Category Archive Health A – Z

ByRx Harun

Technique and Procedure of Intramuscular Injection

Technique and Procedure of Intramuscular Injection/Intramuscular Injection is the method of installing medications into the depth of the bulk of specifically selected muscles. The basis of this process is that the bulky muscles have good vascularity, and therefore the injected drug quickly reaches the systemic circulation and thereafter into the specific region of action, bypassing the first-pass metabolism. It is one of the most common medical procedures to be performed on an annual basis. However, there is still a lack of uniform guidelines and an algorithm in giving IM among health professionals across the world. 

Intramuscular injection, often abbreviated IM, is the injection of a substance directly into the muscle. In medicine, it is one of several methods for parenteral administration of medications. Muscles have larger and more numerous blood vessels than subcutaneous tissue; intramuscular injections usually have faster rates of absorption than subcutaneous or intradermal injections.[rx] The volume of injection is limited to 2-5 milliliters, depending on the injection site.

Anatomy and Physiology of Intramuscular Injection

Anatomical Landmarks

  • There are specific landmarks to be taken into consideration while giving IM injections so as to avoid any neurovascular complications. The specific landmarks for the most commonly used sites are discussed below

Dorsogluteal Region

  • 5 to 7.5 cm below the iliac crest.
  • Upper outer quadrant of the upper outer quadrant within the buttocks

Ventrogluteal Region

  • The heel of the opposing hand is placed in the greater trochanter, the index finger in the anterior superior iliac spine and the middle finger below the iliac crest. The drug is injected in the triangle formed by the index, middle finger, and the iliac crest

Deltoid

  • 2.5 to 5 cm below the acromion process

Vastus Lateralis

  • Possible sites for IM injection include – deltoid, dorsogluteal, rectus femoris, vastus lateralis and ventrogluteal muscles. Sites that are bruised, tender, red, swollen, inflamed or scarred are avoided.
  • The middle third of the line joining the greater trochanter of the femur and the lateral femoral condyle of the knee

Uses of Intramuscular Injection

Drugs may be given intramuscularly both for prophylactic as well as curative purposes, and the most common medications include:

  • Antibiotics- penicillin G benzathine penicillin, streptomycin
  • Biologicals- immunoglobins, vaccines, and toxoids
  • Hormonal agents- testosterone, medroxyprogesterone

Any drugs that are nonirritant and soluble may be given IM during an emergency scenario.

Examples of medications that are sometimes administered intramuscularly are:

  • Atropine
  • Haloperidol (Haldol)
  • Aripiprazole (Abilify)
  • Paliperidone (Invega)
  • Chlorpromazine (Thorazine)
  • Lorazepam (Ativan)
  • Fulvestrant (Faslodex)
  • Codeine
  • Morphine
  • Methotrexate
  • Metoclopramide
  • Magnesium sulfate
  • Olanzapine
  • Streptomycin
  • Diazepam
  • Prednisone
  • Penicillin
  • Interferon beta-1a
  • Sex hormones, such as testosterone, estradiol valerate, and medroxyprogesterone acetate (as Depo Provera)
  • Dimercaprol
  • Ketamine
  • Leuprorelin
  • Naloxone
  • Quinine, in its gluconate form
  • Vitamin B12, as cyanocobalamin, hydroxocobalamin or methylcobalamin
  • Risperidone

Vaccines are often administered as IM injections.

In addition, some vaccines are administered intramuscularly

  • Gardasil
  • Hepatitis A vaccine
  • Rabies vaccine
  • Influenza vaccines based on inactivated viruses are commonly administered intramuscularly (although there is active research being conducted as to the best route of administration).
  • Platelet-rich plasma injections can be administered intramuscularly.
  • Certain substances (e.g. ketamine) are injected intramuscularly for recreational purposes.

Indications of Intramuscular Injection

IM is commonly indicated for patients who are 

  • Noncompliant
  • Uncooperative
  • Reluctant
  • Unable to receive drugs through other commonly utilized routes

Contraindications of Intramuscular Injection

  • Active infection, cellulitis or dermatitis at the site of administration
  • Known allergy or hypersensitivity to the drug
  • Acute myocardial infarction- the release of muscle enzymes may provide a confounding bias in making the diagnosis
  • Thrombocytopenia
  • Coagulation defects
  • Hypovolemic shock- the absorption of the drug may be hampered owing to compromised vascularity to the muscle
  • Myopathies
  • Associated muscular atrophy- leads to delayed drug absorption as well as adds up the risk of neurovascular complications

Equipment

  • 20-25 gauge syringe with a needle length of 16-38 mm
  • Filter needle
  • Alcohol-based antiseptic solution
  • The correct drug in an appropriate dose
  • Dry cotton swab
  • Self-adhesive bandage
  • Needle disposal unit
  • A trained nurse or a paramedics
  • The treating physician

Preparation

Prerequisite-

Ensure the 5 ‘Rs’

  • Right patient
  • Right drug
  • Right dose
  • Right site
  • Right timing

Ask for any adverse reactions in previous such procedures.

Counseling regarding the procedure and preparing the patient– to calm them down and also to minimize the pain associated with the procedure

Site selection

  • Infants- vastus lateralis
  • Children- vastus lateralis and deltoid
  • Adults- ventrolateral and deltoid

Drug volume

  • 2 ml or less- deltoid injection
  • 2 to 5 ml       – Ventrogluteal injection

Needle length

  • Vastus lateralis -16 to 25 mm
  • Deltoid-16 to 32 mm (children), 25 to 38 mm(adults)
  • Ventrogluteal-38 mm

Technique of Intramuscular Injection

The sequential method of IM injection can be summarised as follows

  • Thorough cleaning of the hands
  • Application of sterile gloves
  • Thorough cleansing surrounding the site of injection with an alcohol-based antiseptic solution
  • Perpendicular insertion of a needle of appropriate sized length
  • Prepare the drug and then aspirate it from the filter needle
  • Insure intramuscular positioning of the needle via confirming restricted side to side movement of the needle as opposed to when the needle is in the subcutaneous plane
  • Aspirate to rule out any egress of blood especially in cases of dorsogluteal injection due to inadvertent vascular puncturing of the gluteal artery during the procedure
  • Slow injection of the drug at 10 sec/ml
  • Slow withdrawal the needle and then apply gentle pressure over the injected site with a dry cotton swab
  • Proper disposal of all the equipment used during the procedure
  • Assessment of  the injected region for probable early and late complications

Complications

Common complications  associated with the intramuscular injection can be summarized as :

  • Muscle fibrosis and contracture
  • Abscess at the injection site
  • Gangrene
  • Nerve injury -the sciatic nerve in gluteal injection, the femoral nerve in vastus lateralis injection
  • Vascular injury- the superior gluteal nerve in dorsogluteal injection, the femoral nerve in vastus lateralis injection, radial nerve in deltoid injection
  • Skin slough
  • Periostitis
  • Transmission of HIV, hepatitis virus
  • Persistent pain at the site of injection

Clinical Significance

Advantages

  • Rapid and uniform absorption of the drug especially those of the aqueous solutions
  • Rapid onset of the action compared to that of the oral and the subcutaneous routes
  • IM injection bypasses the first-pass metabolism
  • It also avoids the gastric factors governing the drug absorption
  • Has efficacy and potency comparable to that of the intravenous drug delivery system.
  • Highly efficacious in emergency scenarios such as acute psychosis and status epilepticus
  • Depot injections allow slow, sustained and prolonged  action
  • A large volume of the drug can be administered compared to that of the subcutaneous route

 Disadvantages

  • Expert and a trained person is required for administrating the drug by IM route
  • The absorption of the drug is determined by the bulk of the muscle and its vascularity
  • The onset and duration of the action of the drug is not adjustable
  • In case of inadvertent scenarios such as anaphylaxis or neurovascular injuries, intravenous (IV) assess needs to be secured
  • IM injection at the appropriate landmarks may be difficult in a child as well as in  patients requiring physical restrain
  • Inadvertent injection in the subcutaneous plane of the fascia can lead to delayed action of the drug
  • Painful procedure
  • Suspensions, as well as oily drugs, cannot be administered
  • Can lead to anxiety to the patient especially in children
  • Self-administration of the drug can be difficult
  • The precipitation of the drug following faster absorption of the solvent may lead to delayed and prolonged action of the drug
  • Unintended prolonged sequelae following delayed drug release from the muscular compartment
  • Need for temporary restraint of the patients especially in cases with children

References

ByRx Harun

Intramuscular Injection – Types, Technique, Procedure

Intramuscular Injection is the method of installing medications into the depth of the bulk of specifically selected muscles. The basis of this process is that the bulky muscles have good vascularity, and therefore the injected drug quickly reaches the systemic circulation and thereafter into the specific region of action, bypassing the first-pass metabolism. It is one of the most common medical procedures to be performed on an annual basis. However, there is still a lack of uniform guidelines and an algorithm in giving IM among health professionals across the world. 

Intramuscular injection, often abbreviated IM, is the injection of a substance directly into the muscle. In medicine, it is one of several methods for parenteral administration of medications. Muscles have larger and more numerous blood vessels than subcutaneous tissue; intramuscular injections usually have faster rates of absorption than subcutaneous or intradermal injections.[rx] The volume of injection is limited to 2-5 milliliters, depending on the injection site.

Anatomy and Physiology of Intramuscular Injection

Anatomical Landmarks

  • There are specific landmarks to be taken into consideration while giving IM injections so as to avoid any neurovascular complications. The specific landmarks for the most commonly used sites are discussed below

Dorsogluteal Region

  • 5 to 7.5 cm below the iliac crest.
  • Upper outer quadrant of the upper outer quadrant within the buttocks

Ventrogluteal Region

  • The heel of the opposing hand is placed in the greater trochanter, the index finger in the anterior superior iliac spine and the middle finger below the iliac crest. The drug is injected in the triangle formed by the index, middle finger, and the iliac crest

Deltoid

  • 2.5 to 5 cm below the acromion process

Vastus Lateralis

  • Possible sites for IM injection include – deltoid, dorsogluteal, rectus femoris, vastus lateralis and ventrogluteal muscles. Sites that are bruised, tender, red, swollen, inflamed or scarred are avoided.
  • The middle third of the line joining the greater trochanter of the femur and the lateral femoral condyle of the knee

Uses of Intramuscular Injection

Drugs may be given intramuscularly both for prophylactic as well as curative purposes, and the most common medications include:

  • Antibiotics- penicillin G benzathine penicillin, streptomycin
  • Biologicals- immunoglobins, vaccines, and toxoids
  • Hormonal agents- testosterone, medroxyprogesterone

Any drugs that are nonirritant and soluble may be given IM during an emergency scenario.

Examples of medications that are sometimes administered intramuscularly are:

  • Atropine
  • Haloperidol (Haldol)
  • Aripiprazole (Abilify)
  • Paliperidone (Invega)
  • Chlorpromazine (Thorazine)
  • Lorazepam (Ativan)
  • Fulvestrant (Faslodex)
  • Codeine
  • Morphine
  • Methotrexate
  • Metoclopramide
  • Magnesium sulfate
  • Olanzapine
  • Streptomycin
  • Diazepam
  • Prednisone
  • Penicillin
  • Interferon beta-1a
  • Sex hormones, such as testosterone, estradiol valerate, and medroxyprogesterone acetate (as Depo Provera)
  • Dimercaprol
  • Ketamine
  • Leuprorelin
  • Naloxone
  • Quinine, in its gluconate form
  • Vitamin B12, as cyanocobalamin, hydroxocobalamin or methylcobalamin
  • Risperidone

Vaccines are often administered as IM injections.

In addition, some vaccines are administered intramuscularly:

  • Gardasil
  • Hepatitis A vaccine
  • Rabies vaccine
  • Influenza vaccines based on inactivated viruses are commonly administered intramuscularly (although there is active research being conducted as to the best route of administration).
  • Platelet-rich plasma injections can be administered intramuscularly.
  • Certain substances (e.g. ketamine) are injected intramuscularly for recreational purposes.

Indications of Intramuscular Injection

IM is commonly indicated for patients who are

  • Noncompliant
  • Uncooperative
  • Reluctant
  • Unable to receive drugs through other commonly utilized routes

Contraindications of Intramuscular Injection

  • Active infection, cellulitis or dermatitis at the site of administration
  • Known allergy or hypersensitivity to the drug
  • Acute myocardial infarction- the release of muscle enzymes may provide a confounding bias in making the diagnosis
  • Thrombocytopenia
  • Coagulation defects
  • Hypovolemic shock- the absorption of the drug may be hampered owing to compromised vascularity to the muscle
  • Myopathies
  • Associated muscular atrophy- leads to delayed drug absorption as well as adds up the risk of neurovascular complications

Equipment

  • 20-25 gauge syringe with a needle length of 16-38 mm
  • Filter needle
  • Alcohol-based antiseptic solution
  • The correct drug in an appropriate dose
  • Dry cotton swab
  • Self-adhesive bandage
  • Needle disposal unit
  • A trained nurse or a paramedics
  • The treating physician

Preparation

Prerequisite-

Ensure the 5 ‘Rs’

  • Right patient
  • Right drug
  • Right dose
  • Right site
  • Right timing

Ask for any adverse reactions in previous such procedures.

