L5 Nerve Root

The L5 nerve root arises from the spinal canal, it is part of the lumbosacral plexus. It is also part of the sciatic nerve. The L5 nerve root supplies the muscle that allows extension of the toes and dorsiflexion of the ankle. It is also responsible for supplying sensation to the dorsum of the foot and leg. When the L5 nerve root gets involved, you will have sciatica with a positive straight leg raising. Straight leg raising (tension sign) occurs from L5-S1 involvement.  The tension sign produces pain and paresthesia in the leg at 30-70 degrees of hip flexion.  Injuries to the L5 nerve root include intervertebral disc herniation, spondylolisthesis, sacral fractures and sacroiliac joint injury.  In intervertebral disc herniation the L5 nerve root involvement can cause Trendelenburg gait due to posterolateral disc herniation. This is because it affects the gluteus medius and minimus. Trendelenburg gait can also occur with L5-S1 foraminal disc herniation. Posterolateral disc herniation affects the transversing or the descending nerve root at the level of L4-L5 (affects the L5 nerve root). Foraminal disc herniation, which is far lateral or the extra foraminal, affects the exiting nerve root or upper nerve root (L5-S1 will affect L5 nerve root). The lumbar disc herniation affects L 4-L5, and L5- S1 level in about 95% of the time and it will involve the L5-S1 nerve roots. In general, the L5 nerve root involvement will cause weakness with hip abduction, big toe extension, and ankle dorsiflexion.  If there is a sacroiliac joint injury, the lumbosacral plexus can be injured. That will predominately affect the L5 nerve root causing the patient to have foot drop. When doing surgery on the sacroiliac joint, and the surgeon goes anteriorly to fix the injury and places a retractor in the anterior aspect of the sacrum, the L4-L5 nerve roots can be injured. These nerves are about 1 cm medial to the sacroiliac joint at it inferior part. In displaced sacral fracture, the L5 nerve root can be injured especially if it is a fracture of the ala of the sacrum which occurs about 5% of the time. With degenerative spondylolisthesis, the vertebra do not slip a lot. Degenerative spondylolisthesis occurs at L4-L5, occurs more often in females and involves the L5 nerve root.  In isthmic spondylolisthesis, if it occurs at L5-S1, it may involve the L5 nerve root and cause hamstring tightness.  Spondylolysis is a fracture of the Pars interarticularis. With isthmic spondylolisthesis the vertebra is slipped and it may slip a lot.

Pediatric Femoral Shaft Fractures

Treatment for pediatric femoral shaft fracture varies. Treatment can include casting or surgery, depending on the age of the patient and the pattern of the fracture. A fracture of the femur that occurs in a child before the walking age, there should be concern for non-accidental trauma, suspect abuse.  Pediatric patients 0-6 months of age should be treated with a Pavlik harness, 6months to 5 years of age should be treated with an immediate spica cast. Moderate evidence supports treatment with an early spica cast or traction with delayed spica cast for children aged 6 mo. - 5 years with a diaphyseal femur fracture with less than 2 cm of shortening.  A spica cast is not used for a patient that has shortening of 2-3 cm. If there is excessive shortening or potential shortening, there will be loss of reduction in the spica cast and the child can be treated by traction and delayed spica cast or by a different alternative. In very unstable fractures, you are going to use traction with a delayed spica cast or external fixator.  Children 5 years of age to 11 years, consider using flexible rods, plate, or external fixator. To use flexible IM nails, the fracture must be axially stable and it can be used in children between the ages of 5-11 years, and should not be used in children weighing more than 100 pounds or in children older than 11 years. An alternative technique, different than the flexible IM nail should be used in older children that weigh more than 100 pounds or if the child is more than 11 years old. For the flexible nails to work, the fracture must be short, oblique, or transverse.  It is probably better if the fracture is in the mid-diaphysis area. In comminuted fractures, or very distal or proximal fractures, it may be hard to control the fracture with a flexible IM rod. Approximately 50% of fractures treated with flexible nails have about 15 degrees of malalignment.  The nail size of the IM flexible nail is determined by multiplying the width of the isthmus of the femoral canal by 0.4 and the goal is to have 80% fill.  Sub muscular plate fixation can be used in children more than 5 years old and in the patient that weigh more than 100 pounds. It can also be used in very proximal or very distal fractures where the flexible rod will not work, especially if the fracture is unstable. It can be used in cases of severe comminution when you will use the plate as a bridge plate. It can be used for open fractures, if there is associated vascular injury, if the fract5uer is significantly comminuted, or it can be used in polytrauma patient. With external fixation there is increased risk of re-fracture after removal of the fixator. The main blood supply to the femoral head is the deep branch of the medial femoral circumflex artery and these branches are near the piriformis fossa and are vulnerable to be injured with a piriformis entry nailing. Osteonecrosis of the femoral head can occur with an open proximal physis. Piriformis or near piriformis entry rigid nailing is not usually recommended for the young child. If the IM rod needs to be done, it is better to go through a greater trochanteric entry which can also have its own complication such as coxa valgus or premature fusion of the greater trochanter apophysis.   Rigid trochanteric entry nailing may be an option for children at or near skeletal maturity.  The most common complication in younger patients is leg length discrepancy with over growth of up to 2 cm in patients younger than 10 years of age. It typically occurs within 2 years of the injury. Leg length discrepancy can occur from excessive shortening following a cast treatment. Do not accept more than 2 cm of shortening.  Monitor the child for development of compartment syndrome following spica cast. When you do traction and you delay the spica cast, a proximal tibial traction pin can cause recurvatum due to damage of the anterior part of the tibial tubercle apophysis. 

Low Back Pain

What are the important facts about low back pain? No definitive etiology is found in about 85% of the patients. 90% of patients with a single episode of low back pain return to work within 6 weeks, and most patients get better with time. The history of low back pain is the single most important factor predicting future occupational low back pain. Low back pain is the second most common cause of work absenteeism. Persistent back pain more than 6 months constitutes more than 4% of the cases. Disability is closely linked to compensation and litigation. The least amount of pressure on the disc is measured with the person lying supine. The highest disc pressure is measured while sitting and 20 degree forward leaning with 20 kg load in the arm. By keeping the weight of the load close to the body, this reduces the compressive forces being placed on the lumbar spine. Yoga activities and exercises performed during sitting probably have less pressure being placed on the discs. What are the physical factors that lead to low back pain? Lifting heavy objects. Holding the load close to the body is important to reduce the compressive forces being placed on the lumbar spine.  Cigarette smoking is another factor. Nicotine causes disc degeneration, it interferes with the vascularity of the spine and the nutrition of the discs. Operating motor vehicles, prolonged sitting, lack of fitness, operating vibrating tools also contribute to low back pain. Sports related activities can lead to low back pain. One example includes golf.  Pain results from twisting and excessive forward bending and overarching of the spine during the swing.  At the age of 40, the average person loses 50% of their rotational movement of the spine. It is important to perform stretching and warmups before starting the game. Another example of a sport related activity leading to low back pain is horseback riding. Vibration caused by horseback riding increases the load on the discs. The back muscles work constantly to keep you posture straight. Caring for horses could be bad for the back due to the bending and the lifting associated with their care. The etiology of low back pain. Virtually any structure in the spine and close to the spine can hurt, causing what seems to be low back pain. These structures include facet joints, intervertebral discs, spinal canal/nerve roots, sacroiliac joints, muscles, ligaments, nerves, hip joint/piriformis syndrome, and trochanteric bursitis. Red flags for cancer include patients over the age of 50, pain at rest and at night, unexplained weight loss, history of cancer, bone destruction involving the pedicle in pathognomonic. Look for the winking owl sign of the vertebrae. The red flags for infection include diabetes mellitus, intravenous drug abuse, fever, urinary tract infection, and previous surgery on the spine. The physical examination includes the initial assessment, focus on the red flags such as fractures, tumor, infection, or cauda equina syndrome. Symptoms and signs of cauda equina syndrome are back pain more than leg pain, bladder or bowel disturbances, bilateral leg pain and weakness, saddle anesthesia (rectal and genital area sensory changes). In the absence of red flags, imaging studies are usually not helpful in the first 4-6 weeks. It is hard to explain to the patient why you did not get an x-ray, although not getting and early x-ray is a good patient care, but it may lead to suboptimal patient satisfaction. Intensive work-up may not be necessary in the early stages of routine low back pain. Conservative treatment of low back pain include anti-inflammatory medication and muscle relaxants which are usually helpful, and a soft brace or corset. Physical therapy is an important aspect of the treatment and should be done as soon as pain control is achieved. The combination of physical therapy and return to work is important. If a patient sustained chronic, disabling occupational low back pain without any intensive rehab, there is a 50% chance of going back to work if the person is out of work for 6 months. The chance of returning to work drops to 20% if the person is out of work for 1 year. The chance of returning to work is almost none if the person is out of work for 2 years. It is important to do therapy and encourage the patient to go back to work. The best treatment for acute low back pain is to continue with the ordinary daily activities within the limits permitted by the pain.  The best treatment for low back pain is for the patient to go back to work.

