain if left untreated.
  • Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
  • Conditions that cause demyelination of the brain, including multiple sclerosis and some other autoimmune diseases.
  • Reactions to surgery, medication, or anesthesia.
  • Loss of oxygen to the brain due to choking or anaphylactic shock.
  • Brain cancers.
  • Lesions in the brain, even if non-cancerous, since these lesions can impede function on one side of the brain.
  • Congenital abnormalities, including cerebral palsy and neonatal-onset multi-inflammatory disease.
  • Rarely, psychological causes; some states of catatonia can cause hemiplegia, and people with parasomnia—a sleep disorder leading to unusual nighttime behavior—may experience nighttime episodes of hemiplegia.
  • Head injury
  • Diabetes
  • Brain tumor
  • Infections –> meningitis, encephalitis, meningitis, brain abscess
  • Migraine syndrome -> recurrent headaches of severe intensity occasionally accompanied by sensations of numbness and tingling in one half of the body.
  • Inflammation of the blood vessels -> vasculitis
  • Diseases affecting the nerves -> like Multiple Sclerosis; acute necrotizing myelitis.
  • Conditions presenting from birth -> cerebral palsy. Lack of blood supply damages nerve cells in the brain. Birth trauma, difficult labor, perinatal strokes in infants within 3 days of birth can all cause cerebral palsy.
  • Hereditary diseases –> leukodystrophies. This is a rare disorder affecting the myelin sheath which covers and protects nerve cells in the brain. The condition usually appears in infancy or childhood.
  • Vascular – cerebral hemorrhage
  • Neoplastic – glioma-meningioma
  • Demyelination – disseminated sclerosis, lesions to the internal capsule
  • Traumatic – cerebral lacerations, subdural hematoma rare cause of hemiplegia is due to local anesthetic injections given intra-arterially rapidly, instead of given in a nerve branch.
  • Congenitalcerebral palsy, Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
  • Disseminated – multiple sclerosis
  • Psychological – parasomnia (nocturnal hemiplegia)
  • Severe headache
  • Impairment or loss of vision
  • Memory loss
  • Confusion
  • Loss of balance or co-ordination
  • Poor balance and dizziness
  • Sudden numbness, paralysis or weakness of an arm, leg or side of the face.
  • Slurred or abnormal speech
  • Loss of consciousness
  • Incontinence

Symptoms of Facial Hemiplegia

What Is Hemiplegia?

Rx

The main symptom of hemiplegia is weakness or paralysis on one side of the child’s body. The condition can vary in severity and affects each child differently. It will only affect one side of the child’s body. General symptoms include

  • Total or partial loss of sensation on just one side.
  • Changes in cognition, mood, or perception.
  • Difficulty speaking.
  • Changes on the other side of the body, since those muscles, may begin to atrophy or become painful due to chronic muscle spasms.
  • Spastic attacks during which the muscles move without your conscious control.
  • Seizures.
  • Pusher syndrome – With this symptom, hemiplegics shift their weight to the paralyzed side of the body, resulting in significant loss of motor control.
  • Severe, throbbing pain, often on one side of your head
  • A pins-and-needles feeling, often moving from your hand up your arm
  • Numbness on one side of your body, which can include your arm, leg, and half of your face
  • Weakness or paralysis on one side of your body
  • Loss of balance and coordination
  • Dizziness or vertigo
  • Nausea and vomiting

You may also have problems with your senses, communication, and drowsiness

  • Seeing zigzag lines, double vision, or blind spots
  • Extreme sensitivity to light, sound, and smell
  • Language difficulties, such as mixing words or trouble remembering a word
  • Slurred speech
  • Confusion
  • Loss of consciousness or coma
  • Difficulty walking
  • Poor balance
  • Little or no use of one hand or leg
  • Speech problems
  • Visual problems
  • Behavioral problems
  • Learning difficulties
  • Epilepsy
  • Developmental delay, for example learning to walk later than other children

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Diagnosis of Facial Hemiplegia

To diagnose a stroke doctor hemiplegia will usually make an assessment using several of the following