Counseling regarding the procedure and preparing the patient– to calm them down and also to minimize the pain associated with the procedure

Site selection

  • Infants- vastus lateralis
  • Children- vastus lateralis and deltoid
  • Adults- ventrolateral and deltoid

Drug volume

  • 2 ml or less- deltoid injection
  • 2 to 5 ml       – Ventrogluteal injection

Needle length

  • Vastus lateralis -16 to 25 mm
  • Deltoid-16 to 32 mm (children), 25 to 38 mm(adults)
  • Ventrogluteal-38 mm

Technique of Intramuscular Injection

The sequential method of IM injection can be summarised as follows

  • Thorough cleaning of the hands
  • Application of sterile gloves
  • Thorough cleansing surrounding the site of injection with an alcohol-based antiseptic solution
  • Perpendicular insertion of a needle of appropriate sized length
  • Prepare the drug and then aspirate it from the filter needle
  • Insure intramuscular positioning of the needle via confirming restricted side to side movement of the needle as opposed to when the needle is in the subcutaneous plane
  • Aspirate to rule out any egress of blood especially in cases of dorsogluteal injection due to inadvertent vascular puncturing of the gluteal artery during the procedure
  • Slow injection of the drug at 10 sec/ml
  • Slow withdrawal the needle and then apply gentle pressure over the injected site with a dry cotton swab
  • Proper disposal of all the equipment used during the procedure
  • Assessment of  the injected region for probable early and late complications

Complications

Common complications  associated with the intramuscular injection can be summarized as :

  • Muscle fibrosis and contracture
  • Abscess at the injection site
  • Gangrene
  • Nerve injury -the sciatic nerve in gluteal injection, the femoral nerve in vastus lateralis injection
  • Vascular injury- the superior gluteal nerve in dorsogluteal injection, the femoral nerve in vastus lateralis injection, radial nerve in deltoid injection
  • Skin slough
  • Periostitis
  • Transmission of HIV, hepatitis virus
  • Persistent pain at the site of injection

Clinical Significance

Advantages

  • Rapid and uniform absorption of the drug especially those of the aqueous solutions
  • Rapid onset of the action compared to that of the oral and the subcutaneous routes
  • IM injection bypasses the first-pass metabolism
  • It also avoids the gastric factors governing the drug absorption
  • Has efficacy and potency comparable to that of the intravenous drug delivery system.
  • Highly efficacious in emergency scenarios such as acute psychosis and status epilepticus
  • Depot injections allow slow, sustained and prolonged  action
  • A large volume of the drug can be administered compared to that of the subcutaneous route

 Disadvantages

  • Expert and a trained person is required for administrating the drug by IM route
  • The absorption of the drug is determined by the bulk of the muscle and its vascularity
  • The onset and duration of the action of the drug is not adjustable
  • In case of inadvertent scenarios such as anaphylaxis or neurovascular injuries, intravenous (IV) assess needs to be secured
  • IM injection at the appropriate landmarks may be difficult in a child as well as in  patients requiring physical restrain
  • Inadvertent injection in the subcutaneous plane of the fascia can lead to delayed action of the drug
  • Painful procedure
  • Suspensions, as well as oily drugs, cannot be administered
  • Can lead to anxiety to the patient especially in children
  • Self-administration of the drug can be difficult
  • The precipitation of the drug following faster absorption of the solvent may lead to delayed and prolonged action of the drug
  • Unintended prolonged sequelae following delayed drug release from the muscular compartment
  • Need for temporary restraint of the patients especially in cases with children

References

ByRx Harun

Piriformis Steroid Injection – Indication, Contraindication

Piriformis steroid injection is an injection of a long-lasting steroid into the piriformis muscle of your buttock. This muscle attaches to the side of the sacrum, which is the side, flat bone at the base of your spine just above your tailbone.

Piriformis muscle injections provide diagnostic information and therapeutic relief for those suffering from piriformis syndrome. Common conditions for which this procedure is used include piriformis muscle spasm and inflammation.

Arriving at the diagnosis of piriformis muscle injection requires a thorough history, physical exam, and the exclusion of more common diagnoses, including lumbar stenosis, lumbar radiculopathy, lumbar facet joint arthritis, sacroiliac (SI) joint dysfunction, trochanteric bursitis, and myofascial pain syndrome

Indications of Piriformis Steroid Injection

Piriformis syndrome may be responsible for 0.3% to 6% of all cases of low back pain and/or sciatica. With an estimated amount of new cases of low back pain and sciatica at 40 million annually, the incidence of piriformis syndrome would be roughly 2.4 million per year. In the majority of cases, piriformis syndrome occurs in middle-aged patients with a reported ratio of male to female patients being affected 1:6.

Contraindications of Piriformis Steroid Injection

Two components contribute to the clinical presentation of piriformis syndrome: somatic and neuropathic. The somatic component is a myofascial pain component of the syndrome secondary to any of the surrounding muscles/fascia (i.e. any of the short external rotators of the hip). The neuropathic component refers to the compression or irritation of the sciatic nerve as it courses through above, near, or through, the piriformis muscle itself.

Patients may present acutely in cases of post-traumatic piriformis syndrome or insidiously as in cases of overuse or myofascial pain. Patients will report having gluteal pain with possible associated paresthesias in the back, groin, perineum, buttocks, hip, back of the thigh, calf, foot, and rectum. There is also intense and worsened pain with sitting or squatting.

Preparation of Piriformis Steroid Injection

Initial evaluation should start with a lumbar spine examination. The examination should take into account the patient’s gait, posture, and alignment as well as any leg length discrepancies. Also, the practitioner should examine the patient’s hips, pelvis, and the sacroiliac joint, noting sensory, motor, and deep tendon reflexes.

In piriformis syndrome, sensory, motor, and deep tendon reflexes are normal. The piriformis should be palpated as well just posterior to the hip joint and in the area of the greater sciatic notch.   Straight leg raise may also be positive although there is variable sensitivity and specificity for this provocative maneuver.

There are individual tests that stretch the piriformis and can be used to help aid in the diagnosis of exclusion. One of these is the Freiberg sign, which is performed by putting the hip in extension and internal rotation and having the patient externally rotate against resistance. The positive exam will reproduce pain around the piriformis. This test will have positive results in up to 63% of patients. Another individual test called the Pace sign is performed by resisting abduction and external rotation of the hip while the patient is in a seated position. Pace sign occurs in 30% to 74% in piriformis syndrome. FAIR test or also known as the piriformis stretch may elicit pain. Beatty sign has also been described and is accomplished by elevating the flexed leg on the irritated side while the patient lies on the asymptomatic side. Pain and reproduction of the symptoms are a positive test result.

Technique

No definitive diagnostic criteria has been validated and established for piriformis syndrome.  It remains a diagnosis of exclusion, but many of the following exam findings can aid the clinician in honing in on this diagnosis:

  • Unilateral or bilateral buttock pain with fluctuating periods of pain throughout the day
  • No lower back pain,
  • No pain upon palpation of axial spine
  • Negative results for straight leg raise
  • Prolonged sitting triggering gluteal pain or sciatica
  • Fluctuating sciatica through the course of the day
  • Buttock pain near projection of the piriformis reproduced by FAIR or Freiberg sign or Beatty sign, or palpitations
  • The absence of perineal irradiation
  • Sciatica reproduced by FAIR, Freiberg sign, or Beatty sign.

Standard radiographs of the pelvis and hip should be done to rule out underlying hip pathology. MRI of the lumbar spine is also recommended to evaluate for a discogenic causes of lumbar radiculopathy and to rule out other sources of compression (e.g. soft tissue tumors or masses).  MRI can also evaluate for spinal stenosis, herniated disks, facet arthrosis, SI joint pathology, occult pelvic fractures, and any surrounding tendinopathies or bursitides.

EMG is often normal in patients with acute piriformis syndrome presentations, however, chronically, EMG/NCS can be useful in identifying neuropathic changes and abnormal results in muscles innervated by the sciatic nerve .

Solution (injectable):

  • Corticosteroids: 40-mg of Depo-Medrol or Kenalog
  • Local anesthetics: 3-5-ml of local anesthetic such as lidocaine or bupivacaine
  • It is also done with botulinum toxin for longer relief than steroid and local anesthetic.

Patient Position: Prone

Fluoroscopy starting position:

  • An A-P view is adjusted so that the inferior part of the sacroiliac joint is in the middle of the screen.

Piriformis Muscle Injection with Fluoroscopic Guidance

  • 18-gauge 1.5″ needle tip is placed on the cleaned skin over the inferior SI joint.
  • Create a skin wheal and then anesthetize the deeper subcutaneous skin with 1% lidocaine and a 27-gauge 1.25-inch needle.
  • A 22-gauge 3.5″ or 5″ Quincke needle is used to contact the very tip of the inferior sacroiliac joint. As the procedure is performed, note of the approximate needle depth.
  • After injection, the needle is withdrawn and redirected to a target site 1-cm inferior, 1-cm lateral, and 1-cm deeper than the SI joint.

Caution: Never inject if the patient feels a sharp pain shooting down their leg as the needle tip may be inside the sciatic nerve. The needle should be repositioned and then retry.

Prior to the Procedure

  • All blood-thinning products – (except aspirin) must be stopped prior to your procedure. You will be advised by letter when to stop taking these medications at the time that your admission date is arranged.
  • You are able to take your other regular medications with a sip of water on the morning of your procedure.
  • If you are an insulin-dependent diabetic you will always be at the beginning of the list. Please bring your insulin with you and it will be given to you following your procedure.
  • Hamilton Day Surgery Centre staff will advise you of your fasting and admission times.
  • You must not have anything to eat, drink, smoke or chew prior to your procedure.
  • You will need to organise someone to drive you home after the procedure as you will not be able to drive for 24 hours after your procedure.

What Will Happen?

  • You will be admitted to the day surgery by a nurse and you will be asked to change into a gown.
  • The anesthetist will speak with you and place a cannula (plastic needle) into a vein in your hand.
  • In the procedure room, you will be assisted to position on the procedure table lying on your abdomen with a pillow under your hips and abdomen.
  • The anesthetist will give you some sedation into your vein.
  • An X-ray machine will be used to determine where the doctor will place the needle for your procedure.
  • Local anesthetic and either Botox or steroid will be injected once correct needle placement has been established with the use of X-ray contrast (Omnipaque).
  • The procedure will take approximately 10 minutes to complete.
  • After the procedure, you will be placed on a trolley and taken to recovery, where you will remain for approximately 1 hour.
  • After having something to eat and drink, you will be discharged with a carer.

Post Procedure

  • Gentle activity and rest is recommended in the first 24 hours following the procedure. You may then return to normal activity.
  • The local anesthetic will wear off 12-18 hours following your procedure.
  • Botox will take approximately 5 days to start working. During the first 5 days, you may experience some pain at the site of the injection and some flu-like symptoms. Other possible side effects include headache, temporarily increased pain, irritation of nerves at the site of the injection, and rarely paralysis of muscle outside the area of spasm.
  • The steroid will take approximately 48 hours to start working. During this time there may be a window of increased discomfort or pain.
  • Caution should be taken if any leg heaviness occurs. If this occurs, activity should be kept to a minimum until full leg sensation returns.
  • A nurse from HPC will telephone you 24 to 48 hours following your procedure to check on your progress and organize a follow-up appointment.

Complications

Nonoperative

Treatment for piriformis syndrome begins with nonoperative modalities including:

  • Oral analgesics (e.g. NSAIDs, muscle relaxants, and gabapentin)
  • Physical therapy:

    • Regimens include nerve stretches, isometric exercises, gluteal muscle strengthening
  • Injections

    • Diagnostic and therapeutic modalities
    • Agents used include cortisone, local anesthetic, or botulinum toxin
    • A recent study reported positive outcomes in patients managed with physical therapy and Botulinum toxin injection

Surgical treatment

  • Surgery is considered in refractory cases after exhausting nonoperative modalities
  • A 2005 study reported surgical outcomes in 64 patients managed with surgical intervention for refractory symptoms: 

    • 82% reported initial improvement
    • 76% had long-term positive outcomes
    • 92% of those managed with surgery returned to work or presurgical baseline activity levels within 2 weeks of the surgery

References

ByRx Harun

Popliteal Fossa – Anatomy, Nerve Supply, Muscle Attachment

Popliteal fossa is a shallow depression located posterior to the knee joint. This area is often referred to as the knee “pit” and may develop vascular, nervous, lymphatic, and adipose tissues as well as swelling and masses. The fossa houses several important structures that are essential for lower extremity function.

Anatomic boundaries of the popliteal fossa include the following

  • Superomedially – the semimembranosus, and semitendinosus muscles
  • Superolaterally – the biceps femoris muscle (short and long heads)
  • Inferomedial and inferolateral – the medial and lateral heads of the gastrocnemius muscle contribute to the lower border, respectively.
  • The plantaris muscle – also runs deep to the gastrocnemius to form the inferolateral border.
  • The roof of the fossa – proceeding from most superficial to deep, consists of the skin, superficial fascia, and deep (popliteal) fascia.
  • The floor of the fossa – includes the popliteal surface of the femur, the capsule of the knee joint, popliteal ligament, and fascia encasing the popliteus muscle.