P-Acne Shoulder Infection

Propionibacterium acne is a slow growing, anaerobic gram positive bacteria. acne is skin bacteria responsible for shoulder infections and it usually has a subtle subclinical presentation. They can be rod shaped or branched usually found in the skin pores. Propionibacterium acnes may colonize in the axilla especially in males. There is difficulty in obtaining positive cultures from standard labs. Propionibacterium acnes are generally nonpathogenic but can cause numbers of infection such as acne vulgaris. The Propionibacterium acne infection is one of the most common causes of shoulder infection such as rotator cuff infection. In fact, some people think that it is the most common organism isolated after rotator cuff surgery.  The interesting thing about Propionibacterium acne is that it grows very slowly. Most of the standard labs will read the culture up to 5 days, but the Propionibacterium acne can grow up to 14 days. If the lab states that there is no growth, this could mean that you didn’t give it enough time. The patient may have this infection and the infection may continue despite the fact that the culture came back negative. It game back before the growth of the organisms.  The standard labs will not keep the culture for two weeks unless you tell them to keep the culture.  Allow up to two weeks for the culture to grow and to identify this organism. Ask the lab to hold the culture for a longer time if you strongly suspect the infection in the shoulder. This organism colonizes the shoulder at an increased rate.  Mini open cuff repair after arthroscopic surgery may have increased risk of that infection. A second prep and drape of the surgical field was suggested to reduce the incidence of infection.  Positive culture was found also in revision shoulder arthroplasty. Staphylococcus epidermidis loses the prosthesis, especially in the hip or the knee. P-acne however, loves the prosthesis in the shoulder. The clinical presentation is insidious and nonspecific.  The traditional signs of infection are usually lacking: fever, erythema, severe pain. Blood work is usually not consistently elevated. It is a slow growing bacteria and the cultures take from one to three weeks to become positive. This creates a diagnostic challenge. The initial culture is usually negative. The lab does not usually hold the cultures unless instructed with personal communication with the appropriate personnel. If you suspect infection, ask the lab to hold the culture for at least 2 weeks.  P-acne is a common cause of indolent shoulder infection and shoulder implant failure. Infection of the shoulder with P-acne should be considered as a cause of persistent unexplained shoulder pain. Treatment includes obtaining fluid from aspiration, or obtain a tissue sample (multiple tissue samples are better), keep the culture for two weeks, debridement, IV antibiotics (resistance of the bacteria to antibiotics is a challenge). Any prosthesis may need to be removed.  In summary, the Propionibacterium acne infection is an emerging clinical entity. The harm goes beyond the skin and should not be considered a contaminant. It is becoming an orthopedic pathogen and not just a dermatology pathogen.  It is probably resistant to the standard broad spectrum antibiotics. The clinician should be aware that this bacteria loves to infect the shoulder.

Sudden Cardiac Death in Athletes

The heart is a muscular organ that is about the size of a closed fist that function as the body’s circulatory pump. The heart is divided into four chambers. The two upper chambers are called the atria. The bottom two chambers are the ventricles. The interventricular septum separates the left ventricle from the right ventricle.  The blood return from the entire body deoxygenated and then enters the heart through the right atrium. It then passes to the right ventricle where it is pumped through the pulmonary artery to the lungs to become loaded with oxygen.  Oxygenated blood returns to the left atrium and then passes down into the left ventricle where it is pumped back into the circulation through the aorta. Many conditions may lead to sudden cardiac death including hypertrophic cardiomyopathy (HCM), commotio cordis, coronary artery disease (CAD), and myocarditis. Hypertrophic cardiomyopathy is a disease of the heart muscle that leads to abnormal thickening.  HCM is the most common cause of cardiac sudden deaths in athletes. It is the most common genetic heart malformation in athletes affecting 1/500 individuals.  This abnormal thickening of the heart muscle occurs due to an autosomal dominant genetic abnormality of the muscle cell proteins. Asymmetrical thickening of the interventricular septum may lead to a condition known as Hypertrophic Obstructive Cardiomyopathy or HOCM. It may lead to intermittent cardiac outflow obstruction with may ultimately cause sudden cardiac death.  Abnormal systolic anterior motion (SAM) of the mitral valve leaflet exacerbated by exercise may lead to aortic obstruction and sudden death. Increased heart rate during exercise leads to decreased filling of the left ventricle with blood. This leads to a narrower left ventricular chamber that may increase the chances of aortic obstruction.  Therefore, HCM is an absolute contraindication to vigorous exercises.  Most of the time, patient are asymptomatic and the condition is found incidentally during regular physical examinations. Thorough history taking is one of the most important parts of the examination. Some patients may present with one or more of the following symptoms: dyspnea on exertion, angina/chest pain, palpations, syncope, positive family history, and sudden cardiac death.  Cardiac auscultation may reveal an ejection systolic murmur that is best heard at the left parasternal edge and it increases in intensity with maneuvers such as decreased left ventricular venous return when standing abruptly, or performing the Valsalva maneuver. The ECHO is the best study of choice. The majority of patients have normal life expectancy.  However, risk assessment for the development of sudden cardiac death should be performed. Patients with a high risk of developing sudden cardiac death may benefit from the implantation o f a defibrillator. Vigorous exercise should be avoided in patients with HCM. Genetic testing and physical screening for the family members. Symptomatic patients are treated medically first in order to control their symptoms. Surgical intervention including septal ablation and surgical myomectomy are indicated only after failure of all drug therapies to control the patient’s symptoms.  Sudden death of a healthy individual with no underlying cardiac disease due to ventricular fibrillation following g a blunt, nonpenetrating blow to the precordial area of the chest. Sports with a higher risk of commotion cordis include baseball, hockey, lacrosse, cricket, rugby , boxing, karate, and other martial arts. The chances of developing commotio cordis are influenced by factors such as the injury being from a high energy impact, and the site of impact (anterior chest wall over the heart).  This also translates as the timing of impact relative to the cardiac cycle. The risk of commotio cordis increases when the impact coincides with the first 10-30 milliseconds of the ascending phase of the T wave. Defibrillation should be started as soon as possible, preferably within the first three minutes. Players should be advised to wear proper protective gear and to avoid blocking balls or pucks with thir chest. Furthermore, the presence of automated external defibrillators at sporting events and training grounds have been shown to decrease mortality rates with commotio cordis.

Glute Injection

Glute (buttock) injection is a universal procedure that is commonly used around the world. Selecting the proper site that avoids injury to the neurovascular structures is important. The sciatic nerve could be at risk for injury during a buttock injection.  The buttocks is divided into quadrants. Divide the buttock halfway down the middle and halfway across.  Injection is given in the center of the upper outer quadrant. Avoid the other quadrants. Injection into the other quadrants may cause injury to the neurovascular structures and damage the sciatic nerve.  Another helpful method that could confirm a safe site for injection is to draw a line from the posterior superior edge of the iliac spine to the greater trochanter. This area above the line is considered to be the safe zone for intramuscular injection.

