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- Disc Herniation
The spine is comprised of bony vertebrae separated by discs. The neural structures of the spine include the spinal cord (T12-L1), the conus medullaris—which is the lower end of the spinal cord, and the Cauda Equina, which is the division of multiple nerve roots beginning at the level of L1. Conditions of the lumbar spine including disc herniation are a main cause of lower back pain.
The lumbar spine (lower back) consists of five vertebrae numbered L1-L5. These vertebrae are attached to the sacrum at the lower end of the spine. The discs between the vertebrae are round cushioning pads which act as shock absorbers. In a normal disc, there are two layers—the inner disc layer, which is comprised of soft gelatinous tissue and known as the Nucleus Pulposus, and the outer disc layer—which is made up of thick strong tissue, which is known as the Annulus Fibrosis. Behind this disc lies the spinal nerve root and the cauda equina. A major disc herniation of the lumbosacral region could affect the nerve roots.
In about 95% of all disc herniation cases, the L4-L5 or L5-S1 disc levels are involved. Herniation of the L4-L5 disc will affect the L5 nerve root. Herniation of the L5-S1 disc will affect the S1 nerve root.
There are three types of disc herniation:
- Protrusion/ Bulge
- A bulging disc with intact annular and posterior longitudinal ligament fibers
- Disc Herniation
- Type A—Disruption of inner annular fibers with intact outer annular fibers
- Type B—Disrupted annulus with tail of disc material extending into the disc space
- Free fragment without tail extending into disc space
- Fragment may be reabsorbed spontaneously
- May get better with the use of an epidural
There are three typical locations for disc herniation as well:
- Involves multiple nerve roots
- Predominantly causes low back pain more than leg pain
- May cause incontinence of the bladder and bowel
- Urgent surgical treatment if patient presents with neurological deficits
- Posterolateral—usual location, most commonly involving one nerve root (the lower one)
- For example: L4-L5 posterolateral herniation will involve L5 nerve root
- Occurs in 8-10% of cases
- Involves the exiting nerve
- Example: L4-L5 foraminal herniation will involve the L4 nerve root
Discogenic Back Pain is an internal disc disruption with early disc degeneration. Pain gets worse with flexion and sitting but, gets slightly better with extension. Forward flexion is limited on the exam and there are no radicular symptoms.
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.