Blood Supply and Lymphatics

Popliteal Artery

  • The predominant arterial supply in the popliteal fossa is the popliteal artery. The artery represents the distal continuation of the femoral artery after passing through the adductor hiatus of the adductor Magnus’s muscle. The popliteal artery then ends at the lower border of the popliteus muscle before further dividing into the anterior tibial artery and the common trunk of the posterior tibial and peroneal arteries.
  • Five genicular branches of the popliteal artery provide blood to the capsular structures and ligaments of the knee: superior lateral, superior medial, middle, inferior lateral, and inferior medial genicular arteries. The genicular arteries form a collateral network between the femoral artery and the popliteal artery.

This dense vascular network allows for an alternative pathway for blood to flow from the femoral to popliteal arteries

  • Medial superior genicular artery – branch of the popliteal artery that runs anterior to the semimembranosus and semitendinosus. Anastomoses with lateral superior genicular artery.
  • Lateral superior genicular artery – branch of the popliteal artery that passes above lateral femoral condyle. Anastomoses with medial superior genicular artery, lateral femoral circumflex, and lateral inferior genicular arteries.
  • Medial inferior genicular artery – arises from the popliteal artery and descends with popliteus muscle, then passes the medial tibial condyle. Anastomoses with lateral inferior and medial superior genicular arteries.
  • Lateral inferior genicular artery – arises from the popliteal artery and passes under the gastrocnemius. Anastomoses with inferior medial genicular, superior lateral genicular, and anterior recurrent tibial artery.
  • Middle genicular artery – branch of the popliteal artery that supplies the ligaments and synovial membrane of the knee joint. 

Popliteal Vein

  • The popliteal vein is superficial to the popliteal artery in the fossa. The popliteal vein receives venous circulation from several tributaries. The anterior tibial vein, posterior tibial vein, and the peroneal vein merge at the popliteus muscle to make the popliteal vein. Within the popliteal fossa, the small saphenous vein feeds into the popliteal vein and is located more superficially, but transverses the deep fascia in between both gastrocnemius heads. Similarly to the popliteal artery, the popliteal vein extends superiorly through the adductor hiatus before transitioning into the femoral vein.

Nerves

  • The sciatic nerve branches into the tibial and common peroneal nerve just anterior to the popliteal fossa. The tibial nerve then enters the posterior legs between the heads of the gastrocnemius. The common peroneal nerve passes around the neck of the fibula.

Tibial Nerve

  • The tibial nerve is a branch of the sciatic nerve consisting of nerve roots L4-S3. It is superficial to the popliteal vessels and travels laterally to medially from the superior angle to the inferior angle of the popliteal fossa, respectively.  The tibial nerve contains muscular, articular, and cutaneous branches. Muscular branches in the distal portion of the fossa supply the medial and lateral heads of the gastrocnemius, soleus, plantaris, and popliteal muscles.
  • The sural nerve is the cutaneous branch of the tibial nerve and extends from the middle of the popliteal fossa, providing innervation of the lower posterior half of the lower leg and lateral foot. The three articular branches arise from the superior portion of the fossa. The superior medial genicular is found at the medial femoral condyle, and the middle genicular nerve pierces the posterior capsule of the knee joint innervating intercondylar structures and the inferior genicular nerve which travels to the medial tibial condyle.

Common Peroneal Nerve

  • The common peroneal nerve also referred to as the common fibular nerve, consists of nerve roots L4-S2 and arises from the sciatic nerve as well. It branches approximately at the superior angle of the popliteal fossa and travels to the lateral angle where it wraps around the fibular head, splitting off into the deep and superficial peroneal nerves and innervating the anterior and lateral compartments of the lower leg, respectively

Muscles

The musculoskeletal structures found in the popliteal fossa form its boundaries. The fossa has the shape of a rhombus or diamond and is made up of the following musculoskeletal structures.

  • Superomedial – The semimembranosus and semitendinosus muscles from the superomedial aspect of the fossa. The semimembranosus is the most medial of the hamstring muscles and functions to extend the hip and flex the knee as well as assist in medial rotation of the knee. The semitendinosus muscle is superficial to the semimembranosus and is the middle of the three hamstring muscles. Not surprisingly, it gets its name because of the long tendinous nature of its structure and assists in the same mechanism as the semimembranosus muscle.
  • Superolateral – The biceps femoris forms the superolateral portion of the popliteal fossa and has two functioning heads. The long head is part of the hamstring muscles while the short head is not included in this description. Both structures participate in knee flexion, while the long head additionally assists in hip extension.
  • Inferomedial – The medial head of the gastrocnemius forms the anteromedial border of the fossa. It assists the lower leg in plantar flexion at the ankle and knee flexion when contracted.  Along with the lateral head of the gastrocnemius and soleus, it forms the calf muscle.
  • Inferolateral – The lateral head of the gastrocnemius and the plantaris muscle forms the inferolateral border of the popliteal fossa. Both contribute to plantarflexion of the ankle. The lateral gastrocnemius head also contributes to knee flexion. The plantaris muscle is notably the longest tendon in the body and is not found in every human being.

Function

  • The function of the popliteal fossa is closely associated with the critical anatomic structures it contains. The fossa is a diamond-shaped region directly posterior to the knee and clinically appears as a soft impression behind the knee. It is an important area serving as a transition point/conduit for nerve tissue, vasculature, lymphatic tissue, and musculoskeletal structures, which are discussed at length below.

References

ByRx Harun

Parameniscal Cyst – Causes, Symptoms, Diagnosis, Treatment

Parameniscal Cyst/Baker Cyst also is known as a popliteal or parameniscal cyst, is a fluid-filled sac that forms in the posterior aspect of the knee, typically located between the semimembranosus and medial head of the gastrocnemius. In adults, Baker’s Cysts tend to form in association with degenerative conditions of the knee.  One of the most common associations seen is secondary to degenerative meniscal tears.  Inflammatory conditions and arthritides are also known causes of popliteal cyst formation.  When the cyst forms in association with a meniscal tear, the meniscus serves as a one-way valve and the extruded synovial fluid localizes and consolidates to form a viscous, gel-like material.

Baker cysts, or popliteal cysts, are fluid-filled distended synovial-lined lesions arising in the popliteal fossa between the medial head of the gastrocnemius and the semimembranosus tendons via communication with the knee joint. They are usually located at or below the joint line.

Causes of Parameniscal Cyst

Baker’s cysts are encountered most frequently in adults with a history of

  • Trauma – (e.g., cartilage or meniscus tears, injury to the knee),
  • Degenerative/co-existing knee joint disease – (e.g., osteoarthritis, rheumatoid arthritis, infectious arthritis, pigmented villonodular synovitis, meniscal tears), or asymptomatically as an incidental finding.
  • Swelling in the knee – This happens when the fluid that lubricates your knee joint increases. When pressure builds up, fluid squeezes into the back of the knee and creates the cyst.
  • Arthritis – People with all forms of arthritis often have Baker’s cysts.
  • Injury – A sports-related injury or other blow to the knee can cause A Baker’s cyst.
  • Gout –This a type of arthritis, which results from the buildup of uric acid in the blood, can lead to a Baker’s cyst.
  • Baker’s cysts arise between the tendons of the medial head of the gastrocnemius and the semimembranosus muscles. They are posterior to the medial femoral condyle.

Symptoms of Parameniscal Cyst

In some cases, a Baker’s cyst causes no pain, and you may not notice it. If you do have signs and symptoms, they might include:

  • Swelling behind your knee, and sometimes in your leg
  • Knee pain
  • Stiffness and inability to fully flex the knee
  • mild to severe pain
  • stiffness
  • limited range of motion
  • swelling behind the knee and calf
  • bruising on the knee and calf
  • rupturing of the cyst

Diagnosis of Parameniscal Cyst

A Baker’s cyst can often be diagnosed with a physical exam. However, because some of the signs and symptoms of a Baker’s cyst mimic those of more serious conditions, such as a blood clot, aneurysm or tumor, your doctor may order noninvasive imaging tests, including

  • Ultrasound
  • X-ray
  • Magnetic resonance imaging (MRI)

Treatment of Popliteal Cyst

Treatment is not usually necessary for Baker’s Cyst unless the patient is symptomatic.  Incidental findings in the asymptomatic patient are managed with observation and reassurance alone.

Non-operative management

  • Keep it cold – Apply a cold pack to the affected area. It’ll help keep the swelling down. A compression wrap might also help.
  • Rest your leg – Keep it raised above your heart level when possible. This will keep down swelling. Use a cane or crutch when you walk to keep pressure off your leg.
  • Rest/activity modification
  • NSAIDs – For pain (and to reduce inflammation), take an over-the-counter medication like ibuprofen.
  • PT/rehab – regimens are often effective in patients with minimal symptoms, and in the setting of smaller degenerative meniscal tears
  • Medication – Your doctor may inject corticosteroid medication, such as cortisone, into your knee to reduce inflammation. This may relieve pain, but it doesn’t always prevent the recurrence of the cyst.
  • Fluid drainage – Your doctor may drain the fluid from the knee joint using a needle. This is called needle aspiration and is often performed under ultrasound guidance.
  • Aspiration and steroid injection – The knee joint itself can be treated with a cortisone injection in the setting of moderate to advanced tri  compartmental degenerative knee arthritic conditions.  This can help manage patients’ symptoms and clinically differentiate the contribution of the popliteal cyst itself on the patients daily symptoms
  • Ultrasound-guided aspiration and injection – can be performed by an experienced interventional radiologist

    • Recurrence rates are much lower in younger patient populations
    • Recurrence rates are higher in older patient populations and degenerative meniscal tears with associated cysts

Operative management

  • Arthroscopic debridement, cyst decompression, meniscal repair vs partial meniscectomy

    • less invasive than the open approach
    • often results in cyst recurrence, especially in older patients with moderate-advanced knee degenerative conditions
  • Open cyst excision

    • Posterior approach to the knee is utilized
    • Not indicated in the setting of underlying knee degenerative conditions secondary to the risk of cyst recurrence

It is important to treat the underlying joint disorder, if one exists, in all patients with symptomatic Baker’s cysts. This will help reduce the accumulation of synovial fluid and enlargement of the cyst.

Physical therapy

  • Icing, a compression wrap, and crutches may help reduce pain and swelling. Gentle range-of-motion and strengthening exercises for the muscles around your knee also may help to reduce your symptoms and preserve knee function.

Exercises

Exercises that focus on preserving the knee’s range of motion may ease pain and prevent muscle weakness. However, before trying any exercise for a Baker’s cyst, speak to a doctor or physical therapist. The wrong exercise may injure the knee, intensifying pain. The following exercises may benefit a person with a Baker’s cyst:

Standing calf stretch

  • Stand up straight in front of a chair or another heavy piece of furniture, and use it for balance, if necessary.
  • Step back with the right leg, then bend both knees until there is a stretch.
  • Hold this stretch for 20 seconds, then switch sides.

Heel lift

  • Sit in a chair with both feet flat on the floor and the knees at a 90-degree angle.
  • Lift one heel while keeping the ball of the foot on the floor.
  • Push the top of the knee down to flatten the foot. Repeat this 10 times, then switch sides.

Calf stretch

  • Sit on the floor with the legs extended straight out in front of you.
  • Loop a towel or exercise band under the balls of the feet, then gently pull backward.
  • Hold the stretch for 10 seconds, then switch sides.

Walking

Baker’s cysts often form as a result of a knee injury. During recovery, walking may help a person gradually regain strength and mobility. However, if a person needs to change their gait or contort a knee into an unusual position to walk comfortably, it may not be safe to walk yet. Consult a doctor or physical therapist.

Remedies

The following home care strategies may help alleviate symptoms of a Baker’s cyst or prevent one from forming:

  • Apply ice or cold packs to the cyst to reduce pain and swelling.
  • Apply heat to the area. Some people find that alternating ice and heat works well.
  • Take nonsteroidal anti-inflammatory drugs such as acetaminophen or ibuprofen.
  • Avoid any activities that cause pain. If walking is painful, use crutches to reduce pressure on the injured knee.
  • Gently massage the area around the cyst to ease any pain and help reduce inflammation.

Prevention

A Baker’s cyst often appears following a knee injury. Preventing knee injuries is, therefore, the best way to prevent these cysts from developing.

To avoid injuring the knee:

  • Wear supportive shoes that fit well.
  • Warm-up before exercise and sports, and cool down afterward.
  • Refrain from exercising on a knee that is already tender and painful.
  • Seek treatment for any knee, leg, or foot injuries — an injury to one area of the body can increase the risk of falls and further harm.

References

ByRx Harun

Baker Cyst – Causes, Symptoms, Diagnosis, Treatment

Baker Cyst also is known as a popliteal or parameniscal cyst, is a fluid-filled sac that forms in the posterior aspect of the knee, typically located between the semimembranosus and medial head of the gastrocnemius. In adults, Baker’s Cysts tend to form in association with degenerative conditions of the knee.  One of the most common associations seen is secondary to degenerative meniscal tears.  Inflammatory conditions and arthritides are also known causes of popliteal cyst formation.  When the cyst forms in association with a meniscal tear, the meniscus serves as a one-way valve and the extruded synovial fluid localizes and consolidates to form a viscous, gel-like material.

Baker cysts, or popliteal cysts, are fluid-filled distended synovial-lined lesions arising in the popliteal fossa between the medial head of the gastrocnemius and the semimembranosus tendons via communication with the knee joint. They are usually located at or below the joint line.