Corachobrachialis Muscle Anatomy

The coracobrachialis muscle arises from the tip of the coracoid process. The coracobrachialis muscle may have a conjoint tendon with the short head of the biceps muscle.  The coracobrachialis lies lateral to the pectoralis minor muscle. Close to the origin of the coracobrachialis is the origin of the coraco-clavicular ligaments. The conoid ligament is medial and the trapezoid ligament is lateral. The coracobrachialis muscle inserts into the middle third of the medial border of the humeral shaft.  The innervation of the coracobrachialis, biceps brachii, and brachialis muscle comes from the musculocutaneous nerve.  The brachialis has dual innervation. The medial part of the muscle innervation is from the musculocutaneous nerve and the lateral part of the muscle gets innervation from the radial nerve. The musculocutaneous nerve will also give the lateral antebrachial nerve with its anterior and posterior divisions. It is the primary nerve supply of the muscles of the anterior compartment of the upper arm it supplies sensation to the lateral half of the forearm. The coracobrachialis muscle flexes and adducts the arm at the shoulder joint.  The coracobrachialis muscle originates from the coracoid, and the musculocutaneous nerve is close to the muscle. The musculocutaneous nerve pierces the coracobrachialis about 3-8 cm distal to the coracoid where it then gives a branch to the coracobrachialis muscle. Some studies show that the nerve may be 1-5 cm from the coracoid. The nerve runs between the biceps and the brachialis muscles on the anterior compartment of the arm. The musculocutaneous nerve is close to approaches of the anterior shoulder especially with retraction of the conjoint tendon of the coracobrachialis and short head of the biceps. When the musculocutaneous nerve is injured, we may not be able to measure the deficit except for decreased sensation on the area supplied by the lateral antebrachial cutaneous nerve, which is a terminal branch that will give sensation to the forearm. The lateral antebrachial cutaneous nerve could be injured during distal biceps repair. Be careful when retracting the conjoint tendon during anterior shoulder surgery (avoid injury to the musculocutaneous nerve). Occasional, coracoid osteotomy is done to enhance exposure to the shoulder joint and the conjoint tendon will be easily retracted without compromising the musculocutaneous nerve.

Simple Acts of Kindness to Relieve Patient Pain

In general, doctors treat patients for pain due to injury or surgery. Pain intensity varies from person to person and it can be related to stress, distress, coping strategies, and physiological factors. The physician should work with the patient for better pain control and for safer prescribing of medications.  The best pain relief is self-efficacy and resilience. We have found that giving the patient a teddy bear helps to relieve their pain and anxiety, giving the patient comfort and confidence in the system.

Acetabular Fracture Associated BOTH Columns

https://www.youtube.com/watch?v=5RxEh9yKqes

Associated BOTH column fracture is a fracture of both columns of the acetabulum. Both columns are separated from each other and from the axial skeleton, resulting in a floating acetabulum. This is the most complex type of acetabular fracture. The fracture type used to be called “central acetabular fracture.” This fracture pattern may be associated with central dislocation and no part of the articular surface remains attached to the axial skeleton. The acetabular fragments become free and rotate around each other. They may appear to maintain congruity to the femoral head. There is dissociation of the articular surface from the axial skeleton. Because of this secondary congruity, traction may be used in the treatment of associated both column fracture in the elderly. You will see the “spur sign” above the acetabulum on the obturator oblique view and this is diagnostic for associated BOTH column fracture. In the obturator view, you will find the anterior column (iliopectineal line) is disrupted and you will find the “spur sign.” The “spur sign” is the posterior inferior aspect t of the intact posterior ilium. Another feature of the associated BOTH column acetabular fracture is the Judet sign of the curved line. The Judet sign of the curved line occurs due to interruption by the fracture of the iliopectineal line. The curved line belongs to the greater sciatic notch and if after fixation anteriorly, the patient has a positive curved line sign, and then the posterior column is probably not reduced. The roof of the acetabulum is involved either totally or partially. When you see an x-ray and the roof of the acetabulum is in pieces, then this injury is probably an associated BOTH column fracture. You will see a coronal plane fracture through the iliac wing. In general see coronal for column fracture. If you have BOTH column fracture and there is an additional fracture going to the ilium then this is an associated BOTH column fracture. In CT scan, the fracture will be coronal. T-shaped fracture of the acetabulum is different from an associated BOTH column fracture of the acetabulum. In associated BOTH column fracture of the acetabulum, the fracture goes through the ilium. The acetabulum is floating and is disconnected from the axial skeleton. If you see extension of the transverse fracture of the acetabulum through the medial wall of the acetabulum and the fracture is going through the obturator ring, then this is a T-shaped fracture. The ilioinguinal approach is the main approach used to treat associated BOTH column fractures.

Flexion Distraction Injury of the Lumbar Spine

Flexion Distraction Injury of the Lumbar Spine

It is sometimes called a seat belt injury or “chance fracture”. Usually, the patient is restrained, back seat passenger that is involved in a car accident and the person is wearing only a lap seat belt. The chance fracture is a variant of the flexion/distraction injury. The terminology is sometimes confusing, but a chance fracture could indicate a bony injury. It may present itself with a minimal compression fracture of the vertebral body, however, in this case all three columns of the spine are injured from distraction and tension. When you deal with a traumatic compression fracture in a young patient that is involved in a car accident, rule out a seat belt injury or “chance fracture”. This condition could be misdiagnosed or not diagnosed. Bowel trauma occurs in these cases due to crushing of the bowel between the lap seat belt and the spinal column, which results in devascularization and acute bowel rupture. In flexion/distraction injury, there will be an anterior wedge fracture of the vertebral body plus horizontal fracture of the posterior elements or distraction of the facet and the spinous processes. If it goes unrecognized, it may lead to progressive kyphosis with pain and deformity. This injury usually occurs in the thoracolumbar junction or in the midlumbar are. The posterior column fails first because of the axis of rotation is anterior to the vertebral body. The flexion/distraction injury is unstable in flexion and usually needs surgery to restore the disrupted tension band and prevent progressive deficit and pain, as well as enhance the functional recovery of the patient. In patients with flexion/distraction injury of the lumbar spine, up to 50% of these patients have associated potential life threatening injures such as visceral and gastrointestinal injury. Look for transabdominal ecchymosis; you will probably need to consult a general surgeon, and this condition occurs more in children. The hallmark of this injury is the axial split of the pedicle which is seen on the sagittal CT scan. There will be little comminution and since the center of rotation is the anterior longitudinal ligament, the posterior ligaments will be disrupted or the posterior neural arch is fractured transversely. Flexion/distraction injury or seat belt injury can be purely bony, purely ligamentous, or mixed. The treatment of flexion/distraction injury, especially if the injury is ligamentous, is usually a posterior reconstruction of the tension part of the spine with short segment fusion with instrumentation. Ligamentous injuries of the spine do not heal (needs to be fused). The bony chance fracture can be stable in extension and the fracture can heal. The fracture could heal, but the fracture will probably need long term follow-up. The fracture could be treated in a TLSO (Thoracic Lumbar Sacral Orthosis) brace and watch the fracture for the development of kyphosis.

Brown-Sequard Syndrome

Brown-Sequard Syndrome (BSS)

Brown-Sequard Syndrome results from an injury to one half of the spinal cord as seen in penetrating injuries. The spinothalamic tract fibers cross the midline below the level of the lesion resulting in contralateral loss of pain and temperature sensation. The posterior column and the corticospinal tracts carry vibration, position, light touch sensation, and motor function that are lost from the ipsilateral side of the body. The prognosis is usually good. 90% of the patients recover. If the patient has a wound on the right side, the patient will feel it on the left side. It is a hemisection lesion. There is loss of vibratory, light touch and motor on the same side while pain and temperature is lost on the other side.

Open Fractures of the Tibia

Open Fractures of the Tibia

25% of tibial shaft fractures can be open. Open fractures can lead to complications including wound problems, osteomyelitis, nonunions, and infected nonunions. The treatment of open fractures of the tibia can be challenging. A lot of the concepts are not black and white; they may be in the grey zone. We don’t know the best time for debridement. We don’t know what the optimal irrigation solution is and what the optimal pressure for the fluid is. We don’t know for sure the ideal duration of giving antibiotic prophylaxis, but we know that it is important to give the appropriate antibiotics early and do meticulous debridement. We know that the IM rod is better than the plate fixation or external fixator, and the result of the reamed IM rod or unreamed IM rod is the same. We need to close or cover the wound before 1 week and the vac can be used provisionally when we cannot close the wound, primarily at the optimal time. A grade I fracture is less than 1 cm. a grade II fracture is 1-10cm. A grade III fracture is more than 10 cm, and there is contamination. Grade III fractures are divided into three types. Grade IIIa fractures require adequate tissue for closure (or skin graft). Grade IIIb fractures require extensive periosteal stripping and the patient will need a flap (rotational or free flap). Grade IIIc fractures have a vascular injury that requires repair or amputation. The relative indication for amputation is warm ischemia for more than 6 hours, absent plantar sensation and severe ipsilateral foot trauma.