Treatment of Facial Hemiplegia

Some potential hemiplegia exercises to consider include

  • Strength Training Exercises – Some strength training exercises can prove to be beneficial for hemiplegics. The training recommended may vary depending on the type of hemiplegia, but common exercises include knee rolling, single-leg dropouts, and single-leg bridges, among others. In some cerebral hemiplegia patients, this can help improve range of motion and functionality in the affected limbs—though this isn’t certain.
  • Muscle Stretches – Stretching specific muscle groups helps hemiplegics stave off some of the side effects of hemiplegia, such as joint/muscle pain from not moving limbs for too long and muscular atrophy. Spastic hemiplegics may need assistance in safely moving their contracted muscles without injury.
  • Seated Aerobics – Seated aerobics provide a relatively safe way to burn calories and improve health from virtually anywhere. This form of exercise is recommended for hemiplegics recovering from a spinal cord injury.
  • Water Aerobics – This hemiplegia exercise allows hemiplegics to relax their muscles and support the full weight of their bodies relatively easily as they stretch and work on their range of motion. Some rehabilitation programs use water aerobics as a chance to help people with paralysis to get out of the chair and experience some freedom of movement as they work muscles that are often neglected during in-chair exercises.
  • Muscle relaxant – that help to increase muscle strength. It can be done either by any drugs or manually applying heat and electromagnetic radiation.
  • Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
  • Support groups – family education, and advocacy by family support, friend circle, etc.
  • Psychotherapy – to help you deal with the psychological effects of the disease.
  • Exercise therapy – to help you remain healthy in spite of your disability.

Initial Treatment of Hemiplegia

Immediate treatment is aimed at limiting the size of the stroke and preventing further stroke. Acute stroke therapies try to stop a stroke while it is happening by quickly dissolving the blood clot causing an ischaemic stroke or by stopping the bleeding of a hemorrhagic stroke.  This will involve administering medications and may involve surgery in some cases.

Medications

Facial Hemiplegia

RX

  • Thrombolytic therapy – These medications dissolve blood clots allowing blood flow to be re-established
  • Anticoagulants (eg: heparin) or aspirin These medications help to prevent blot clots from getting bigger and prevent new blood clots from forming
  • Antihypertensives  In cases of hemorrhagic stroke these medications may be prescribed to help lower high blood pressure
  • Medications– to reduce swelling in the brain and medications to treat underlying causes for the stroke eg: heart rhythm disorders may also be given.
  • Blood thinners – to reduce cardiovascular blockages and decrease the chances of future strokes.
  • Antibiotics usually delivered intravenously, to combat brain infections.
  • Muscle relaxant drugs – Tolperisone or eperisone hcl
  • Surgery to address secondary issues-particularly involuntary muscle contractions, spinal damage, or damage to the ligaments or tendons on the unaffected side of the body.
  • Physical therapy – designed to help the brain work around the injuries. Physical therapy can also strengthen the unaffected side and help you reduce the loss of muscle control and tone.
  • Support groups – family education, and advocacy.
  • Psychotherapy to help you deal with the psychological effects of the disease.
  • Exercise therapy to help you remain healthy in spite of your disability.

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Treatment of Facial Hemiplegia

Brain cells do not generally regenerate. Following a stroke, surviving brain cells can take over the function of areas that are dead or damaged, but only to a certain degree. The adaptive ability of the brain requires the relearning of various skills. As each person who suffers a stroke is affected differently, individual rehabilitation plans are developed in conjunction with the patient, family, and healthcare team. These aim to teach skills and maximize function so that the person can achieve maximum independence.

Physiotherapy

Treatment of hemiplegia requires coordination of several health professionals. A physiotherapist, occupational therapist, a physician, a surgeon and support from family, etc.