Causes of Baker Cyst

Baker’s cysts are encountered most frequently in adults with a history of

  • Trauma – (e.g., cartilage or meniscus tears, injury to the knee),
  • Degenerative/co-existing knee joint disease – (e.g., osteoarthritis, rheumatoid arthritis, infectious arthritis, pigmented villonodular synovitis, meniscal tears), or asymptomatically as an incidental finding.
  • Swelling in the knee – This happens when the fluid that lubricates your knee joint increases. When pressure builds up, fluid squeezes into the back of the knee and creates the cyst.
  • Arthritis – People with all forms of arthritis often have Baker’s cysts.
  • Injury – A sports-related injury or other blow to the knee can cause A Baker’s cyst.
  • Gout –This a type of arthritis, which results from the buildup of uric acid in the blood, can lead to a Baker’s cyst.
  • Baker’s cysts arise between the tendons of the medial head of the gastrocnemius and the semimembranosus muscles. They are posterior to the medial femoral condyle.

Symptoms of Baker Cyst

In some cases, a Baker’s cyst causes no pain, and you may not notice it. If you do have signs and symptoms, they might include:

  • Swelling behind your knee, and sometimes in your leg
  • Knee pain
  • Stiffness and inability to fully flex the knee
  • mild to severe pain
  • stiffness
  • limited range of motion
  • swelling behind the knee and calf
  • bruising on the knee and calf
  • rupturing of the cyst

Diagnosis of Baker Cyst

A Baker’s cyst can often be diagnosed with a physical exam. However, because some of the signs and symptoms of a Baker’s cyst mimic those of more serious conditions, such as a blood clot, aneurysm or tumor, your doctor may order noninvasive imaging tests, including

  • Ultrasound
  • X-ray
  • Magnetic resonance imaging (MRI)

Treatment  of Baker Cyst

Treatment is not usually necessary for Baker’s Cyst unless the patient is symptomatic.  Incidental findings in the asymptomatic patient are managed with observation and reassurance alone.

Non-operative management

  • Keep it cold – Apply a cold pack to the affected area. It’ll help keep the swelling down. A compression wrap might also help.
  • Rest your leg – Keep it raised above your heart level when possible. This will keep down swelling. Use a cane or crutch when you walk to keep pressure off your leg.
  • Rest/activity modification
  • NSAIDs – For pain (and to reduce inflammation), take an over-the-counter medication like ibuprofen.
  • PT/rehab – regimens are often effective in patients with minimal symptoms, and in the setting of smaller degenerative meniscal tears
  • Medication – Your doctor may inject corticosteroid medication, such as cortisone, into your knee to reduce inflammation. This may relieve pain, but it doesn’t always prevent the recurrence of the cyst.
  • Fluid drainage – Your doctor may drain the fluid from the knee joint using a needle. This is called needle aspiration and is often performed under ultrasound guidance.
  • Aspiration and steroid injection – The knee joint itself can be treated with a cortisone injection in the setting of moderate to advanced tri  compartmental degenerative knee arthritic conditions.  This can help manage patients’ symptoms and clinically differentiate the contribution of the popliteal cyst itself on the patients daily symptoms
  • Ultrasound-guided aspiration and injection – can be performed by an experienced interventional radiologist

    • Recurrence rates are much lower in younger patient populations
    • Recurrence rates are higher in older patient populations and degenerative meniscal tears with associated cysts

Operative management

  • Arthroscopic debridement, cyst decompression, meniscal repair vs partial meniscectomy

    • less invasive than the open approach
    • often results in cyst recurrence, especially in older patients with moderate-advanced knee degenerative conditions
  • Open cyst excision

    • Posterior approach to the knee is utilized
    • Not indicated in the setting of underlying knee degenerative conditions secondary to the risk of cyst recurrence

It is important to treat the underlying joint disorder, if one exists, in all patients with symptomatic Baker’s cysts. This will help reduce the accumulation of synovial fluid and enlargement of the cyst.

Physical therapy

  • Icing, a compression wrap, and crutches may help reduce pain and swelling. Gentle range-of-motion and strengthening exercises for the muscles around your knee also may help to reduce your symptoms and preserve knee function.

Exercises

Exercises that focus on preserving the knee’s range of motion may ease pain and prevent muscle weakness. However, before trying any exercise for a Baker’s cyst, speak to a doctor or physical therapist. The wrong exercise may injure the knee, intensifying pain. The following exercises may benefit a person with a Baker’s cyst:

Standing calf stretch

  • Stand up straight in front of a chair or another heavy piece of furniture, and use it for balance, if necessary.
  • Step back with the right leg, then bend both knees until there is a stretch.
  • Hold this stretch for 20 seconds, then switch sides.

Heel lift

  • Sit in a chair with both feet flat on the floor and the knees at a 90-degree angle.
  • Lift one heel while keeping the ball of the foot on the floor.
  • Push the top of the knee down to flatten the foot. Repeat this 10 times, then switch sides.

Calf stretch

  • Sit on the floor with the legs extended straight out in front of you.
  • Loop a towel or exercise band under the balls of the feet, then gently pull backward.
  • Hold the stretch for 10 seconds, then switch sides.

Walking

Baker’s cysts often form as a result of a knee injury. During recovery, walking may help a person gradually regain strength and mobility. However, if a person needs to change their gait or contort a knee into an unusual position to walk comfortably, it may not be safe to walk yet. Consult a doctor or physical therapist.

Remedies

The following home care strategies may help alleviate symptoms of a Baker’s cyst or prevent one from forming:

  • Apply ice or cold packs to the cyst to reduce pain and swelling.
  • Apply heat to the area. Some people find that alternating ice and heat works well.
  • Take nonsteroidal anti-inflammatory drugs such as acetaminophen or ibuprofen.
  • Avoid any activities that cause pain. If walking is painful, use crutches to reduce pressure on the injured knee.
  • Gently massage the area around the cyst to ease any pain and help reduce inflammation.

Prevention

A Baker’s cyst often appears following a knee injury. Preventing knee injuries is, therefore, the best way to prevent these cysts from developing.

To avoid injuring the knee:

  • Wear supportive shoes that fit well.
  • Warm-up before exercise and sports, and cool down afterward.
  • Refrain from exercising on a knee that is already tender and painful.
  • Seek treatment for any knee, leg, or foot injuries — an injury to one area of the body can increase the risk of falls and further harm.

References

ByRx Harun

Popliteal Cyst – Causes, Symptoms, Treatment

Popliteal Cyst/Baker Cyst also is known as a popliteal or parameniscal cyst, is a fluid-filled sac that forms in the posterior aspect of the knee, typically located between the semimembranosus and medial head of the gastrocnemius. In adults, Baker’s Cysts tend to form in association with degenerative conditions of the knee.  One of the most common associations seen is secondary to degenerative meniscal tears.  Inflammatory conditions and arthritides are also known causes of popliteal cyst formation.  When the cyst forms in association with a meniscal tear, the meniscus serves as a one-way valve and the extruded synovial fluid localizes and consolidates to form a viscous, gel-like material.

Baker cysts, or popliteal cysts, are fluid-filled distended synovial-lined lesions arising in the popliteal fossa between the medial head of the gastrocnemius and the semimembranosus tendons via communication with the knee joint. They are usually located at or below the joint line.

Causes of Popliteal Cyst

Baker’s cysts are encountered most frequently in adults with a history of

  • Trauma – (e.g., cartilage or meniscus tears, injury to the knee),
  • Degenerative/co-existing knee joint disease – (e.g., osteoarthritis, rheumatoid arthritis, infectious arthritis, pigmented villonodular synovitis, meniscal tears), or asymptomatically as an incidental finding.
  • Swelling in the knee – This happens when the fluid that lubricates your knee joint increases. When pressure builds up, fluid squeezes into the back of the knee and creates the cyst.
  • Arthritis – People with all forms of arthritis often have Baker’s cysts.
  • Injury – A sports-related injury or other blow to the knee can cause A Baker’s cyst.
  • Gout –This a type of arthritis, which results from the buildup of uric acid in the blood, can lead to a Baker’s cyst.
  • Baker’s cysts arise between the tendons of the medial head of the gastrocnemius and the semimembranosus muscles. They are posterior to the medial femoral condyle.

Symptoms of Popliteal Cyst

In some cases, a Baker’s cyst causes no pain, and you may not notice it. If you do have signs and symptoms, they might include:

  • Swelling behind your knee, and sometimes in your leg
  • Knee pain
  • Stiffness and inability to fully flex the knee
  • mild to severe pain
  • stiffness
  • limited range of motion
  • swelling behind the knee and calf
  • bruising on the knee and calf
  • rupturing of the cyst

Diagnosis of Popliteal Cyst

A Baker’s cyst can often be diagnosed with a physical exam. However, because some of the signs and symptoms of a Baker’s cyst mimic those of more serious conditions, such as a blood clot, aneurysm or tumor, your doctor may order noninvasive imaging tests, including

  • Ultrasound
  • X-ray
  • Magnetic resonance imaging (MRI)

Treatment of Popliteal Cyst

Treatment is not usually necessary for Baker’s Cyst unless the patient is symptomatic.  Incidental findings in the asymptomatic patient are managed with observation and reassurance alone.

Non-operative management

  • Keep it cold – Apply a cold pack to the affected area. It’ll help keep the swelling down. A compression wrap might also help.
  • Rest your leg – Keep it raised above your heart level when possible. This will keep down swelling. Use a cane or crutch when you walk to keep pressure off your leg.
  • Rest/activity modification
  • NSAIDs – For pain (and to reduce inflammation), take an over-the-counter medication like ibuprofen.
  • PT/rehab – regimens are often effective in patients with minimal symptoms, and in the setting of smaller degenerative meniscal tears
  • Medication – Your doctor may inject corticosteroid medication, such as cortisone, into your knee to reduce inflammation. This may relieve pain, but it doesn’t always prevent the recurrence of the cyst.
  • Fluid drainage – Your doctor may drain the fluid from the knee joint using a needle. This is called needle aspiration and is often performed under ultrasound guidance.
  • Aspiration and steroid injection – The knee joint itself can be treated with a cortisone injection in the setting of moderate to advanced tri  compartmental degenerative knee arthritic conditions.  This can help manage patients’ symptoms and clinically differentiate the contribution of the popliteal cyst itself on the patients daily symptoms
  • Ultrasound-guided aspiration and injection – can be performed by an experienced interventional radiologist

    • Recurrence rates are much lower in younger patient populations
    • Recurrence rates are higher in older patient populations and degenerative meniscal tears with associated cysts

Operative management

  • Arthroscopic debridement, cyst decompression, meniscal repair vs partial meniscectomy

    • less invasive than the open approach
    • often results in cyst recurrence, especially in older patients with moderate-advanced knee degenerative conditions
  • Open cyst excision

    • Posterior approach to the knee is utilized
    • Not indicated in the setting of underlying knee degenerative conditions secondary to the risk of cyst recurrence

It is important to treat the underlying joint disorder, if one exists, in all patients with symptomatic Baker’s cysts. This will help reduce the accumulation of synovial fluid and enlargement of the cyst.

Physical therapy

  • Icing, a compression wrap, and crutches may help reduce pain and swelling. Gentle range-of-motion and strengthening exercises for the muscles around your knee also may help to reduce your symptoms and preserve knee function.

Exercises

Exercises that focus on preserving the knee’s range of motion may ease pain and prevent muscle weakness. However, before trying any exercise for a Baker’s cyst, speak to a doctor or physical therapist. The wrong exercise may injure the knee, intensifying pain. The following exercises may benefit a person with a Baker’s cyst:

Standing calf stretch

  • Stand up straight in front of a chair or another heavy piece of furniture, and use it for balance, if necessary.
  • Step back with the right leg, then bend both knees until there is a stretch.
  • Hold this stretch for 20 seconds, then switch sides.

Heel lift

  • Sit in a chair with both feet flat on the floor and the knees at a 90-degree angle.
  • Lift one heel while keeping the ball of the foot on the floor.
  • Push the top of the knee down to flatten the foot. Repeat this 10 times, then switch sides.

Calf stretch

  • Sit on the floor with the legs extended straight out in front of you.
  • Loop a towel or exercise band under the balls of the feet, then gently pull backward.
  • Hold the stretch for 10 seconds, then switch sides.

Walking

Baker’s cysts often form as a result of a knee injury. During recovery, walking may help a person gradually regain strength and mobility. However, if a person needs to change their gait or contort a knee into an unusual position to walk comfortably, it may not be safe to walk yet. Consult a doctor or physical therapist.

Remedies

The following home care strategies may help alleviate symptoms of a Baker’s cyst or prevent one from forming:

  • Apply ice or cold packs to the cyst to reduce pain and swelling.
  • Apply heat to the area. Some people find that alternating ice and heat works well.
  • Take nonsteroidal anti-inflammatory drugs such as acetaminophen or ibuprofen.
  • Avoid any activities that cause pain. If walking is painful, use crutches to reduce pressure on the injured knee.
  • Gently massage the area around the cyst to ease any pain and help reduce inflammation.

Prevention

A Baker’s cyst often appears following a knee injury. Preventing knee injuries is, therefore, the best way to prevent these cysts from developing.

To avoid injuring the knee:

  • Wear supportive shoes that fit well.
  • Warm-up before exercise and sports, and cool down afterward.
  • Refrain from exercising on a knee that is already tender and painful.
  • Seek treatment for any knee, leg, or foot injuries — an injury to one area of the body can increase the risk of falls and further harm.