The most predictive factor for amputation is the severity of the soft tissue injury in the ipsilateral extremity. When comparing limb salvage versus amputation, the patient’s outcome is generally the same at 1-5 years. Lack of plantar sensation does not predict poor outcome after limb salvage. Segmental fractures are Grade III fractures, even if the open fracture is 1 cm. The ideal irrigation solution and the pressure used to controversial. Timing of the initial debridement is controversial. Irrigation and debridement within 6 hours was the gold standard in the past. Debridement is performed as a priority procedure no later than the morning after admission. There is no difference in infection rate for a patient who has the initial surgery before or after 6 hours, including patients with Type III open fractures. More than 40% of the patients usually wait longer than 6 hours for their initial surgery after arrival at the hospital. Delayed surgery for less severe fractures is acceptable as long as the debridement is done as a priority the following day. Unless there is a gross contamination, evidence is not clear as to when is the best time for the debridement. It seems like giving the patient antibiotics promptly is more important than the time of debridement. The preferred solution is normal saline and low pressure irrigation. Low pressure lavage may reduce reoperation rates due to infection, nonunions, and wound healing problems. Normally the tradition is to use 3, 6, and 9 liters of solution for Type I, Type II, and Type III open fractures (just recommendations). There is increased risk of wound healing with antibiotic solution. Meticulous irrigation and debridement of open fractures is important in decreasing the infection risk. Prophylaxis should be started as soon as possible. All patients with open fractures should receive first generation Cephalosporin’s that will cover gram-positive bacteria. You can give penicillin for farm injuries and clostridia prone wounds. You will give clindamycin if there is a penicillin allergy. In Type III open fractures, add aminoglycoside, such as gentamicin. It was found that local antibiotics delivery at the site of injury decreased the infection risk, such as cement beaded loaded with antibiotics. Antibiotic should be given within 3 hours of the time of injury (preferably given as soon as possible). There is reduction of 59% of acute infection in patients with open fractures treated with antibiotics. The infection rate is 1.6 times greater if antibiotics are given after 3 hours. Type I and Type II open fractures require antibiotic coverage for 24 hours after wound closure. For Type III open fractures, antibiotic administration should be given for a period of 72 hours after the injury and no more than 24 hours after wound closure. After the initial debridement, the patient will need staged debridement within 24-48 hours. There is a reduction infection rate, acute and chronic, for Type III open fractures with the use of systemic antibiotics and aminoglycoside cement beads compared with antibiotics alone. This combination of antibiotics lowers the infection rate for any open tibial fracture that is treated with an IM rod. Its affect is more noticed in Type III injuries. Plating of open fractures may cause chronic infection and infected nonunion. The healing time is doubled with plated open fractures. The IM rod resulted in a better alignment and lower reoperation rate than using external fixator. Also, no difference in the infection rate between the IM rod and the external fixator. You can use a reamed nail or an unreamed nail. They both have a comparable result and no difference in the outcome.

When reaming, you can use a bigger rod that provides better stability. Reamed nailing is superior in closed tibial fractures, but it is not superior in open tibial fractures. Reaming can cause increased pressure and disruption of the endosteal blood supply, can cause thermal necrosis and fat embolism with increased intramedullary risk of infection. The unreamed rod uses smaller nails and results in less stability but preserves the endosteal blood supply. Unreamed IM tibial rod appears to have a shorter time to union and fewer incidence of knee contractures when compared with circular wire external fixator. Nowadays, more and more orthopedic surgeons are using reamed nails for open fractures of the tibia. If you have a spiral fracture of the distal 1/3 of the tibia, you will need to get a CT scan of the ankle to identify a posterior malleolar fracture, which should be fixed before insertion of the IM rod. There is a lack of evidence to support the value of external fixator over the IM rod in open factures of the tibia. Due to patient discomfort, the high incidence of pin tract infection and loss of alignment, external fixator should not be used as a definitive fixation. Use external fixator temporarily (less than 4 weeks) and replace it with a rod in about 14 days. External fixator may be utilized for severely contaminated open fractures. Tibial fractures treated with a shorter duration of external fixator has reduction of the infection risk by 80%. When there is a shorter interval between removal of the external fixator and insertion of the IM rod of the tibia, there is a reduction of the risk of infection by 85%. In less severe soft tissue injuries, you do primary closure without tension. In cases of delayed closure, soft tissue coverage should be done within 7 days. Soft tissue coverage beyond 7 days will increase the infection. There is no difference in the incidence of infection in patients who had primary closure and delayed closure of the wound. It is recommended to do primary closure for Type I, Type II, and Type IIIa fractures with tension free closure and after timely antibiotic prophylaxis and adequate debridement. Intraoperative culture after debridement has no value. It does not predict future infection. In the upper 1/3 of the tibia, you can treat it by a medial gastrocnemius flap. In the middle 1/3 of the tibia, you can treat it by a soleus rotational flap. The use of a free flap for soft tissue coverage was less likely to have wound complications than the use of a rotational flap. The zone of injury may be larger than expected, and it may include the rotated muscle flap. The negative pressure wound therapy (the vac) is used frequently. The vac provides provisional coverage for wounds where the physician cannot do primary closure. There is decreased infection rate when using the vac. The vac is used for coverage after the initial debridement of the open fracture until the definitive coverage is done. It is a good temporizing dressing and can also be used in fasciotomy wounds. The vac promotes local wound healing. Bone morphogenetic protein (BMP2) decreases the need for secondary surgery and is used in acute open tibial fractures treated with IM rod.

Syndesmotic Injuries of the Ankle

Syndesmotic Injuries of the Ankle

The syndesmosis gives stability to the ankle. It resists external rotation and axial and lateral displacement of the talus. Syndesmotic injuries of the ankle can be challenging in the diagnosis and in the treatment. It may not be easy to obtain and maintain reduction of the syndesmosis. Approximately 50% of the patients with operatively treated supination/external rotation type fracture of the ankle have syndesmotic injury on stress radiographs intraoperatively. Anatomic reduction of the syndesmosis is crucial for a good clinical outcome. Restoration of the normal fibular length and alignment, as well as obtaining and maintaining the alignment of the syndesmosis significantly impacts the functional outcome of the patient. Malreductions of the tibiofibular syndesmosis is not uncommon, and it can occur in up to 30% of the patients. Fluoroscopy, direct visualization and reduction of the syndesmosis could improve the anatomic reduction. Syndesmotic injuries are common. They are found in sports injuries (high ankle sprain) or in ankle fractures such as supination/ external rotation Type IV, pronation/ external rotation and pronation/ abduction injuries. It does not occur with supination/adduction injury. In this injury, you will see vertical fracture of the medial malleolus and the talus will go medially. Syndesmotic fixation probably is needed more with an ankle fracture that has a high fibular fracture and deltoid ligament injury, than an ankle fracture that has fracture of the fibula with medial malleolus fracture. The higher the fracture in the fibula, the more incidence of syndesmotic disruption and the need for syndesmotic fixation. In fact, the high fibular fracture plus deltoid injury equals syndesmotic screw fixation (means syndesmotic screw fixation is needed more). To diagnose a syndesmotic injury, you will find an unstable mortise; it can be evident or occult.