  • Treatment is focused – to find the causative factor and check its further progression. Secondly, after a few days, rehabilitation therapy helps to minimize disability.
  • Several medicines – are prescribed to control the primary cause such as antihypertensive, anti-thrombolytic agents to dissolve the clot, drugs to control cerebral edema, etc.
  • Intensive physical therapy – is begun after a few days. Activities such as walking, standing are done repeatedly under the guidance of a physiotherapist. It helps to improve the muscular functions which have become rigid. It is aimed to make the patient self-sufficient to perform his daily activities.
  • The patient is taught – to move his affected arm with his strong arm. With exercise, it is possible to maintain the flexibility of joints and it also prevents tightening and shortening of muscles. Speech therapy is simultaneously begun to improve communication and speaking skills.
  • Speech therapy – to improve communication
  • Occupational therapy to improve daily functions such as eating, cooking, toileting, and washing.
Recovery can take months and it may be several days or weeks after the stroke before doctors are able to give an accurate prediction for recovery.

Occupational therapy

  • Occupational therapy – Occupational Therapists may specifically help with hemiplegia with tasks such as improving hand function, strengthening the hand, shoulder, and torso, and participating in activities of daily living (ADLs), such as eating and dressing.
  • Therapists – may also recommend a hand splint for active use or for stretching at night. Some therapists actually make the splint; others may measure your child’s hand and order a splint. OTs educate patients and family on compensatory techniques to continue participating in daily living, fostering independence for the individual – which may include, environmental modification, use of adaptive equipment, sensory integration, etc.

Rehabilitation & Therapy for Hemiplegia

1. Improving motor control

a. Neurofacilitatory Techniques

In Stroke Physical Therapy these therapeutic interventions use sensory stimuli (e.g. quick stretch, brushing, reflex stimulation, and associated reactions), which are based on neurological theories, to facilitate movement in patients following stroke. The following are the different approaches

  • Bobath Concept- Berta & Karel Bobath’s approach focuses to control responses from the damaged postural reflex mechanisms. Emphasis is placed on affected inputs facilitation and normal movement patterns (Bobath, 1990).
  • ii.Brunnstrom – Brunnstrom approach is one form of neurological exercise therapy in the rehabilitation of stroke patients. The relative effectiveness of Neuro-developmental treatment versus the Brunnstrom method was studied by Wagenaar and colleagues from the perspective of the functional recovery of stroke patients. The result of this study showed no clear differences in the effectiveness of the two methods within the framework of functional recovery.
  • iii.Rood – Emphasise the use of activities in developmental sequences, sensation stimulation, and muscle work classification. Cutaneous stimuli such as icing, tapping, and brushing are employed to facilitate activities.
  • iv. Proprioceptive neuromuscular facilitation (PNF) – Developed by Knott and Voss, they advocated the use of peripheral inputs as stretch and resisted movement to reinforce existing motor response. Total patterns of movement are used in the treatment and are followed in a developmental sequence.

b. Learning theory approach

  • i. Conductive education – In Stroke Physical Therapy, Conductive education is one of the methods in treating neurological conditions including hemiplegic patients. Cotton and Kinsman (1984) demonstrated a neuropsychological approach using the concept of CE for adult hemiplegia. The patient is taught how to guide his movements towards each task-part of the task by using his own speech – rhythmical intention.
  • ii. Motor relearning theory – Carr & Shepherd, both are Australian physiotherapists, developed this approach in 1980. It emphasizes the practice of functional tasks and the importance of relearning real-life activities for patients. Principles of learning and biomechanical analysis of movements and tasks are important. There is no evidence adequately supporting the superiority of one type of exercise approach over another. However, the aim of the therapeutic approach is to increase physical independence and to facilitate the motor control of skill acquisition and there is strong evidence to support the effect of rehabilitation in terms of improved functional independence and reduced mortality.

c. Functional electrical stimulation (FES) 

  • FES is a modality that applied a short burst of electrical current to the hemiplegic muscle or nerve. In Stroke Physical Therapy, FES has been demonstrated to be beneficial to restore motor control, spasticity, and reduction of hemiplegic shoulder pain and subluxation.  A recent meta-analysis of the randomized controlled trial study showed that FES improves motor strength. A study by Faghri has identified that FES can significantly improve arm function, electromyographic activity of posterior deltoid, the range of motion and reduction of severity of subluxation and pain of the hemiplegic shoulder.

d. Biofeedback

  • Biofeedback is a modality that facilitates the cognizant of electromyographic activity in selected muscle or awareness of joint position sense via visual or auditory cues. In Stroke Physical Therapy the result of studies in biofeedback is controversial. A meta-analysis of 8 randomized controlled trials of biofeedback therapy demonstrated that electromyographic biofeedback could improve motor function in stroke patients.
  • A conflicting meta-analysis study by showing that biofeedback was not efficacious in improving the range of motion in the ankle and shoulder in a stroke patient. Moreland conducted another meta-analysis that concluded that EMG biofeedback alone or with conventional therapy did not superior to conventional physical therapy in improving upper- extremity function in the adult stroke patient.