References

ByRx Harun

Popliteal Artery Entrapment Syndrome (PAES)

Popliteal artery entrapment syndrome (PAES) is a rare cause of exercise-induced leg pain. Entrapment occurs because of an abnormal relationship between the popliteal artery and the surrounding myofascial structures in the popliteal fossa. Arterial insufficiency in the affected limb arises with entrapment of the artery, commonly giving leg symptoms with exertion.

Popliteal Artery Entrapment Syndrome (PAES) described by Stuart in1879, is an uncommon limb-threatening vascular entity comprising approximately 0.17%-3.5% of the general population in the United States (US). This embryologically developmental anomaly results mainly due to an aberrant relationship of the popliteal artery with the surrounding popliteal fossa myofascial structures. Surprisingly, PAES predominantly affects active young males without a previous history of cardiovascular risk factors.

Pathophysiology of Popliteal Artery Entrapment Syndrome (PAES)

Generally, the majority of the PAES cases are due to the embryological anomalies while fewer patients have been documented having acquired (fibrous bands) causes for the PAES. Additionally, the PAES are further classified into six different types based on the relationship of the medial head of the gastrocnemius muscle with the popliteal artery.

  • Type I: An aberrant medial course of the popliteal artery around a normally positioned MHG
  • Type II: MHG attaches abnormally and more laterally on the femur causing the popliteal artery to pass medially and inferiorly
  • Type III: Abnormal fibrous band or accessory muscle arising from the medial or lateral condyle encircling the popliteal artery
  • Type IV: Popliteal artery lying in its primitive deep or axial position within the fossa, becoming compromised by the popliteus muscle or fibrous bands
  • Type V: The entrapment of both the popliteal artery and vein due to any of the causes mentioned above
  • Type VI: The muscular hypertrophy, resulting in a functional compression of both the popliteal artery and vein

The functional PAES (Type VI or F) describes another subtype of the disease that is not due to inherited anatomic abnormalities. It has been postulated that repeated microtrauma results in the growth of connective tissue, destruction of the internal elastic lamina, and damage to the smooth muscles resulting in fibrosis and scar formation. The resulting injury leads to thrombosis, embolization, and aneurysmal degeneration.

A more straightforward and practical classification system for the PAES was also introduced by Heidelberg.. According to this classification, the PAES is classified into the following three main types

  • Type 1: The problem lies in the course of the popliteal artery
  • Type 2: The muscular insertion is atypical
  • Type 3: Both of the abovementioned conditions are present

Causes of Popliteal Artery Entrapment Syndrome (PAES)

  • Both congenital and acquired mechanisms have been proposed in the development of PAES. An in-depth understanding of the various stages of human embryological development has successfully demonstrated the precise etiology of the congenital PAES.
  • Developmentally, the popliteal artery and the medial head of the gastrocnemius muscle develop about the same time. Both femoral and sciatic artery contributes significantly to the development of the popliteal artery. It originates from the extension of the femoral artery proximally and the sciatic artery distally.
  • Additionally, the sciatic artery contributes to the development of the tibial arteries as well. Over time, the sciatic artery regresses, and the femoral artery becomes the main contributor to the development of the popliteal artery.
  • Popliteal artery entrapment syndrome is a rare abnormality of the anatomical relationship between the popliteal artery and adjacent muscles or fibrous bands in the popliteal fossa.

Symptoms of Popliteal Artery Entrapment Syndrome (PAES)

The main symptom of popliteal artery entrapment syndrome (PAES) is pain or cramping in the back of the lower leg (the calf) that occurs during exercise and goes away with rest. Other signs and symptoms may include:

  • Cold feet after exercise
  • Tingling or burning in your calf (paresthesia)
  • Numbness in the calf area
  • Heavy feeling in the leg
  • Lower leg cramping at night
  • Swelling in the calf area
  • Changes in skin color around the calf muscle
  • Blood clots in the lower leg (deep vein thrombosis)

Symptoms typically affect young, otherwise healthy people under age 40.

Diagnosis of Popliteal Artery Entrapment Syndrome (PAES)

Your doctor will carefully examine you and ask questions about your symptoms and health history. However, because most people with popliteal artery entrapment syndrome (PAES) are young and usually healthy, diagnosing the condition can sometimes be challenging. The findings from a physical exam usually are normal.

Your doctor will rule out other causes of leg pain, including muscle strains, stress fractures, chronic exertional compartment syndrome and peripheral artery disease, which results from clogged arteries.

Tests used to rule out other conditions and diagnose PAES include the following

  • Ankle-brachial index (ABI) measurement is usually the first test done to diagnose PAES. Blood pressure measurements are taken in your arms and legs during and after walking on a treadmill. The ABI is determined by dividing ankle pressure by arm pressure. The blood pressure in your legs should be higher than that in your arms. But if you have PAES, your ankle pressure drops during exercise.
  • Duplex ultrasound of the calf – uses high-frequency sound waves to determine how fast blood is flowing through the leg arteries. This noninvasive test may be done before or after exercise or while you flex your foot up and down, which puts your calf muscle to work.
  • Magnetic resonance angiography (MRA) – shows the calf muscle that is trapping the artery. It can also reveal how much of the popliteal artery is narrowed. You may be asked to flex your foot or press it against aboard during this test. Doing so helps your doctor determine how blood is flowing to your lower leg.
  • CT angiography – also shows which leg muscle is causing the artery entrapment. As with MRA, you may be asked to change the position of your foot during this test.
  • Catheter-based angiography – allows your doctor to see how blood is flowing to and from the lower leg in real-time. It’s done if the diagnosis is still unclear after other, less invasive imaging tests.

Treatment of Popliteal Artery Entrapment Syndrome (PAES)

The management of the PAES is tailored based on the presence and absence of the symptoms. For asymptomatic patients with incidental findings of popliteal artery entrapment, management is typically expectant, as the majority of these patients never experience symptoms or disease progression. On the contrary, if muscle insertion abnormalities are the cause of the PAEs even in an asymptomatic patient, surgical correction is the preferred method of treatment.

Furthermore, for symptomatic PAES patients, surgical resection has been the management of choice . Surgery with popliteal artery release allows for the definitive re-establishment of normal anatomy and often portends excellent results. Through either a posterior or medial approach, the MHG or musculotendinous band can be divided. The artery can then be palpated to determine its patency and determine if the bypass is required. Reconstruction of the adjacent muscles is not necessary as this is well tolerated without functional limitation.

Also, the open surgical procedures offer the best results to address the PAES and assess the artery for repair or bypass. In cases where there is extensive arterial wall damage, occlusion, or aneurysm development interposition bypass grafting, using autogenous vein via a posterior approach or medial bypass to extend farther down the below-knee popliteal artery have been advocated. The medial approach may be better for the management of Type I and II, while a posterior approach may be better for type III and IV.

Moreover, the management of functional PAES is still controversial although some have had success with gastrocnemius debulking. Also, postoperatively, surveillance is performed using arterial duplex imaging at 1, 3, 6, and 12 months, and annually after that.

References

ByRx Harun

Achilles Tendonitis – Causes, Symptoms, Diagnosis, Treatment

Achilles Tendonitis is one of the most frequently ankle and foot overuse injuries, which is a clinical syndrome characterized by the combination of pain, swelling, and impaired performance. The two main categories of Achilles tendinopathy are classified according to anatomical location and broadly include insertional and non insertional tendinopathy. The etiology of Achilles Tendonitis multifactorial including both intrinsic and extrinsic factors. Failed healing response and degenerative changes were found in the tendon. The failed healing response includes three different and continuous stages (reactive tendinopathy, tendon disrepair, and degenerative tendinopathy).

Causes of Achilles Tendonitis

The causes and mechanisms of Achilles Tendonitis (AT) include the following

  • Intrinsic factors – This includes anatomic factors, age, sex, metabolic dysfunction, foot cavity, dysmetria, muscle weakness, imbalance, gastrocnemius dysfunction, anatomical variation of the plantaris muscle, tendon vascularization, torsion of the Achilles tendons, slippage of the fascicle, and lateral instability of the ankle.
  • Extrinsic factors – These include mechanical overload, constant effort, inadequate equipment, obesity, medications (corticosteroids, anabolic steroids, fluoroquinolones,), improper footwear, insufficient warming or stretching, hard training surfaces, and direct trauma, among others.

Factors related to a high risk of rupture of the Achilles tendon link to advanced age due to a lack of uniformity of the tendons, slippage of the fascicles, and excessive exercise in athletes, Sports minded individuals tend to have an injury at the Achilles tendon insertion site.

Systemic Factors

Systemic diseases that may be associated with Achilles tendonitis injuries include the following

  • Chronic renal failure
  • Collagen deficiency
  • Diabetes mellitus
  • Gout
  • Infections
  • Lupus
  • Parathyroid disorders
  • Rheumatoid arthritis
  • Thyroid disorders

Foot problems that increase the risk of Achilles tendon injuries include the following

  • Cavus foot
  • Insufficient gastroc soleus flexibility and strength
  • limited ability to perform ankle dorsiflexion
  • Tibia vara
  • Varus alignment with functional hyper pronation

Symptoms of Achilles Tendonitis

  • You hear a snap, crack or popping sound when pushing off with your leg, often accompanied by a sharp pain in the back of your leg or ankle
  • Trouble moving your foot to walk or go upstairs. You’re unable to stand on your toes (“tippy-toe”)
  • Pain, bruising and swelling at the back of your leg or heel
  • Chronic, recurrent calf or Achilles tendon ̶ area pain
  • Previous rupture of the affected tendon
  • Loss of plantarflexion power in the foot
  • Swelling of the calf
  • The recent increase in physical activity/training volume
  • Recent use of fluoroquinolones, corticosteroids, or corticosteroid injections

Diagnosis of Achilles Tendonitis

Physical exploration

  • Clinical signs and symptoms of Achilles Tendonitis include localized pain, focal or diffuse sensitivity,  swelling, stiffness/morning pain, perceived rigidity in the Achilles’ tendon, positive arc sign, Royal London Hospital test, and Thompson test.

Tests used to diagnose Achilles tendinopathy

  • Lateral and axial calcaneus x-rays – May detect calcifications in the proximal extension of the tendon insertion or bony prominences in the upper portion of the calcaneus. Also, x-rays can help exclude pathological bone tumors.
  • Ultrasound – Can help assess injury to the tendon; can be used to predict the risk of tendinopathy and rupture. Ultrasound may reveal the increased thickness of the Achilles tendon with hyperemia associated with hypervascularity, a decrease in the gastrocnemius-soleus rotation angle and a decrease in the length of the Kager fat pad. Ultrasound is also useful during interventional treatment.
  • Magnetic Resonance Imaging – Provides significant information about the state of joint structures with a study in multiple planes in static and dynamic views. One study found that MRI had lower sensitivity than ultrasound in the detection of early changes of enthesopathy.. Another study found an excellent agreement between tendon thickness measurement between magnetic resonance and ultrasound.
  • Computed Tomography (CT) – The CT scan is useful to rule out trabecular structural alterations of the calcaneus in Achilles pathology of insertion. However, it exposes the patient to radiation.
  • Victoria Institute of Sports Assessment – Achilles (VISA-A) remains the gold standard for assessing pain and function, but it requires additional studies to increase its reliability. Nevertheless, it is an essential tool for patient post-treatment follow-up.

Differential Diagnosis

  • Achilles bursitis
  • Ankle fracture
  • Ankle impingement syndrome
  • Ankle osteoarthritis
  • Ankle sprain
  • Calf injuries
  • Calcaneofibular ligament injury
  • Calcaneus fractures
  • Deep venous thrombosis (DVT)
  • Exertional Compartment Syndrome
  • Fascial tears
  • Gastrocsoleus muscle strain or rupture
  • Haglund deformity
  • Plantaris tendon tear
  • Psoriatic arthritis
  • Reiter syndrome
  • Retrocalcaneal bursitis
  • Ruptured Baker cyst
  • Syndesmosis
  • Talofibular Ligament Injury

Treatment of Achilles Tendinopathy

Management of Achilles tendinopathy can divide into conservative and surgical. Additionally, one must consider whether it is an acute or chronic condition. Finally, for those with a full rupture, the treatment is usually surgical.