You also need to suspect syndesmotic injury in proximal fibular fracture, which is called Maisonneuve fracture. Look at the disruption of the interosseous membrane and the syndesmosis. You do this by looking at the ankle and get an x-ray. You also suspect syndesmotic injury with sports injuries where there is a positive squeeze test (high ankle sprain). 20% of syndesmotic injuries of the ankle can be undetected on clinical examination. You should get stress-rays. You also suspect it in supination/external rotation Type II injury that has a fibular fracture. Provocative tests or the stress views are used in fibular fractures supination/external rotation Type II to see if it is really a Type II injury or if the injury is a Type IV and there is a hidden occult deltoid and syndesmotic injury. To do the provocative tests to diagnose an occult injury or syndesmotic injury of the ankle, do the gravity test or do the abduction/external rotation stress views or do weight bearing film. In weight bearing films, the dorsiflexion of the ankle can eliminate any errors on the medial side. Sometimes when the ankle is plantar flexed, the medial side looks widened, but it is not a true widening. Look for the tibiofibular clear space, look for the tibiofibular overlap, and look for the widened medial clear space (more than 5mm). The tibiofibular clear space will be greater than 5mm with syndesmotic injury. The tibiofibular clear space is probably the best radiologic measure because it is not affected by the position of the leg. If the syndesmosis is unstable, you need to fix it. It is the last part of ankle fracture fixation. You must have anatomic reduction of the syndesmosis. Before you fix the syndesmosis, you will need to evaluate the reduction of the syndesmosis. This can be done by direct inspection and reduction or by x-rays. You may need x-rays of the other side to assess accuracy of reduction of the syndesmosis intraoperatively. In surgery, you can test the stability of the syndesmosis. You can use the cotton test, use a bone hook, or pull on the fibula by levering it out by hemostat, by a freer or an elevator, or you can see the movement of the fibula. You can also do the abduction/external rotation test. You will do x-ray intraoperatively and check if the syndesmosis is stable or not and if it is reduced or not. So you want to restore the fibular length and see if the medial clear space and tibiofibular overlap are OK or not. Make sure that you do not have mortise instability, which is displacement of the talus out of the mortise. You want to restore the fibular length because this is key. The fibula must sit properly in the incisura. The morphology of the incisura is variable and that encourages malreduction. If the incisura is shallow, the fibula can be pushed anteriorly. If the incisura is deep, then the fibula can be pushed posteriorly, and this can cause malreductions and malrotation. Syndesmotic malreduction can occur from positioning of the reduction clamps. Anterior clamps can cause malreduction. Avoid translation of the fibula anteriorly when using anteriorly based clamps. Clamp placement in a neutral anatomical axis reduces syndesmotic malreduction. While oblique placed clamps results in syndesmotic malreduction, variation in the angulation of the reduction clamp and screw placement can cause iatrogenic syndesmotic malreduction and displaces the fibula in external rotation. Fixation of the fibula in as much as 30 degrees of external rotation may go undetected using intraoperative fluoroscopy. The malreduction may not be clinically significant if it is minimal; however, it can be very significant if the malreduction is significant. Screw fixation is supposed to be the gold standard for syndesmotic fixation; however, this is no longer the gold standard fixation method. You can fix the syndesmosis by screws, by suture buttons, and by a variety of different techniques. Patients with suture buttons return to work early and less frequently need their implant removed. The controversy is that there is no gold standard for the number of screws used, the number of cortices, the level of placement of the screws, the type of screws (3.5 or 4.5). I personally use 3.5 screws and rarely use 4.5 screws. I may also use cross screws in severe situations. I also use a plate in Maisonneuve fractures, not just screws over the fibula, the screws have to go through a plate to help the stability of the screws. You must have anatomic reduction of the fibula, as well as alignment. Achieving the fibular length can be a problem, especially if the fibula is comminuted. In this situation, you need to fix the medial malleolus first, then restore the fibular length.

The Dime Sign, the Shenton’s line, and the uninterrupted subcortical line. Syndesmotic screws are rigid, and they can break or loosen. The tight rope fixation avoids the problem of the rigid fixation, so it maintains the reduction while allowing physiological movement of the fibula (tight rope fixation has its own problems). I used to remove all syndesmotic screws, but now I don’t remove them unless it is necessary for pain or stiffness. I make the patient walk on it around 10-12 weeks. 17% of the screws will break, 13% become loosened, and ¼% of the screws are removed due to symptoms. The screws look bad on x-rays when they are broken or loosened, but these screws don’t cause a lot of trouble. If you keep the screws, it is just an x-ray problem and not a functional problem. If you leave the screws or if you remove the screws, there is no difference in functional outcome between screw removal and nonremoval. They found that when the syndesmosis is malreduced and then you remove the screws, then the patient feels better and the movement gets better. Retained, broken screws had a better functional outcome than the retained, intact screws. Fixation of the posterior malleolus adequately stabilizes the syndesmosis. If the fragment is minimally displaced, then the screws can be directed anteriorly to posteriorly. If the fragment is large, you can fix it with a buttress plate posteriorly. The posterior malleolar fixation restores the stiffness to 70% and the syndesmotic screw fixation restores the stiffness to 40% compared to intact specimens. There is a strong association between obesity and loss of syndesmotic reduction. Obese patients are 12 times more likely to lose syndesmotic reduction than nonobese patients. In regards to the syndesmotic injury, you will need to recognize it and fix it when the syndesmosis is unstable. Evaluate the reduction of the syndesmosis. Avoid malreduction. Remove syndesmotic screws only if needed.

Neonatal Compartment Syndrome

There are only a few cases of compartment in the neonate. This can be a difficult diagnosis. Compartment syndrome in the neonate does not present itself with the classic “P’s” as seen in adult patients. Compartment syndrome in the neonate does not present itself with the classic “P’s” as seen in adult patients. There are 5 P’s: pain/swelling, paresthesia, pulselessness, pallor, and paralysis. Diagnosis in neonate is usually made retrospectively after the patient has complications. The condition of compartment syndrome usually occurs within the first 24 hours of birth. It usually occurs in the forearm, is usually unilateral and occurs more in the dorsal aspect of the forearm. Risk factors are the mother may be diabetic, some hypercoagulable state (like polycythemia), and prematurity. The actual cause is not known, however it can be a combination of extrinsic compression and hypercoagulable state. Make sure to avoid missing the diagnosis of compartment syndrome. The infant will have a swollen, tense forearm associated with skin lesions on the forearm. The skin may have erythema, bullae, and edema. The skin lesions will be present at birth and usually at the forearm. The patient may also have pseudoparalysis, may lack spontaneous limb movement, and there might be some nerve injury involved also. The clinical diagnosis of compartment syndrome will be made after exclusion of other conditions such as infection, vascular injury, and amniotic band syndrome. The clinical diagnosis of compartment syndrome will be made after exclusion of other conditions such as infection, vascular injury, and amniotic band syndrome. Infection could be cellulitis or can be necrotizing fasciitis. Both should be excluded! Treatment of neonatal compartment syndrome of the forearm should be early diagnosis and immediate fasciotomy. Ischemic muscle contracture will develop from missing the diagnosis and delaying the treatment.

Anatomy of the Acetabulum

The column principle divides the acetabulum into an anterior and posterior column which becomes important when considering acetabular fractures and their management. The anterior column is composed of the anterior ilium, the anterior wall and dome of the acetabulum and the superior pubic ramus. The posterior column extends from the obturator foramen through the posterior aspect of the weight bearing dome of the acetabulum and then obliquely through the greater sciatic notch. The ischiopubic ramus is a complex structure that consists of the inferior pubic ramus and the inferior ramus of the ischium. It forms the inferior border of the obturator foramen. The pelvis is oriented to form an inverted “Y” shape. The obturator artery is a branch of the anterior division of the internal iliac artery. It arises in the pelvis and it enters the obturator canal. The obturator artery the divides into two branches: the anterior and posterior branches of the obturator artery form a vascular circle around the outer surface of the obturator membrane. An acetabular branch reaches the hip joint and joins the ligamentum teres to supply the head of the femur. It usually supplies a small portion of the head of the femur. Corona mortis is a connection between the internal iliac branch (obturator) and the external iliac or its branch, the inferior epigastric. Corona mortis is predominantly a venus connection and the arterial connection is much less. Its location on the superior pubic ramus is variable. It is about 3-7 cm from the symphysis pubis. It is located behind and on top of the superior pubic ramus and one must be careful with lateral dissection of the superior pubic ramus. The Corona Mortis is susceptible to injury in pelvic trauma and in pelvic surgery especially during the ilioinguinal approach.  Be aware that the sciatic nerve can be split, and this can be a normal variant. Keep the knee flexed and the hip extended during posterior approach to the acetabulum. This will protect the sciatic nerve. The sciatic nerve is posterior to the obturator internus muscle and anterior to the piriformis muscle. When using the sciatic nerve retractor in the lesser sciatic notch, the muscle and tendon of the obturator internus protects the sciatic nerve. It acts as a buffer layer between the retractor and the nerve, because the nerve is posterior to the muscle. Sliding trochanteric osteotomy allows exposure of the dome and the superior aspect of the acetabulum. This type of osteotomy keeps the muscles intact and this will balance its pulling forces. There will be less of a chance of displacement of the greater trochanter this way. The superior gluteal nerve is close to the superior gluteal artery at the greater sciatic notch. The superior gluteal nerve can be injured from approaches that involve more than 5 cm above the acetabulum. Excessive traction or attempt to control the bleeding from the superior gluteal artery at the greater sciatic notch, may injure the nerve by a suture or by a vascular clip that may entangle the nerve. Injury to this nerve may affect the gluteus minimus. Injury to this nerve affects the abductors of the hip joint and the patient may end up with Trendelenburg Gait. The inferior gluteal nerve may also be injured. It innervates the gluteus maximus muscle. The Lateral Femoral Cutaneous Nerve can become injured during the ilioinguinal approach for acetabular fixation. The Lateral Femoral Cutaneous Nerve usually passes under the ilioinguinal medial to the anterior superior iliac spine (ASIS).