2. Hemiplegic shoulder management

Shoulder subluxation and pain of the affected arm is not uncommon in at least 30% of all patient after stroke, whereas subluxation is found in 80% of stroke patients. It is associated with the severity of the disability and is common in patients in rehabilitation settings. Suggested interventions are as follows:

  • a. Exercise – Active weight-bearing exercise can be used as a means of improving motor control of the affected arm; introducing and grading tactile, proprioceptive, and kinesthetic stimulation; and preventing edema and pain. In Stroke Physical Therapy, Upper extremity weight bearing can be used to lengthen or inhibit tight or spastic muscles while simultaneously facilitating muscles that are not active (Donatelli, 1991). According to Robert (1992), the amount of shoulder pain in hemiplegia was related most to loss of motion. He advocated that the provision of ROM exercise (caution to avoid improvement) as treatment as early as possible.
  • b. Functional electrical stimulation – Functional electrical stimulation (FES) is an increasingly popular treatment for hemiplegic stroke patients. It has been applied in stroke physical therapy for the treatment of shoulder subluxation spasticity and functionally, for the restoration of function in the upper and lower limb. In Stroke Physical Therapy, Electrical stimulation is effective in reducing pain and severity of subluxation, and possibly in facilitating recovery of arm function
  • c. Positioning & proper handling – In Stroke Physical Therapy, proper positioning and handling of the hemiplegic shoulder, whenever in bed, sitting and standing or during lifting, can prevent shoulder injury is recommended in the AHCPR & SIGN guidelines for stroke rehabilitation. In Stroke Physical Therapy, positioning can be therapeutic for tone control and neuro-facilitation of stroke patients (Davies, 1991). Braus et al 94 found shoulder hand syndrome reduced from 27% to 8% by the instruction to everyone including family on handling technique.
  • d. Neuro-facilitation
  • e. Passive limb physiotherapy – Maintenance of a full pain-free range of movement without traumatizing the joint and the structures can be carried out. In Stroke Physical Therapy, at no time should pain in or around the shoulder joint be produced during treatment.
  • f. Pain relief physiotherapy – Passive mobilization as described by Maitland can be useful in gaining relief of pain and range of movement. In Stroke Physical Therapy other treatment modalities such as thermal, electrical, cryotherapy, etc. can be applied for shoulder pains or musculoskeletal in nature.
  • g. Reciprocal pulley – The use of reciprocal pulley appears to increase the risk of developing shoulder pain in stroke patients. It is not related to the presence of subluxation or to muscle strength.
  • h. Sling – In Stroke Physical Therapy the use of a sling is controversial. No shoulder support will correct a glenohumeral joint subluxation. However, it may prevent the flaccid arm from hanging against the body during functional activities, thus decreasing shoulder joint pain. They also help to relieve downward traction on the shoulder capsule caused by the weight of the arm.

3. Limb physiotherapy

  • Limb physiotherapy/Stroke Physical Therapy includes passive, assisted-active and active range-of-motion exercise for the hemiplegic limbs. This can be effective management for the prevention of limb contractures and spasticity and is recommended within AHCPR. Self-assisted limb exercise is effective for reducing spasticity and shoulder protection. Adams and coworkers recommended passive full-range-of-motion exercise for a paralyzed limb for potential reduction of complication for stroke patients

4. Chest physiotherapy

  • In Stroke Physical Therapy, evidence shows that both cough and forced expiratory technique (FET) can eliminate induced radio aerosol particles in the lung field. Directed coughing and FET can be used as a technique for bronchial hygiene clearance in stroke patients.