Conservative therapy:  It is the first line of management and includes the following

  • Reduction of activity levels
  • Adaptation of footwear, manual therapy directed at local sites may enhance the rehabilitation
  • Eccentric stretching exercises should comprise an integral component of physiotherapy and can achieve a 40% reduction in pain; moderate level evidence favors eccentric exercise over concentric exercise for reducing pain
  • Tendon loading exercise at short- and long-term follow-up
  • If unresponsive to initial management, extracorporeal shock wave therapy reduces pain by 60%, with 80% patient satisfaction, improving functionality and quality of life, with a follow-up at 4 weeks; this might be the first choice because of its safety and effectiveness
  • Physiotherapy improves the pain and functionality of the Achilles tendinopathy of the middle portion; however, studies do not show preferences for any particular exercise over another – overall, use of a splint to an eccentric exercise protocol or the use of orthoses to improve pain and function is not a recommendation
  • Current evidence shows a lack of efficacy on the use of platelet-rich plasma for Achilles tendinopathy

Nonoperative Management

  • Braces and immobilization – with a cast or pneumatic walking boot are combined with modified activity []. Immobilization is frequently used in the acute setting to control exacerbating factors, but prolonged immobilization should be avoided[].
  • Ultrasound – is a commonly prescribed program of physical therapy. In animal studies, ultrasound could stimulate collagen synthesis in tendon fibroblasts and cell division during the period of rapid cell proliferation []. Therapeutic ultrasound has been shown to reduce the swelling in the acute inflammatory phase of soft-tissue disorders, relieve pain, and increase function in patients with chronic tendon injuries and may enhance tendon healing [, ].
  • Low-level laser therapy (LLLT) – could reduce the expression of proinflammatory markers such as IL-6 and TNF-α in gene level []. In the cellular level, LLLT may increase collagen production [], stimulate tenocyte proliferation [], downregulate MMPs, decrease the capillary flow of neovascularization, and finally preserve the resistance and elasticity of tendon [, ].
  • Extracorporeal shockwave therapy (ESWT) – How ESWT works is still poorly understood, but it is known to cause selective dysfunction of sensory unmyelinated nerve fibers, alteration in the dorsal root ganglia, and cavitation in interstitial and extracellular disruption, which could promote the healing response [].
  • Deep friction massage (DFM) – and tendon mobilization may also be helpful in the treatment of Achilles tendinopathy. DFM has been advocated for tendinopathy and para tendinopathy. Friction has been shown to increase the protein output of tendon cells []. In combination with stretching, deep friction massage helps to restore tissue elasticity and reduce the strain in the muscle-tendon unit [, ]. Future randomized comparison studies are necessary to compare DFM in isolation with other modes of treatment.
  • Cryotherapy – might play a role in reducing the increased capillary blood flow in Achilles tendinopathy, reducing the metabolic rate of the tendon, and applying for relief of pain [, ]. However, recent evidence in upper limb tendinopathy indicated that the addition of ice did not offer any advantage over an exercise program consisting of eccentric and static stretching exercises [].

Medication

  • NSAIDs – used in chronic tendinopathy is questionable because the histological examination in the tendinopathic tissue shows no inflammatory cells []. The benefits of NSAIDs use are relieving pain in the acute phase and reducing the possibility of leg stiffness []. However, there are some studies that indicated that the NSAIDs may inhibit tendon cell migration and proliferation and impair tendon healing [].
  • Corticosteroid injections – are reported to reduce pain and swelling and improve the ultrasound appearance of the tendon. The mechanism behind any positive effect of local steroids on chronic Achilles tendinopathy remains unclear. Some authors have hypothesized that any beneficial effects of corticosteroids in this condition are owed to other local steroid effects rather than suppression of inflammation, including lyses of tendon and peritendon adhesions or alteration of the function of pain generating nociceptor in the region [].
  • Platelet-rich plasma (PRP) – at the site of tendon injury is thought to facilitate healing because it contains several different growth factors and other cytokines that can stimulate the healing of soft tissue []. Animal studies indicated that PRP could increase the expression of collagen types I and III and vascular endothelial growth factor and improve the healing and remodeling process of the tendon [, ].
  • Intratendinous hyperosmolar dextrose (prolotherapy) – is thought to produce a local inflammatory response and an increase in tendon strength. Clinical results indicated that intratendinous injections of hyperosmolar dextrose could reduce the pain at rest and during tendon-loading activities in patients with chronic of the Achilles tendinopathy [, ]. Moreover, after the injection of dextrose, there were reductions in the size and severity of hypoechoic regions and intratendinous tears and improvements in neovascularity [].
  • Nitric oxide – is a small-free radical generated by a family of enzymes, the nitric oxide synthases. It can induce apoptosis in inflammatory cells and cause angiogenesis and vasodilation. Moreover, oxygen-free radicals can stimulate fibroblast proliferation []. Nitric oxide can enhance tendon healing. Inhibition of nitric oxide synthase can reduce the healing process, which resulted in a decreased cross-sectional area and reduced failure load [].
  • The sclerosing agent – that selectively targets the vascular may cause thrombosis of the vessel. As the concomitant sensory nerves have been implicated as possible pain generators, to destroy local nerves adjacent to neovessels may decrease pain []. As vessel number has been shown to correlate with tendon thickness, a treatment that decreases vessel number is likely to also affect the tendon thickness. Moreover, the sclerosing agent injected at multiple sites around the tendon and neovessels initiates a local inflammatory response, which induces the proliferation of fibroblasts and the synthesis of collagen.
  • Aprotinin – is a broad-spectrum serine protease inhibitor capable of blocking trypsin, plasmin, kallikrein, and a range of MMPs []. Most previous studies using Aprotinin injection in the management of Achilles tendinopathy showed a trend towards improved clinical results [, ]. The major potential negative of using Aprotinin is the side effect of allergy [], but the allergic reactions can be reduced by minimizing repeat injections and recommending a delay of at least 6 weeks between injections [].
  • Autologous blood injections – results have not been highly encouraging and there is little evidence for their use.[rx]

Surgery

Surgical therapy is optional for 10 to 30% of patients who fail conservative therapy after six months. The success rate is higher than 70%, but reports show complication rates of 3 to 40%. The Achilles tendon should undergo reattachment with a tendon rupture of more than 50%.

Noninsertional Achilles Tendonitis

  • The goal of surgery is to resect degenerative tissue, stimulate tendon healing by means of controlled, low-grade trauma, and/or augment the Achilles tendon with grafts. It has been suggested that noninvasive treatment should be tried for at least 4 months prior to operative interventions []. Conventional surgical treatment has consisted of open release of adhesions with or without resection of the paratenon. If >50% of the tendon has been debrided, augmentation or reconstruction is recommended [].

Insertional Achilles Tendonitis

  • Patients who do not respond to conservative treatment may need operative management []. The operative strategy for insertional Achilles tendinopathy is the removal of the degenerative tendon and associated calcification, excision of the inflamed retrocalcaneal bursa, resection of the prominent posterior calcaneal prominence, reattachment of the insertion as required, and/or augmentation of the tendo-Achilles with a tendon transfer/graft [, ]. Calcaneoplasty and resection of the retrocalcaneal bursa can be performed endoscopically [].

Complications

Re-rupture

  • While newer level 1 evidence has reported no difference in re-rupture rates, prior studies have suggested a 10% to 40% re-rupture rate with nonoperative management (compared to 1% to 2% rate of re-rupture after surgery)
  • Lantto et al. recently demonstrated in a randomized controlled trial of 60 patients from 2009 to 2013 at 18-month follow-up: 

    • Similar Achilles tendon performance scores
    • Slightly increased calf muscle strength differences favoring the operative cohort (10% to 18% strength difference) at 18-month follow-up
    • Slightly better health-related quality of life scores in the domains of physical functioning and bodily pain favoring the operative cohort

Wound Healing Complications

  • Overall, a 5-10% risk following surgery
  • Risk factors for postoperative wound complications include:

    • Smoking (most common and most significant risk factor)
    • Female gender
    • Steroid use
    • Open technique (vs percutaneous procedures)

Sural Nerve Injury

  • Increased rate of injury associated with the percutaneous procedure (compared to open technique)

References

ByRx Harun

Achilles Tendinopathy – Symptoms, Diagnosis, Treatment

Achilles tendinopathy is one of the most frequently ankle and foot overuse injuries, which is a clinical syndrome characterized by the combination of pain, swelling, and impaired performance. The two main categories of Achilles tendinopathy are classified according to anatomical location and broadly include insertional and non insertional tendinopathy. The etiology of Achilles tendinopathy is multifactorial including both intrinsic and extrinsic factors. Failed healing response and degenerative changes were found in the tendon. The failed healing response includes three different and continuous stages (reactive tendinopathy, tendon disrepair, and degenerative tendinopathy).

Causes of Achilles Tendinopathy

The causes and mechanisms of Achilles tendinopathy (AT) include the following

  • Intrinsic factors – This includes anatomic factors, age, sex, metabolic dysfunction, foot cavity, dysmetria, muscle weakness, imbalance, gastrocnemius dysfunction, anatomical variation of the plantaris muscle, tendon vascularization, torsion of the Achilles tendons, slippage of the fascicle, and lateral instability of the ankle.
  • Extrinsic factors – These include mechanical overload, constant effort, inadequate equipment, obesity, medications (corticosteroids, anabolic steroids, fluoroquinolones,), improper footwear, insufficient warming or stretching, hard training surfaces, and direct trauma, among others.

Factors related to a high risk of rupture of the Achilles tendon link to advanced age due to a lack of uniformity of the tendons, slippage of the fascicles, and excessive exercise in athletes, Sports minded individuals tend to have an injury at the Achilles tendon insertion site.

Systemic Factors

Systemic diseases that may be associated with Achilles tendon injuries include the following:

  • Chronic renal failure
  • Collagen deficiency
  • Diabetes mellitus
  • Gout
  • Infections
  • Lupus
  • Parathyroid disorders
  • Rheumatoid arthritis
  • Thyroid disorders

Foot problems that increase the risk of Achilles tendon injuries include the following

  • Cavus foot
  • Insufficient gastrocsoleus flexibility and strength
  • limited ability to perform ankle dorsiflexion
  • Tibia vara
  • Varus alignment with functional hyper pronation

Symptoms of Achilles Tendinopathy

  • You hear a snap, crack or popping sound when pushing off with your leg, often accompanied by a sharp pain in the back of your leg or ankle
  • Trouble moving your foot to walk or go upstairs. You’re unable to stand on your toes (“tippy-toe”)
  • Pain, bruising and swelling at the back of your leg or heel
  • Chronic, recurrent calf or Achilles tendon ̶ area pain
  • Previous rupture of the affected tendon
  • Loss of plantarflexion power in the foot
  • Swelling of the calf
  • The recent increase in physical activity/training volume
  • Recent use of fluoroquinolones, corticosteroids, or corticosteroid injections

Diagnosis of Achilles Tendinopathy

Physical exploration

Clinical signs and symptoms of Achilles tendinopathy include localized pain, focal or diffuse sensitivity,  swelling, stiffness/morning pain, perceived rigidity in the Achilles tendon, positive arc sign, Royal London Hospital test, and Thompson test.

Tests used to diagnose Achilles tendinopathy

  • Lateral and axial calcaneus x-rays – May detect calcifications in the proximal extension of the tendon insertion or bony prominences in the upper portion of the calcaneus. Also, x-rays can help exclude pathological bone tumors.
  • Ultrasound – Can help assess injury to the tendon; can be used to predict the risk of tendinopathy and rupture. Ultrasound may reveal the increased thickness of the Achilles tendon with hyperemia associated with hypervascularity, a decrease in the gastrocnemius-soleus rotation angle and a decrease in the length of the Kager fat pad. Ultrasound is also useful during interventional treatment.
  • Magnetic Resonance Imaging – Provides significant information about the state of joint structures with a study in multiple planes in static and dynamic views. One study found that MRI had lower sensitivity than ultrasound in the detection of early changes of enthesopathy.. Another study found an excellent agreement between tendon thickness measurement between magnetic resonance and ultrasound.
  • Computed Tomography (CT) – The CT scan is useful to rule out trabecular structural alterations of the calcaneus in Achilles pathology of insertion. However, it exposes the patient to radiation.
  • Victoria Institute of Sports Assessment – Achilles (VISA-A) remains the gold standard for assessing pain and function, but it requires additional studies to increase its reliability. Nevertheless, it is an essential tool for patient post-treatment follow-up.

Differential Diagnosis

  • Achilles bursitis
  • Ankle fracture
  • Ankle impingement syndrome
  • Ankle osteoarthritis
  • Ankle sprain
  • Calf injuries
  • Calcaneofibular ligament injury
  • Calcaneus fractures
  • Deep venous thrombosis (DVT)
  • Exertional Compartment Syndrome
  • Fascial tears
  • Gastrocsoleus muscle strain or rupture
  • Haglund deformity
  • Plantaris tendon tear
  • Psoriatic arthritis
  • Reiter syndrome
  • Retrocalcaneal bursitis
  • Ruptured Baker cyst
  • Syndesmosis
  • Talofibular Ligament Injury

Treatment of Achilles Tendinopathy

Management of Achilles tendinopathy can divide into conservative and surgical. Additionally, one must consider whether it is an acute or chronic condition. Finally, for those with a full rupture, the treatment is usually surgical.