Injury to the Corona mortis may lead to significant hemorrhage which may be difficult to control. The superior gluteal artery passes through the greater sciatic notch. Injury to the superior gluteal artery can be associated with acetabular fractures, especially fractures that involve the posterior column of the acetabulum. The superior gluteal artery cam ne damaged by aggressive retraction of the abductor muscles during posterior approach to the hip. The Medial Femoral Circumflex Artery (MFCA) can be damaged due to dislocation of the femoral head or from taking down the quadratus femoris from the femur instead of the ischium. You need to leave a tag of 1 cm for the piriformis and the obturator internus from the greater trochanter to preserve the deep branch of the medial circumflex artery. If you detach these two tendons too close to the trochanter, this could injure the deep branch of the medial femoral circumflex artery. The medial femoral circumflex is the main blood supply to the femoral head. The sciatic nerve is close to the acetabulum and can be injured. In fact, sciatic nerve injury is the most common traumatic and iatrogenic nerve injury connected to the acetabulum. Sciatic nerve injury can be approximately 10% with hip dislocation. The incidence may be higher with posterior acetabular fractures. When you examine a patient with an acetabular fracture, always check the sciatic nerve function. Check dorsiflexion of the ankle and the toes. It is peroneal division of the sciatic nerve that will be affected. Check for numbness on the top of the foot. Repeat the exam again just before surgery. Partial sciatic nerve injury can get worse from acetabular surgery. The sciatic nerve anatomy is variable but well described. There may be variations in its anatomy. These diagrams show the incidence of the most common patterns of the relationship between the sciatic nerve and the piriformis muscle.

Anatomy of the Adductor Longus Muscle

The adductor longus muscle is one of the adductor muscles of the hip located within the thigh. There are six adductor muscles for the hip and here is a diagram showing the arrangement of these adductor muscles. The adductor longus muscle arises from the anterior surface of the superior pubic ramus, just lateral to pubic symphysis. It is inserted into the middle third of the medial lip of the linea aspera on the posterior surface of the shaft of the femur. The adductor longus muscle is innervated by the obturator nerve which arises from the L2, L3, and L4 ventral rami of the lumbar plexus. Outside the obturator foramen in the proximal part of the thigh, the obturator nerve divides into anterior and posterior divisions. It is the anterior division of the obturator nerve which supplies the adductor longus muscle. The adductor longus muscle adducts and flexes the thigh, and helps to laterally rotate the hip joint. Adductor strains may occur in hockey players or soccer players. It is sometimes called a “pulled groin.” Adductor strains usually involve the adductor muscles, especially the adductor longus muscle. It occurs due to eccentric contraction of the muscle. The injury occurs due to external rotation of an abducted leg. The patient will have groining pain and pain at the site of the injury, usually near the pubic ramus. The patient will also have weak adduction. It may be difficult to differentiate an adductor strain from a sport hernia. X-rays are usually normal. MRI will show avulsion of the adductor muscles from the pubic ramus. Adductor strain treatment includes: ice, rest, protected weight bearing, and patient will go through a rehabilitation program. Surgery is rarely done and the role of surgery is not well defined.

Anatomy of Coracobrachialis Muscle

The brachialis muscle is a muscle in the upper arm that flexes the forearm at the elbow joint. The brachialis muscle originates from the lower half of the anterior humerus, near the insertion of the deltoid muscle. The brachialis muscle is located underneath of the biceps brachii muscle.
It is inserted into the tuberosity on the anterior surface of the coronoid process of the ulna.
The function of the brachialis is that it flexes the forearm at the elbow joint. It doesn’t aid in pronation or supination. The biceps muscle is a strong supinator. There is dual innervation of the brachialis muscle. The musculocutaneous nerve arises from the lateral cord of the brachial plexus. It is the primary nerve supply to the brachialis muscle as well as the coracobrachialis and biceps muscles. The musculocutaneous nerve lies underneath the biceps muscle and on top of the brachialis muscle. Part of the brachialis is also innervated by the radial nerve. The dual innervation of the brachialis allows it to be split during anterior approached to the humeral shaft. The medial part lies in the flexor compartment with the musculocutaneous nerve. As the limb develops, rotation of the lateral brachialis to become flexor and the lateral part brings with it the radial nerve supply. Structures of the cubital fossa located around the brachialis muscle.

The cubital fossa is a triangular hollow area on the anterior surface of the elbow. The brachialis muscle makes up part of the floor of the cubital fossa region. The cubital fossa makes up four main structures from lateral to medial. Radial nerve, biceps brachii tendon, brachial artery, and median nerve. Anterior approach to the humerus (splitting the brachialis):  curved incision is made from the tip of the coracoid process along the anterolateral aspect of the humerus. During part of this procedure, the brachialis is split in the middle after retraction of the biceps muscle. How to approach the radial nerve on the distal humerus? The lower part of the humeral shaft is approached between the brachialis and the brachioradialis muscle with the brachialis retracted medially and the brachioradialis retracted laterally. The radial nerve is identified and protected. Because there is a dual innervation for the muscle, the brachialis is not denervated. When the brachialis is retracted, this may endanger the nerve supply to the lateral brachialis. Coronoid process fractures are usually associated with elbow dislocations and can occur from hyperflexion with avulsion of the brachialis tendon insertion or shearing off of the trochlea.

Femoral Triangle

The femoral triangle is a superficial triangular space located on the anterior aspect of the thigh just inferior to the inguinal ligament. The boundaries of the femoral triangle include the lateral border, medial border, and base. The lateral border is formed by the medial border of the Sartorius M. The Sartorius muscle is a thin, small muscle going that goes from lateral to medial. The Sartorius muscle inserts on the medial side of the proximal tibia. The medial border of the femoral triangle is formed by the medial border of the adductor longus M. The adductor longus muscle goes from medial to lateral direction. The base of the femoral triangle is formed by the inguinal ligament. The floor of the triangle is formed by the iliacus M., psoas major M., pectineus M., and the adductor longus M. The roof of the femoral triangle is covered by skin, superficial and deep fascia. The femoral triangle contains three important structures. From lateral to medial, it is the femoral nerve, femoral artery, and femoral vein, which contains deep inguinal lymph nodes. The femoral nerve lies within the groove between the iliacus and psoas major muscles. Two other nerves are located within the femoral triangle, and they are the lateral cutaneous nerve on the thigh and the femoral branch of the genitofemoral nerve.

The lateral cutaneous nerve of the thigh crosses the lateral corner of the triangle. It supplies the skin on the lateral part of the thigh. The femoral branch of the genitofemoral nerve runs in the lateral compartment of the femoral sheath. It supplies the majority of the skin over the femoral triangle. The femoral triangle also contains the femoral sheath which is a funnel shaped sleeve of fascia enclosing the upper 4 cm of the femoral vessels. The neurovascular bundle is medial to the sartorius muscle. Therefore, in the anterior approach to the hip, it is always safe to go lateral to the sartorius muscle in order to avoid the important structures within the femoral triangle. Do not go medial to the sartorius muscle. You will injure the structures if you go medial to the sartorius muscle. It is important to remember when performing this approach to avoid the lateral cutaneous nerve of the thigh. The sartorius muscle is almost like the teres minor muscle in the shoulder. Do not go inferior to the teres minor muscle in the shoulder, you will injure the axillary nerve and the posterior circumflex artery.

Tarsal Coalition

Tarsal coalition is fusion of the tarsal bones that leads to a ridged flat foot, foot pain and multiple ankle sprains. Tarsal coalition is a congenital anomaly. There are two types of tarsal coalition are talocalcaneal coalition and calcaneonavicular coalition. Talocalcaneal coalition is a coalition between the talus and the calcaneus. Calcaneonavcular coalition is a coalition between the calcaneus and the navicular. When talocalcaneal coalition occurs, it usually happens around 12-15 years of age. The calcaneonavicular coalition presents at an earlier age. 50% of coalitions are bilateral. About 20% have multiple coalition in the same foot. Coalition may be fibrous, cartilaginous or bony. It occurs due to failure of segmentation. It could be associated with fibular hemimelia or Apert’s syndrome. The patient usually complains of a painful foot, a history of repeated ankle sprains, as well as flatfoot deformity. Tarsal coalition may result in peroneal spastic flat foot. You may also find hind foot valgus. On toe standing the arch does not reconstitute. Heel cord contracture might also be evident during the examination. Furthermore, there might be restricted subtalar joint range of motion. Always check both feet, the condition may be bilateral.