5. Positioning

  • In Stroke, Physical Therapy consistent “reflex-inhibitory” patterns of posture in resting is encouraged to discourage physical complication of stroke and to improve recovery (Bobath, 1990).
  • Meanwhile, therapeutic positioning is a widely advocated strategy to discourage the development of abnormal tone, contractures, pain, and respiratory complications. It is an important element in maximizing the patient’s functional gains and quality of life.

6. Tone management

  • A goal of Stroke Physical Therapy interventions has been to “normalize tone to normalize movement.” Therapy modalities for reducing tone include stretching, prolonged stretching, passive manipulation by therapists, weight-bearing, ice, contraction of muscles antagonistic to spastic muscles, splinting, and casting.
  • Research on tone-reducing techniques has been hampered by the inadequacies of methods to measure spasticity and the uncertainty about the relationship between spasticity and volitional motor control.
  • The manual stretch of finger muscles, pressure splints, and dantrolene sodium do not produce apparent long-term improvement in motor control. Dorsal resting hand splints reduced spasticity more than volar splints, but the effect on motor control is uncertain while TENS stimulation showed improvement for chronic spasticity of lower extremities.

7. Sensory re-education

  • Bobath and other therapy approaches recommend the use of sensory stimulation to promote the sensory recovery of stroke patients.

8. Balance retraining

  • Re-establishment of balance function in patients following stroke has been advocated as an essential component in the practice of stroke physical therapy. Some studies of patients with hemiparesis revealed that these patients have a greater amount of postural sway, the asymmetry with greater weight on the non-paretic leg, and a decreased ability to move within a weight-bearing posture. Meanwhile, research has demonstrated moderate relationships between balance function and parameters such as gait speed, independence, wheelchair mobility, reaching, as well as dressing. Some tenable support on the effectiveness of treatment of disturbed balance can be found in studies comparing the effects of balance retraining plus physiotherapy treatment and physiotherapy treatment alone.

9. Fall prevention

  • In Stroke Physical Therapy, falls are one of the most frequent complications and the consequences of which are likely to have a negative effect on the rehabilitation process and its outcome.
  • According to the systematic review of the Cochrane Library, which evaluated the effectiveness of several fall prevention interventions in the elderly, there was significant protection against falling from interventions that targeted multiple, identified, risk factors in individual patients. The same is true for interventions which focused on behavioral interventions targeting environmental hazards plus other risk factors

10. Gait re-education

  • Recovery of independent mobility is an important goal for the immobile patient, and much therapy is devoted to gait-reeducation. Bobath assumes abnormal postural reflex activity is caused by dysfunction so gait training involved tone normalization and preparatory activity for gait activity.
  • In contrast, Carr and Shepherd advocate task-related training with methods to increase strength, coordination and flexible MS system to develop skill in walking while Treadmill training combined with the use of a suspension tube. Some patient’s body weight can effective in regaining walking ability when used as an adjunct to convention therapy 3 months after active training.

11. Functional Mobility Training

  • To handle the functional limitations of stroke patients, functional tasks are taught to them based on movement analysis principles. In Stroke Physical Therapy these tasks include bridging, rolling to sit to stand and vice versa, transfer skills, walking and staring, etc.
  • Published studies report that many patients improve during rehabilitation. The strongest evidence of benefit is from studies that have enrolled patients with chronic deficits or have included a no-treatment control group.
  • Meanwhile, early mobilization helps prevent compilations e.g. DVT, skin breakdown contracture and pneumonia. Evidence has shown better orthostatic tolerance and earlier ambulation.

12. Upper limb training

By 3 months poststroke, approximately 37% of the individuals continue to have decreased upper extremities (UE) function. Recovery of UE function lags behind that of the lower extremities because of the more complex motor skill required of the UE in daily life tasks. That means many individuals who have a stroke are at risk for a lowered quality of life. Many approaches to the physical rehabilitation of adults post-stroke exist that attempt to maximize motor skill recovery. However, the literature does not support the efficacy of any single approach. The followings are the current approaches to motor rehabilitation of the UE.