Conservative therapy:  It is the first line of management and includes the following

  • Reduction of activity levels
  • Adaptation of footwear, manual therapy directed at local sites may enhance the rehabilitation
  • Eccentric stretching exercises should comprise an integral component of physiotherapy and can achieve a 40% reduction in pain; moderate level evidence favors eccentric exercise over concentric exercise for reducing pain
  • Tendon loading exercise at short- and long-term follow-up
  • If unresponsive to initial management, extracorporeal shock wave therapy reduces pain by 60%, with 80% patient satisfaction, improving functionality and quality of life, with a follow-up at 4 weeks; this might be the first choice because of its safety and effectiveness
  • Physiotherapy improves the pain and functionality of the Achilles tendinopathy of the middle portion; however, studies do not show preferences for any particular exercise over another – overall, use of a splint to an eccentric exercise protocol or the use of orthoses to improve pain and function are not a recommendation
  • Current evidence shows a lack of efficacy on the use of platelet-rich plasma for Achilles tendinopathy

Nonoperative Management

  • Braces and immobilization – with a cast or pneumatic walking boot are combined with modified activity []. Immobilization is frequently used in the acute setting to control exacerbating factors, but prolonged immobilization should be avoided[].
  • Ultrasound – is a commonly prescribed program of physical therapy. In animal studies, ultrasound could stimulate collagen synthesis in tendon fibroblasts and cell division during the period of rapid cell proliferation []. Therapeutic ultrasound has been shown to reduce the swelling in the acute inflammatory phase of soft-tissue disorders, relieve pain, and increase function in patients with chronic tendon injuries and may enhance tendon healing [, ].
  • Low-level laser therapy (LLLT) – could reduce the expression of proinflammatory markers such as IL-6 and TNF-α in gene level []. In the cellular level, LLLT may increase collagen production [], stimulate tenocyte proliferation [], downregulate MMPs, decrease the capillary flow of neovascularization, and finally preserve the resistance and elasticity of tendon [, ].
  • Extracorporeal shockwave therapy (ESWT) – How ESWT works is still poorly understood, but it is known to cause selective dysfunction of sensory unmyelinated nerve fibers, alteration in the dorsal root ganglia, and cavitation in interstitial and extracellular disruption, which could promote the healing response [].
  • Deep friction massage (DFM) – and tendon mobilization may also be helpful in the treatment of Achilles tendinopathy. DFM has been advocated for tendinopathy and paratendinopathy. Friction has been shown to increase the protein output of tendon cells []. In combination with stretching, deep friction massage helps to restore tissue elasticity and reduce the strain in the muscle-tendon unit [, ]. Future randomized comparison studies are necessary to compare DFM in isolation with other modes of treatment.
  • Cryotherapy – might play a role in reducing the increased capillary blood flow in Achilles tendinopathy, reducing the metabolic rate of the tendon, and applying for relief of pain [, ]. However, recent evidence in upper limb tendinopathy indicated that the addition of ice did not offer any advantage over an exercise program consisting of eccentric and static stretching exercises [].

Medication

  • NSAIDs – used in chronic tendinopathy is questionable because the histological examination in the tendinopathic tissue shows no inflammatory cells []. The benefits of NSAIDs use are relieving pain in the acute phase and reducing the possibility of leg stiffness []. However, there are some studies that indicated that the NSAIDs may inhibit tendon cell migration and proliferation and impair tendon healing [].
  • Corticosteroid injections – are reported to reduce pain and swelling and improve the ultrasound appearance of the tendon. The mechanism behind any positive effect of local steroids on chronic Achilles tendinopathy remains unclear. Some authors have hypothesized that any beneficial effects of corticosteroids in this condition are owed to other local steroid effects rather than suppression of inflammation, including lyses of tendon and peritendon adhesions or alteration of the function of pain generating nociceptor in the region [].
  • Platelet-rich plasma (PRP) – at the site of tendon injury is thought to facilitate healing because it contains several different growth factors and other cytokines that can stimulate the healing of soft tissue []. Animal studies indicated that PRP could increase the expression of collagen types I and III and vascular endothelial growth factor and improve the healing and remodeling process of the tendon [, ].
  • Intratendinous hyperosmolar dextrose (prolotherapy) – is thought to produce a local inflammatory response and increase in tendon strength. Clinical results indicated that intratendinous injections of hyperosmolar dextrose could reduce the pain at rest and during tendon-loading activities in patients with chronic of the Achilles tendinopathy [, ]. Moreover, after the injection of dextrose, there were reductions in the size and severity of hypoechoic regions and intratendinous tears and improvements in neovascularity [].
  • Nitric oxide – is a small-free radical generated by a family of enzymes, the nitric oxide synthases. It can induce apoptosis in inflammatory cells and cause angiogenesis and vasodilation. Moreover, oxygen-free radicals can stimulate fibroblast proliferation []. Nitric oxide can enhance tendon healing. Inhibition of nitric oxide synthase can reduce the healing process, which resulted in a decreased cross-sectional area and reduced failure load [].
  • The sclerosing agent – that selectively targets the vascular may cause thrombosis of the vessel. As the concomitant sensory nerves have been implicated as possible pain generators, to destroy local nerves adjacent to neovessels may decrease pain []. As vessel number has been shown to correlate with tendon thickness, a treatment that decreases vessel number is likely to also affect the tendon thickness. Moreover, the sclerosing agent injected at multiple sites around the tendon and neovessels initiates a local inflammatory response, which induces the proliferation of fibroblasts and the synthesis of collagen.
  • Aprotinin – is a broad-spectrum serine protease inhibitor capable of blocking trypsin, plasmin, kallikrein, and a range of MMPs []. Most previous studies using Aprotinin injection in the management of Achilles tendinopathy showed a trend towards improved clinical results [, ]. The major potential negative of using Aprotinin is the side effect of allergy [], but the allergic reactions can be reduced by minimizing repeat injections and recommending a delay of at least 6 weeks between injections [].
  • Autologous blood injections – results have not been highly encouraging and there is little evidence for their use.[rx]

Surgery

Surgical therapy is optional for 10 to 30% of patients who fail conservative therapy after six months. The success rate is higher than 70%, but reports show complication rates of 3 to 40%. The Achilles tendon should undergo reattachment with a tendon rupture of more than 50%.

Noninsertional Achilles Tendinopathy

  • The goal of surgery is to resect degenerative tissue, stimulate tendon healing by means of controlled, low-grade trauma, and/or augment the Achilles tendon with grafts. It has been suggested that noninvasive treatment should be tried for at least 4 months prior to operative interventions []. Conventional surgical treatment has consisted of open release of adhesions with or without resection of the paratenon. If >50% of the tendon has been debrided, augmentation or reconstruction is recommended [].

Insertional Achilles Tendinopathy

  • Patients who do not respond to conservative treatment may need operative management []. The operative strategy for insertional Achilles tendinopathy is the removal of the degenerative tendon and associated calcification, excision of the inflamed retrocalcaneal bursa, resection of the prominent posterior calcaneal prominence, reattachment of the insertion as required, and/or augmentation of the tendo-Achilles with a tendon transfer/graft [, ]. Calcaneoplasty and resection of the retrocalcaneal bursa can be performed endoscopically [].

Complications

Re-rupture

  • While newer level 1 evidence has reported no difference in re-rupture rates, prior studies have suggested a 10% to 40% re-rupture rate with nonoperative management (compared to 1% to 2% rate of re-rupture after surgery)
  • Lantto et al. recently demonstrated in a randomized controlled trial of 60 patients from 2009 to 2013 at 18-month follow-up: 

    • Similar Achilles tendon performance scores
    • Slightly increased calf muscle strength differences favoring the operative cohort (10% to 18% strength difference) at 18-month follow-up
    • Slightly better health-related quality of life scores in the domains of physical functioning and bodily pain favoring the operative cohort

Wound Healing Complications

  • Overall, a 5-10% risk following surgery
  • Risk factors for postoperative wound complications include:

    • Smoking (most common and most significant risk factor)
    • Female gender
    • Steroid use
    • Open technique (vs percutaneous procedures)

Sural Nerve Injury

  • Increased rate of injury associated with the percutaneous procedure (compared to open technique)

References

ByRx Harun

SLR Test – Types, Technique, Clinical Outcome

SLR Test/The straight leg raise test also called the Lasegue test is a fundamental neurological maneuver during the physical examination of the patient with lower back pain aimed to assess the sciatic compromise due to lumbosacral nerve root irritation. This test which was first described by Dr. Lazarevic and wrongly attributed to Dr. Lasegue can be positive in a variety of conditions, being lumbar disc herniation the most common. Nonetheless, there are multiple causes of a positive test such as facet joint cyst or hypertrophy.. Overall, this test is one of the most commonly performed maneuvers across clinical practice and provides important information when making the clinical decision to refer a patient to a specialist as well as among spinal surgeons to guide therapeutic decision-making.

Lasegue sign or Straight Leg Raising Test (SLRT) is a neurodynamic exam to assess nerve root irritation in the lumbosacral area. It is an integral element to the neurological exam for patients presenting with low back pain with or without radicular pain. The other less commonly used name is Lazarevic sign.

Anatomy and Physiology of Straight Leg Raising Test (SLRT)

The Lasegue test is basically a provocation test that evidences radicular irritation in the lumbosacral region by lower limb flexion and can be due to multiple causes. Radicular symptoms are primarily produced by nerve root inflammation by surrounded structures. The foramina are formed by the pedicle superiorly and inferiorly, ligamentum flavum posteriorly, disc and vertebral body anteriorly, and this small space normally allows the nerve root excursion of 4 mm, however during the straight leg raise test this root excursion can be compromised by several factors. Mechanical compression solely does not always generate radicular symptoms as many patients have asymptomatic foraminal stenosis in MRI, therefore, positive leg raise test may undergo influence by nerve root irritation secondary to inflammation as well as mechanical compression.

The straight leg raise test is attributed to Charles Lasegue, a French clinician who described two cases of sciatica aggravated by weight-bearing, hip, and knee flexion in “Thoughts of Sciatica” in 1864. Nonetheless, Dr. Lasegue did not describe the test as a provoked pain; instead, his student JJ Forst described the test in his doctoral thesis in 1881, and it was Forst who considered the pain to be produced by hamstring muscle compression to the sciatic nerve.

Nevertheless, it is believed that a Serbian neurologist, Dr. Lazar Lazarevic, was the first who documented the straight leg raise test as it is known today in the article named “Ischiac postica council”, initially published in the Serbian Archives of Medicine (1880), and republished in Vienna (1884). Dr. Lazarevic described the straight-leg-raising test by explaining sciatic pain by stretching the sciatic nerve based on his experience with six patients. Based on this misinterpretation of the original description, it is recommended to describe the maneuver as the straight leg raise test.

Indications of Straight Leg Raising Test (SLRT)

The Technique of Straight Leg Raising Test (SLRT)

The straight leg raise test is performed with the patient in a supine position. The examiner gently raises the patient’s leg by flexing the hip with the knee in extension, and the test is considered positive when the patient experiences pain along the lower limb in the same distribution of the lower radicular nerve roots (usually L5 or S1).

Furthermore, a positive straight leg raise test is determined when pain is elicited by lower limb flexion in an angle lower than 45 degrees. During the test, if the pain is reproduced during the leg straightening, patients usually request that the examiner aborts the maneuver and by flexing the patient’s knee, the buttock pain is usually relieved(Figure 1).

Additional maneuvers have been described to enhance the sensitivity of the test such as the Bragaad’s sign, which consists of concomitant foot dorsiflexion to increase the pain while the examiner completes the leg raise.

An additional maneuver is the crossed straight leg test (crossed over Lasegue), in which the examiner passively flexes the patient’s uninvolved limb while maintaining the knee in extension. A positive test is when the patient reports pain in the involved limb at 40 degrees of hip flexion with the uninvolved limb. A crossed straight test is positive in central disc herniation in cases of severe nerve root irritation.

Currently, the following technique is popular in practice

The patient should be informed about the steps of the test, what to expect during the exam, and to describe the pain distribution. The patient should be examined in a neutral supine position with the head slightly extended. During the exam, the hips and legs should stay neutral. No hips abduction or adduction is allowed as well as no leg internal or external rotation is permitted. The affected leg is then passively and slowly raised by the ankle with the knee fully extended. Upon eliciting pain, the examiner stops further leg elevation and records the range of motion along with the area of pain distribution.

It is noteworthy that ankle dorsiflexion during SLRT may exaggerate the pain, notwithstanding, it is not part of the Lasegue sign.

Causes of Pain While Performing SLRT

  • Stretching of the sciatic nerve
  • Displacement of the medulla and conus medullaris
  • Nerve compression leads to sensitization at the dorsal root ganglion and posterior horn, which in turn leads to the lowering of the pain threshold.

Causes of Positive SLRT

  • Nerve root irritation – Intervertebral disc prolapse being the most common cause
  • Intraspinal tumor
  • Inflammatory radiculopathy

Criteria for a true positive SLRT

  • Radicular leg pain should occur (radiating below the knee).
  • Pain occurs when the leg is between 30 and 60 or 70 degrees from horizontal.

What findings should not qualify as a positive SLRT?

  • Pain occurring in the low back alone.
  • Pain occurring in the posterior thigh alone.
  • Pain occurring at an angle less than 30 degrees – May indicate non-organicity or hip joint pathology.
  • Pain occurring at an angle more than 70 degrees from the horizontal – More likely cause is tight hamstring or gluteal muscles.
  • Pain occurs in a normal person at an angle of 80 to 90 degrees.