The best study is CT scan. It can determine the size and location of the coalition. MRI is also useful in detecting a fibrous or cartilaginous coalition. AP, lateral, and oblique x-ray views should be obtained. On lateral view x-rays, the calcaneonavicular coalition will show the characteristic “anteater nose sign” which is an elongation of the anterior calcaneal process. The lateral view of a talocalcaneal coalition may show talar beaking which is a type of traction spur that occurs due to limited motion of the subtalar joint. Additionally, the C sign is a radiological sign which may be seen on lateral radiographs. It is the outline of the talar dome and the sustentaculum. A 45 degree oblique view is the best for showing calcaneonavicular coalition. No operative treatment usually consists of NSAIDS, modified activities, or the use of a brace or cast. Surgical treatment for calcaneonavicular coalition usually consists of resection with interposition of the extensor digitorum brevis muscle or a fat graft no matter what the size of the coalition is. Talocalcaneal coalitions that involve less than 50% of the subtalar joint are also resected. A triple arthrodesis is performed for large coalitions, failed resections, or advanced conditions.

Diabetic Ankle Fractures

There are some problems associated with diabetic ankle fractures. The biggest problem occurs when what is believed to be a simple ankle fracture is actually a Charcot ankle. The condition of Charcot ankle may not be diagnosed and my lead to a bad outcome such as possible amputation. Diabetic neuropathy often occurs with the loss of protective sensationis and is a risk factor for Charcot ankle. Diabetic ankle fractures have a lot of complications (40% complication rate). The amputation rate is about 6% for closed injuries and about 40% for open injuries. Most significant factor in patients with ankle fractures who are diabetic is a high risk of infection (up to 20% in diabetic patients). There is an increased risk of superficial and deep wound infections. Peripheral neuropathy is the most significant risk factor for post-operative complications. If the patient is treated with a splint or a cast, this must be padded very well in order to avoid ulcers or skin complications. Keep the diabetic patient with an ankle fracture non-weight bearing for longer period of time. The amount of time spent non-weight bearing is double the time for a diabetic patient. Diabetic patients with an ankle fracture usually have a higher incidence of nonunions, malunions, and hardware failures than with nondiabetic patients. Examine the pulses and check the circulation. In general, surgery is better for treatment. It is going to take longer for the fracture to heal, so a good stable fixation is needed that will support the fracture until it heals (fixation will not be traditional). In regard to fixation, add more fixation; more screws with the screws going from the fibula to the tibia. Use spanning external fixator, and use K-wires from the calcaneus to the tibia. I personally like to use minimally invasive techniques. I try not to open the fracture in diabetic patients unless necessary (do it percutaneously with small incision). I start with getting the fibular length. Next, I fix the medial malleolus percutaneously. The syndesmosis could also be fixed percutaneously. Red blood cells contain hemoglobin and when the hemoglobin binds with glucose in the blood, it becomes glycated. When the hemoglobin binds to oxygen, the cells appear red. The term HbA1c refers to the glycated hemoglobin. We find that HbA1c levels appear to be predictive of risk and complication rates in the surgical treatment and outcome of diabetic patients with ankle fractures. Complication rates are higher among patients with elevated HbA1c which is more than 6.5%. The normal range of HbA1c is 4-6%. More than 7% is high. For diabetic ankle fractures, recognize the Charcot ankle, make sure to examine the circulation and the pulses, and cast or splint must be well padded. There is a high risk of complication that may lead to amputation. Loss of protective sensation and peripheral neuropathy is an important risk factor for Charcot ankle. Delay weight bearing because the fracture does not heal quickly. When surgery is done, use percutaneous techniques or good fixation that will allow non-failure of the hardware during healing time.

Femoral Triangle

The femoral triangle is a superficial triangular space located on the anterior aspect of the thigh just inferior to the inguinal ligament. The boundaries of the femoral triangle include the lateral border, medial border, and base. The lateral border is formed by the medial border of the Sartorius M. The Sartorius muscle is a thin, small muscle going that goes from lateral to medial. The Sartorius muscle inserts on the medial side of the proximal tibia. The medial border of the femoral triangle is formed by the medial border of the adductor longus M. The adductor longus muscle goes from medial to lateral direction. The base of the femoral triangle is formed by the inguinal ligament. The floor of the triangle is formed by the iliacus M., psoas major M., pectineus M., and the adductor longus M. The roof of the femoral triangle is covered by skin, superficial and deep fascia. The femoral triangle contains three important structures. From lateral to medial, it is the femoral nerve, femoral artery, and femoral vein, which contains deep inguinal lymph nodes. The femoral nerve lies within the groove between the iliacus and psoas major muscles. Two other nerves are located within the femoral triangle, and they are the lateral cutaneous nerve on the thigh and the femoral branch of the genitofemoral nerve. The lateral cutaneous nerve of the thigh crosses the lateral corner of the triangle. It supplies the skin on the lateral part of the thigh. The femoral branch of the genitofemoral nerve runs in the lateral compartment of the femoral sheath. It supplies the majority of the skin over the femoral triangle. The femoral triangle also contains the femoral sheath which is a funnel shaped sleeve of fascia enclosing the upper 4 cm of the femoral vessels. The neurovascular bundle is medial to the sartorius muscle. Therefore, in the anterior approach to the hip, it is always safe to go lateral to the sartorius muscle in order to avoid the important structures within the femoral triangle. Do not go medial to the sartorius muscle. You will injure the structures if you go medial to the sartorius muscle. It is important to remember when performing this approach to avoid the lateral cutaneous nerve of the thigh. The sartorius muscle is almost like the teres minor muscle in the shoulder. Do not go inferior to the teres minor muscle in the shoulder, you will injure the axillary nerve and the posterior circumflex artery.

Jone's Fracture

Jones Fracture is a fracture of the proximal fifth metatarsal bone. Sir Robert Jones (British surgeon) sustained an acute fracture at the base of the fifth metatarsal bone while dancing and the fracture was then named after him. The Jones fracture occurs at the metaphyseal/diaphyseal junction and it extends into the intermetatarsal joint proximal to the metatarsocuboid joint. The joints are connected to the base of the fifth metatarsal bone. One joint articulates with the cuboid bone (metatarsocuboid) and the second joint (intermetatarsal) articulates with the fourth metatarsal. For the Jones fracture to be called “Jones Fracture,” the fracture must enter the intermetatarsal joint (fracture must be distal to the metatarsocuboid joint and must enter the intermetatarsal joint). The Jones fracture occurs about 1 ½ cm distal to the tuberosity of the fifth metatarsal bone. The metatarsal bone is divide into the head, neck, shaft, and the tuberosity. Jones fractures of the proximal fifth metatarsal occurs in the watershed area within 1.5 cm of the tuberosity. The area where the Jones fracture occurs is an area of limited blood supply. There are multiple metaphyseal arteries in the tuberosity. There is a nutrient artery with intramedullary branches provides retrograde blood flow to the proximal fifth metatarsal. Fracture distal to the tuberosity will disrupt the nutrient artery supply resulting in relative avascularity.

The Peronius Tertius tendon is inserted into the dorsal metaphysis of the fifth metatarsal bone . The Peroneus Brevis tendon is inserted into the tuberosity of the fifth metatarsal bone. The plantar fascia is connected of the fifth metatarsal bone. When a Jones fracture occurs, the tendons will pull the fracture apart and prevent healing. This fracture could be mistaken for sprain, because a sprain is common on this side of the foot. There are three types of fractures at the proximal fifth metatarsal bone.

Fracture in zone I which is the tubersority avulsion fracture. Fracture in zone II which is the two Jones fracture. Laslty, fracture in zone III which is the stress fracture.  In zone I avulsion fractures (psuedo Jones fracture). The Peroneus Brevis insertion site and one treats that fracture conservatively. If one takes fracture in zone II, that is the two Jones fracture. They are usually acute fractures that occur at the metaphyseal-diaphyseal junction and involve  the fourth and fifth metatarsal articulation. Zone III stress fractures are chronic fractures that occur distal to the foruth and fifth metatarsal articulation and may be associated with cavovarus foot deformity. In children, it is important not to make the wrong diagnosis of a fracture of the proximal fifth metatarsal base while looking at a normal growth plate. The growth plate is usually present between the ages of 9-14 years of age and it is parallel and lateral to the metatarsal.