  • a. Facilitation models – They are the most common methods of intervention for the deficits in UE motor skills including Bobath, proprioceptive neuromuscular facilitation, Brunnstrom’s movement therapy, and Rood’s sensorimotor approach. There is some evidence that practice based on the facilitation models can result in improved motor control of UE. However, an intervention based on the facilitation models has not been effective in restoring the fine hand coordination required for the performance of actions.
  • b. Functional electric stimulation – In Stroke Physical Therapy, Functional electric stimulation (FES) can be effective in increasing the electric activity of muscles or increased active range of motion in individuals with stroke. Some evidence showed that FES may be more effective than facilitation approaches.
  • c. Electromyographic biofeedback – In Stroke Physical Therapy, biofeedback can contribute to improvements in motor control at the neuromuscular and movement levels. Some studies have shown improvements in the ability to perform actions during post-testing after biofeedback training. However, the ability to generalize these skills and incorporate them into daily life is not measured.
  • d. Constraint-induced therapy – Constraint-Induced (CI) therapy was designed to overcome the learned nonuse of the affected UE. In the most extreme form of CI therapy, individual post-stroke is prevented from using the less affected UE by keeping it in a splint and sling for at least 90% of their waking hours. Studies have found that the most extreme of CI therapy can effect rapid improvement in UE motor skill and that is retained for at least as long as 2 years. However, CI therapy currently is effective only in those with distal voluntary movement.

13. Mobility appliances and equipment

  • Small changes in an individual’s local ‘environment’ can greatly increase independence, use of a wheelchair or walking stick. However, little research has been done for these ‘treatments’. It is acknowledged that walking aids and mobility appliances may benefit selected patients.

14. Acupuncture 

  • The World Health Organisation (WHO) has listed acupuncture as a possible treatment for pariesis after stroke. Studies had sown its beneficial effects on stroke rehabilitation.
  • Hua had reported a significant difference in changes of neurological score between the acupuncture group and the control group after 4 weeks of treatment in an RCT and no adverse effects were observed in patients treated with acupuncture.

15. Vasomotor training 

  • Early stimulation of the muscle pump can reduce the venous stasis and enhance the general circulation of the body. It then hastens the recovery process.

16. Edema management

  • Use of intermittent pneumatic pump, elastic stocking or bandages and massage can facilitate the venous return of the oedematous limbs. Therefore, the elasticity and flexibility of the musculoskeletal system can be maintained and enhance the recovery process and prevent complications like pressure ulcers.

Homeopathic Medicines for Hemiplegia

Homeopathic medicines cannot cure hemiplegia. However, the medicines can be administered to improve the state of paralysis, improve blood circulation, help control loss of power, improve the power of muscles to come extent and improve the overall health of the patient.

Some common medicines for hemiplegia and such states of paralysis are:

  • Plumbum Metallicum – This medicine is sourced by processing and potentizing the metal lead. It helps the neuro-muscular system of the body. It is administered with the intention to improve some muscle power. Plumbum met, as it is called, may be indicated all kinds of paralysis such as hemiplegia, paraplegia, and quadriplegia. As said earlier, it cannot cure paralysis as such.
  • Causticum Similar to the above medicine, Causticum is also a friend to all paralysis patients. It is aimed at improving some muscle power and not cure it.
  • Nux vomicaThis herbal medicine helps in the early stages of hemiplegia and not after some months or years.
  • Lathyrus sativus – This is another example of a toxin transformed into medicine. It is safe, There are some spasticity and stiffness in some muscles, in the cases of hemiplegia, where Lathyrus may be called for.
  • GelsemiumThis plant remedy is useful for early cases of paralysis including hemiplegia. It is supposed to improve muscle strength in the cases of paralysis.

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Prevention

Reducing the number of controllable risk factors is the best way to prevent a stroke.  This can include:

  • Stopping smoking
  • Losing weight
  • Eating a balanced diet low in sodium and saturated and trans fat
  • Moderating alcohol intake (no more than 2 small drinks per day)
  • Exercising regularly in order to stay physically fit
  • Maintaining good control of existing medical conditions such as diabetes, high blood pressure and high cholesterol.

Referances

What Is Facial Hemiplegia?

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