Issues of Concern of Straight Leg Raising Test (SLRT)

SLRT modifications and its variants: the accuracy of SLRT can be better if it is interpreted with other nerve root tension tests:

  • Crossed SLRT – AKA well-leg raising test or Fajersztajn sign. When the contralateral leg is lifted, the patient experiences pain on the affected side. This test is more specific than ipsilateral SLRT. It becomes positive usually in severe compression and centrally located prolapse. Fajersztajn believed that this sign is due to disc prolapse in the axilla of the root.
  • Reverse SLRT – AKA femoral stretch or Ely test. While the patient is in a prone position, the leg is lifted off the table with both hip and knee joints extended. Some authors may allow knee flexion. This maneuver may reproduce radicular pain in case of upper lumbar radiculopathy, far lateral lumbar disc, or femoral neuropathy. The pain will present in the femoral nerve distribution on the side of the lesion.
  • Braggard test – AKA Sciatic stretch test or Flip test. While raising the leg, the foot is held in a dorsiflexed position, so that the sciatic nerve is stretched more, thereby increasing the intensity of pain or making it possible to elicit the sign early.
  • Reverse flip test – While raising the leg, the foot is held in a plantar-flexed position; this will lessen the pain. But if the patient is complaining of an increase in pain, it can suggest malingering.
  • Bowstring sign – Also known as the popliteal compression test or posterior tibial nerve stretch sign. The patient can be examined in sitting or in a supine position. The examiner flexes the knee and applies pressure on the popliteal fossa, evoking sciatica. Some examiners do it after SLRT by flexing the knee to relieve the buttock pain. The pain would be reproduced by a quick snap on the posterior tibial nerve in the popliteal fossa.

Less frequently used nerve root irritation tests

For the sake of completion, other tests and signs of nerve root tension or irritation are discussed succinctly below:

  • Sitting SLRT (Bechterew test) – the patient is made to sit at the edge of a table with both hip and knee flexed, then made to extend the knee joint or elevate the extended knee, which reproduces the radicular pain. He/she may be able to extend each leg alone, but extending both together causes radicular pain.
  • Distracted SLRT – the sitting SLRT is performed without the patient’s awareness. The patient is distracted as if the surgeon is examining the foot or pulsation, and slowly, the examiner extends the knee. If the patient is experiencing true radiculopathy, the same pain will be reproduced. Otherwise, we can assume that the patient may be malingering.
  • Neri’s sign – while bending forward, the patient flexes the knee to avoid stretching the nerve.
  • The buckling sign – the patient may flex the knee during SLRT to avoid sciatic nerve tension.
  • Sicard sign – passive dorsiflexion of ipsilateral great toe just at the angle of SLRT will produce more pain.
  • Kraus-Weber test – the patient may be able to do a sit-up with the knees flexed but not extended.
  • Minor sign – the patient may rise from a seated position by supporting himself/herself on the unaffected side, bending forward, and placing one hand on the affected side of the back.
  • Bonnet phenomenon – the pain may be more severe or elicited sooner if the test is carried out with the thigh and leg in a position of adduction and internal rotation.

Clinical Significance of Straight Leg Raising Test (SLRT)

Interpretation of SLRT

  • Pain radiating down the buttock to the lateral thigh and medial calf – L4 nerve root irritation
  • Pain radiating down the buttock to the posterior thigh and lateral calf – L5 nerve root irritation
  • Pain radiating down the buttock to the posterior thigh and calf, and lateral foot – S1 nerve root irritation

Interpretation of Positive Reverse SLRT

  • L2, L3 or L4 root irritation
  • Femoral nerve irritation

Sensitivity and Specificity of the Test

The sensitivity of ipsilateral SLRT is 72 to 97%, and specificity is 11 to 66%; whereas the crossed SLRT  sensitivity is 23 to 42%  which is less than ipsilateral SLRT but more specific (85 to 100%).

Tests to Confirm Non-organicity While Performing SLRT

  • Pain occurring at an angle less than 30 degrees
  • A significant discrepancy between the supine and sitting SLRT
  • Touch-me-not or Waddell sign – Widespread and excessive tenderness
  • Back pain on pressing down on the top of the head
  • Overreaction during testing
  • Non-dermatomal and non-myotomal neurologic signs
  • Pain during simulated spinal rotation: The patient’s hands remain to the sides with hips rotated. There will not be any spine rotation with this maneuver. But the patient will complain of pain.

References

ByRx Harun

Lasegue sign/ Straight Leg Raising Test (SLRT)

Lasegue sign/Straight Leg Raising Test (SLRT)/The straight leg raise test also called the Lasegue test is a fundamental neurological maneuver during the physical examination of the patient with lower back pain aimed to assess the sciatic compromise due to lumbosacral nerve root irritation.  Nonetheless, there are multiple causes of a positive test such as facet joint cyst or hypertrophy.. Overall, this test is one of the most commonly performed maneuvers across clinical practice and provides important information when making the clinical decision to refer a patient to a specialist as well as among spinal surgeons to guide therapeutic decision-making.

Lasegue sign or Straight Leg Raising Test (SLRT) is a neurodynamic exam to assess nerve root irritation in the lumbosacral area. It is an integral element to the neurological exam for patients presenting with low back pain with or without radicular pain. The other less commonly used name is Lazarevic sign.

Anatomy and Physiology of Straight Leg Raising Test (SLRT)

The Lasegue test is basically a provocation test that evidences radicular irritation in the lumbosacral region by lower limb flexion and can be due to multiple causes. Radicular symptoms are primarily produced by nerve root inflammation by surrounded structures. The foramina are formed by the pedicle superiorly and inferiorly, ligamentum flavum posteriorly, disc and vertebral body anteriorly, and this small space normally allows the nerve root excursion of 4 mm, however during the straight leg raise test this root excursion can be compromised by several factors. Mechanical compression solely does not always generate radicular symptoms as many patients have asymptomatic foraminal stenosis in MRI, therefore, positive leg raise test may undergo influence by nerve root irritation secondary to inflammation as well as mechanical compression.

The straight leg raise test is attributed to Charles Lasegue, a French clinician who described two cases of sciatica aggravated by weight-bearing, hip, and knee flexion in “Thoughts of Sciatica” in 1864. Nonetheless, Dr. Lasegue did not describe the test as a provoked pain; instead, his student JJ Forst described the test in his doctoral thesis in 1881, and it was Forst who considered the pain to be produced by hamstring muscle compression to the sciatic nerve.

Nevertheless, it is believed that a Serbian neurologist, Dr. Lazar Lazarevic, was the first who documented the straight leg raise test as it is known today in the article named “Ischiac postica council”, initially published in the Serbian Archives of Medicine (1880), and republished in Vienna (1884). Dr. Lazarevic described the straight-leg-raising test by explaining sciatic pain by stretching the sciatic nerve based on his experience with six patients. Based on this misinterpretation of the original description, it is recommended to describe the maneuver as the straight leg raise test.

Indications of Straight Leg Raising Test (SLRT)

The Technique of Straight Leg Raising Test (SLRT)

The straight leg raise test is performed with the patient in a supine position. The examiner gently raises the patient’s leg by flexing the hip with the knee in extension, and the test is considered positive when the patient experiences pain along the lower limb in the same distribution of the lower radicular nerve roots (usually L5 or S1).

Furthermore, a positive straight leg raise test is determined when pain is elicited by lower limb flexion in an angle lower than 45 degrees. During the test, if the pain is reproduced during the leg straightening, patients usually request that the examiner aborts the maneuver and by flexing the patient’s knee, the buttock pain is usually relieved(Figure 1).

Additional maneuvers have been described to enhance the sensitivity of the test such as the Bragaad’s sign, which consists of concomitant foot dorsiflexion to increase the pain while the examiner completes the leg raise.

An additional maneuver is the crossed straight leg test (crossed over Lasegue), in which the examiner passively flexes the patient’s uninvolved limb while maintaining the knee in extension. A positive test is when the patient reports pain in the involved limb at 40 degrees of hip flexion with the uninvolved limb. A crossed straight test is positive in central disc herniation in cases of severe nerve root irritation.

Currently, the following technique is popular in practice

The patient should be informed about the steps of the test, what to expect during the exam, and to describe the pain distribution. The patient should be examined in a neutral supine position with the head slightly extended. During the exam, the hips and legs should stay neutral. No hips abduction or adduction is allowed as well as no leg internal or external rotation is permitted. The affected leg is then passively and slowly raised by the ankle with the knee fully extended. Upon eliciting pain, the examiner stops further leg elevation and records the range of motion along with the area of pain distribution.

It is noteworthy that ankle dorsiflexion during SLRT may exaggerate the pain, notwithstanding, it is not part of the Lasegue sign.

Causes of Pain While Performing SLRT

  • Stretching of the sciatic nerve
  • Displacement of the medulla and conus medullaris
  • Nerve compression leads to sensitization at the dorsal root ganglion and posterior horn, which in turn leads to the lowering of the pain threshold.

Causes of Positive SLRT

  • Nerve root irritation – Intervertebral disc prolapse being the most common cause
  • Intraspinal tumor
  • Inflammatory radiculopathy

Criteria for a true positive SLRT

  • Radicular leg pain should occur (radiating below the knee).
  • Pain occurs when the leg is between 30 and 60 or 70 degrees from horizontal.

What findings should not qualify as a positive SLRT?

  • Pain occurring in the low back alone.
  • Pain occurring in the posterior thigh alone.
  • Pain occurring at an angle less than 30 degrees – May indicate non-organicity or hip joint pathology.
  • Pain occurring at an angle more than 70 degrees from the horizontal – More likely cause is tight hamstring or gluteal muscles.
  • Pain occurs in a normal person at an angle of 80 to 90 degrees.

Issues of Concern of Straight Leg Raising Test (SLRT)

SLRT modifications and its variants: the accuracy of SLRT can be better if it is interpreted with other nerve root tension tests:

  • Crossed SLRT – AKA well-leg raising test or Fajersztajn sign. When the contralateral leg is lifted, the patient experiences pain on the affected side. This test is more specific than ipsilateral SLRT. It becomes positive usually in severe compression and centrally located prolapse. Fajersztajn believed that this sign is due to disc prolapse in the axilla of the root.
  • Reverse SLRT – AKA femoral stretch or Ely test. While the patient is in a prone position, the leg is lifted off the table with both hip and knee joints extended. Some authors may allow knee flexion. This maneuver may reproduce radicular pain in case of upper lumbar radiculopathy, far lateral lumbar disc, or femoral neuropathy. The pain will present in the femoral nerve distribution on the side of the lesion.
  • Braggard test – AKA Sciatic stretch test or Flip test. While raising the leg, the foot is held in a dorsiflexed position, so that the sciatic nerve is stretched more, thereby increasing the intensity of pain or making it possible to elicit the sign early.
  • Reverse flip test – While raising the leg, the foot is held in a plantar-flexed position; this will lessen the pain. But if the patient is complaining of an increase in pain, it can suggest malingering.
  • Bowstring sign – Also known as the popliteal compression test or posterior tibial nerve stretch sign. The patient can be examined in sitting or in a supine position. The examiner flexes the knee and applies pressure on the popliteal fossa, evoking sciatica. Some examiners do it after SLRT by flexing the knee to relieve the buttock pain. The pain would be reproduced by a quick snap on the posterior tibial nerve in the popliteal fossa.

Less frequently used nerve root irritation tests

For the sake of completion, other tests and signs of nerve root tension or irritation are discussed succinctly below:

  • Sitting SLRT (Bechterew test) – the patient is made to sit at the edge of a table with both hip and knee flexed, then made to extend the knee joint or elevate the extended knee, which reproduces the radicular pain. He/she may be able to extend each leg alone, but extending both together causes radicular pain.
  • Distracted SLRT – the sitting SLRT is performed without the patient’s awareness. The patient is distracted as if the surgeon is examining the foot or pulsation, and slowly, the examiner extends the knee. If the patient is experiencing true radiculopathy, the same pain will be reproduced. Otherwise, we can assume that the patient may be malingering.
  • Neri’s sign – while bending forward, the patient flexes the knee to avoid stretching the nerve.
  • The buckling sign – the patient may flex the knee during SLRT to avoid sciatic nerve tension.
  • Sicard sign – passive dorsiflexion of ipsilateral great toe just at the angle of SLRT will produce more pain.
  • Kraus-Weber test – the patient may be able to do a sit-up with the knees flexed but not extended.
  • Minor sign – the patient may rise from a seated position by supporting himself/herself on the unaffected side, bending forward, and placing one hand on the affected side of the back.
  • Bonnet phenomenon – the pain may be more severe or elicited sooner if the test is carried out with the thigh and leg in a position of adduction and internal rotation.

Clinical Significance of Lasegue sign/Straight Leg Raising Test (SLRT)

Interpretation of SLRT

  • Pain radiating down the buttock to the lateral thigh and medial calf – L4 nerve root irritation
  • Pain radiating down the buttock to the posterior thigh and lateral calf – L5 nerve root irritation
  • Pain radiating down the buttock to the posterior thigh and calf, and lateral foot – S1 nerve root irritation

Interpretation of Positive Reverse SLRT

  • L2, L3 or L4 root irritation
  • Femoral nerve irritation

Sensitivity and Specificity of the Test

The sensitivity of ipsilateral SLRT is 72 to 97%, and specificity is 11 to 66%; whereas the crossed SLRT  sensitivity is 23 to 42%  which is less than ipsilateral SLRT but more specific (85 to 100%).

Tests to Confirm Non-organicity While Performing SLRT

  • Pain occurring at an angle less than 30 degrees
  • A significant discrepancy between the supine and sitting SLRT
  • Touch-me-not or Waddell sign – Widespread and excessive tenderness
  • Back pain on pressing down on the top of the head
  • Overreaction during testing
  • Non-dermatomal and non-myotomal neurologic signs
  • Pain during simulated spinal rotation: The patient’s hands remain to the sides with hips rotated. There will not be any spine rotation with this maneuver. But the patient will complain of pain.

References

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