During radiology, x-rays will show the fracture and its location. An acute jones fracture will have sharp margins with no intramedullary sclerosis. A stress fracure will have a wide fracture line with medullary sclerosis. Treatment of Jones fracture, if the fracture is nondisplaced one should use a boot or a cast. A person should be nonweight baring for 6-8 weeks and 75% will heal. In athletes or if the fracture is displaced, a screw fixation of the fracture should be performed. This technique is a very popular one. In the lateral view, the canal appears to be straight and narrow. In the AP view, the fifth metatarsal appears to be curved (lateral bow). Lateral bow of the fifth metatarsal may cause complications during surgery. There is vulnerability at the midshaft for perforation of the medial cortex. The canal us narrower in the dorsal view plantar dimension, which is narrow in the lateral view. The point of entry for the wire or the screw is not centered. The fifth metatarsocuboid joint blocks the proximal canal projection and this situation can cause complications. Each paitent’s metatarsal  should be evlauated indivdually for proper screw selection. For surgery and screw placement, drill parallel with the shaft in the lateral plane and avoid the plantar direction and avoid the Sural nerve. One will probably need to use a 4.5 mm cancellous screw. The appropriate length of the screw that should be used is usually around 40-50 mm. The diameter of the screw depends on the width of the canal. Smaller screw fixation is unstable and a larger screw may displace the fracture. The screw threads must cross the fracture site. Failure of the procedure is attributed to poor blood supply or return of the athlete to activity before complete radiographic union.

Lumbar Plexus

Lumbar Plexus

The lumbosacral plexus starts from L4 to S4. The lumbar plexus starts from L1 to L4. It has 6 branches. To remember this, think “I Twice Got Lunch on Friday”. Knee extension is done by muscles that are innervated by the L2, L3, and L4 nerve roots via the femoral nerve. The femoral nerve innervates the muscles of the anterior compartment of the thigh (quadriceps). ^th lumbar nerve root. All nerves except the genitofemoral nerve and the obturator nerve emerge from the lateral aspect of the psoas major muscle. The genitofemoral nerve emerges anteriorly, and the obturator nerve emerges medially in relationship to the psoas major muscle. L2, L3, and L4 will give the obturator and femoral nerves. The obturator nerve and the femoral nerve are equal.

The femoral nerve also provides sensation to this area. These muscles cause hip adduction: adductor brevis, adductor longus, and adductor magnus. They are innervated by the L2, L3, and L4 nerve roots via the obturator nerve. This is the area of sensation supplied by the obturator nerve. With its origin coming from the nerve roots of L2 and L3, the lateral femoral cutaneous nerve of the thigh innervates the skin on the lateral part of the thigh. Risk of injury to this nerve can occur with bone graft, with hip or acetabular procedures, and with external fixator of the pelvis. The genitofemoral nerve comes from the L1 and L2 nerve roots. Six branches come from the lumbar plexus. Two branches come from one nerve root. Two branches come from three nerve roots. Two branches come from two nerve roots. The two nerves that arise from one nerve root are: iliohypogastric and iliolinguinal. Both of these nerves arise from L1 nerve root. The iliohypogastric nerve is above the iliolinguinal nerve. The two nerves that arise from two nerve roots are the genitofemoral (L1, L2) and the lateral femoral cutaneous nerve of the thigh (L2, L3). The two nerves that arise from three nerve roots are the obturator and the femoral. Both arise from the L2, L3, and L4 nerve roots. There is also contribution from T12. The fourth lumbar nerve root also passes a branch to the lumbosacral trunk at the 5

Guyon's Canal Syndrome

Guyon’s Canal Syndrome- Ulnar Tunnel Syndrome

The ulnar nerve arises from the medial cord of the brachial plexus. After the ulnar nerve passes through the arm, it runs from the medial epicondyle to the pisiform bone in the wrist in a direct trajectory. Two carpal bones are important in relation to the ulnar nerve in the wrist: the pisiform and the hamate. Both the ulnar nerve and the ulnar artery enter the Guyon’s canal. The Guyon’s canal is approximately 4 cm long. The ulnar nerve enters the wrist medial to the ulnar artery. The Guyon’s canal has one proximal entrance and two distal exits, one superficial and one deep. The Guyon’s canal contains the ulnar nerve with its superficial sensory and deep motor branches. ^th lumbricals. The deep branch of the ulnar nerve also innervates the hypothenar muscles, the adductor pollicis muscle, and the deep head of the flexor pollicis brevis muscle. The superficial branch of the ulnar nerve is mainly sensory. It gives supply to the digital nerves of the 4^th and 5^th fingers and a motor branch to the palmaris brevis muscle. Based on the location of compression in the Guyon’s canal, the affected area of the nerve may be purely motor, purely sensory, or a mixture of motor and sensory. Pain and paresthesia in the ulnar 1 ½ digits or clawing of the 4^th and 5^th fingers can be symptoms. Another symptom can be loss of function of the intrinsics (it normally flexes the MCP and extends the IP joints). In low ulnar nerve injury, the flexor digitorum profundus is working (functional). It flexes the 4^th and 5^th fingers and causes clawing (unopposed by the intrinsic muscles). Ulnar nerve palsy results in paralysis of the intrinsic muscles; test the first dorsal interosseous muscle and check for atrophy. 70% of pinch is lost due to loss of adductor muscles.^th and 5^th fingers and causing clawing of these two fingers. High ulnar nerve palsy has less clawing of the 4^th and 5^th fingers and sensory deficit to dorsum of the hand. In cubital tunnel syndrome (high ulnar nerve involvement) you can also find Tinel’s sign at the elbow and positive elbow flexion test. The dorsal cutaneous branch arises before the Guyon’s canal. If you have high ulnar nerve palsy, there will be sensory deficit on the dorsum of the hand, because that nerve will be affected. If you have a low ulnar nerve palsy, that nerve will not be affected because it already branched out or came off from the ulnar nerve and escaped (sensation on that part of the dorsum of the hand). Nonoperative treatments include activity modification, NSAIDS, and splinting. Surgical treatment includes release of the carpal tunnel .In patients diagnosed with both carpal tunnel and ulnar tunnel syndrome, the Guyon’s canal is adequately decompressed by the release of the carpal tunnel. Local decompression can be done especially if nonoperative treatment fails. Decompression of the ulnar nerve by addressing the cause; success of surgery depends on finding a cause. To determine the cause of compression, explore and release of all three zones in the Guyon’s canal, vascular treatment of ulnar artery thrombosis, hook of hamate excision, decompress ganglion cysts, and release hypothenar muscle origin. All of these things are possible causes that need to be addressed. Tendon transfer can be a treatment in late cases; it will correct claw fingers, restore power pinch, and improve Wartenberg’s sign.

The Froment’s test is positive. When pinching a piece of paper between the thumb and index finger, the thumb IP joint will flex if the adductor pollicis muscle is weak due to ulnar nerve palsy. Symptoms also include weak grasp due to intrinsic weakness, Wartenberg’s Sign, and the Allen’s test. Carpal tunnel view x-rays and CT scans are useful to evaluate hook of the hamate fractures and nonunions. MRI is useful to evaluate ganglion cysts. Ultrasound is useful to check vascular status of the hand and to diagnose ulnar artery thrombosis. EMG and nerve studies are helpful. High or low ulnar nerve injury is a differential diagnosis. In low ulnar nerve injury or compression, the flexor digitorum profundus muscle is working; flexing the 4

The Guyon’s canal contains the ulnar nerve with its superficial sensory and deep motor branches. Ulnar nerve compression neuropathy can occur in the Guyon’s canal. The most common causes include volar ganglion, hook of hamate fracture, repetitive trauma, ulnar artery thrombosis, palmaris brevis muscle hypertrophy, or pisiform fracture or dislocation. Volar ganglion cysts may protrude or grow into the canal, which could compress the ulnar nerve. Hook of hamate fracture can lead to neuropathy of the nerve in the tunnel. Compression and inflammation also can result from repetitive trauma such as using a hammer. Trauma over the hook of hamate, where the superficial branch of the palmar artery lies, leads to vascular insufficiency of the ulnar side of the hand. Ulnar nerve compression may occur as a result of pisiform dislocation or fracture. The Guyon’s canal is bound on the floor by the transverse carpal ligament, on the roof by the volar carpal ligament, on the ulnar border by the pisiform and pisohamate ligament, and on the radial border by the hook of hamate. There are three zones of Guyon’s canal compression. Zone I is located proximal bifurcation of the nerve; it is characterized by mixed motor and sensory symptoms, and it is caused by ganglia and hook of hamate fractures. Zone II is located in the deep motor branch; it is characterized by motor symptoms only, and it is caused by ganglia and hook of hamate fractures. Zone III is located by superficial sensory branch; it is characterized by sensory symptoms only, and it is caused by ulnar artery thrombosis or aneurysm. The deep branch of the ulnar nerve innervates all of the interosseous muscles and the 34d and 4