The Ideal Patient With Low Back Pain

Low back pain is very common, and the majority of the patients get better with time. The ideal patient will get better with time and has no radiation below the knee, no history of trauma, no fever or chills or weight loss, no bladder or bowel dysfunction, no neurological deficits, and no pathological reflexes.

In order to optimize recovery, management of the patient should consist of early return to activity as tolerated, as the symptoms allow. You will give the patient reassurance with limited analgesia, early range of motion, and muscle relaxants. A healthy patient with an acute onset of non-traumatic low back pain, you do not need early diagnostic imaging before proceeding with the therapeutic treatment. Diagnostic imaging is not necessary unless the initial treatment is unsuccessful, and the symptoms are prolonged. X-rays may not be needed in the first six weeks unless there is a reason for it, such as red flags. In fact, the use of x-rays can lead to better patient satisfaction but doesn’t necessarily lead to better patient outcome. X-rays and MRIs may show changes in the intervertebral discs and may be associated with the patient’s pain, but these changes are also commonly seen in cross-sectional studies of asymptomatic people. There are a lot of false positive MRIs, and you need to correlate the MRI findings with the clinical findings. Don’t rely on the MRI alone! Just because you have MRI changes or disc protrusion, it does not mean that the patient needs surgery!

A nonspecific pain does not require surgery; therefore, it does not require further work-up. There are risk factors associated with low back pain that includes Poor physical fitness; Smoking; History of repetitive bending or stooping on the job and whole-body vibration exposure. If the patient has a simple low back pain, 50% of the patients resolve their pain in one week. Resolution of the acute back pain occurs in 90% of the patients within one month. If the patient has leg pain greater than back pain, then the patient has sciatica. Sciatica means nerve root irritation, probably due to a herniated disc.

MRSA Screening & Decolonization

The best way to prevent surgical site infection, is optimizing the patient prior to surgery. The physician will want to make sure that the patient is nutritionally fit. Specific protocols will need to be followed for patients with conditions such as diabetes, are overweight, or who smoke. It is also important to improve the skin and soft tissue condition (area where the incision will be). The physician should try to reduce the bacterial burden that the patient is carrying. Immediately before surgery, the patient should be given prophylactic preoperative antibiotics and try to decrease the contamination in the operating room. The patient may bring organisms on themselves into the operating room (about 80% of these organisms are brought in by the patient). A screening for Methicillin-Sensitive Staphylococcus Aureus (MSSA) or Methicillin Resistant Staphylococcus Aureus (MRSA) and decolonization. Identifying the patients carrying diseases and treating the condition prior to going into the hospital will reduce the infection rate. Once patients are in the hospital, it is possible for them to spread bacteria to other patients. The best way to prevent the spread of bacteria is with PROPER HAND WASHING PRACTICES!

How can we decrease the bacterial burden of the patient bringing these organisms to the operating room? What are the tests that we should do? How can we help the situation when the patient is in the clinic or in the office?

areasThe patient should be screened for MSSA or MRSA and then a decolonization should be done. Some patients have large reservoirs of bacteria (carriers) and these are the patients who will have an increased risk of surgical site infection. These reservoirs are located in the nose, axilla, groin, and perianal area. These patients will need to be identified so the bacteria can be eradicated and the risk of surgical site infection can decrease. Being a MRSA carrier will increase the chances of infection (about 10x more risk for surgical site infection). You wouldn’t know that the patient is a MRSA carrier unless you test them. It is important to identify these MRSA carriers so that proper antibiotics can be given. A MRSA “carrier” is an individual who can carry the bacteria without necessarily becoming ill. About 2% of the population are MRSA carriers.

MRSA is a contagious bacteria that is difficult to treat because it is resistant to most commonly used antibiotics. In the bacteria cell wall, there is a penicillin binding protein. When penicillin is able to bind to the binding protein of the cell wall, disruption of the cell wall and destruction of the bacteria is possible. However, if the staph aureus acquires the mecA gene, then it can alter the penicillin binding protein, making the bacteria resistant to all penicillin. The primary way of transmitting MRSA is through direct contact from another person, an object that has it, or from sneeze droplets of an infected person. 30% of staph bacteria lives in the nose. About 25-30% of the population is colonized with S. aureus.


This means that the bacteria is present; however, it is not causing an infection with S. aureus. Ironically, if you are a carrier, you are only 6 times as likely to receive an infection, while non-carriers are 10 times as likely. MRSA carriers are diagnosed by examining a swab or culture of the nose. The physician will want to identify these patients before bringing them to the hospital, and eradicate or decolonize the organisms by using a 2-4% chlorhexidine bath for 5 days. The patient should leave the chlorhexidine on the surface of the skin (it works better if kept on for a longer time), so it is better not to wash it off. A 2% nasal mupirocin for five days may also be used. By the screening and eradication program, you can drop the infection rate by about 40-60% or more depending on the compliance of the patient. Our institution showed that empiric treatment is less costly than S. aureus screening and decolonization in total joint arthroplasty patients. They find that the cost is much less than the cost of the standard screening and decolonization of the S. aureus. They found that the empiric treatment allows for more efficient workflow without compromising the patient.


AVN of the Femoral Head- Causes, Trauma to the Hip

AVNAvascular necrosis (AVN), or osteonecrosis, is death of a segment of bone due to disruption of the blood supply. Extraosseous or intraosseous interruption of the venous or arterial blood flow. AVN may be caused due to fractures of the femoral neck or dislocations of the hip, or due to mechanical disruption of blood vessels. Trauma to the deep branch of the Medial Femoral Circumflex Artery may occur with antegrade rod placement during piriformis entry in children. Posterior dislocation of the femoral head should be reduced in an expedited way to decrease the risk of thrombosis of the vessels which supply the femoral head. Osteonecrosis develops in about 2-20% of hips that are reduced within 6 hours. The risk of osteonecrosis will increase with delay in reduction of the hip. Osteonecrosis appears within two years after the injury. It is evident within one year in most patients.

acute femoral neck fracture

With a Pipken fracture, the patient should be informed about the complications of AVN preoperatively. Fixation failure is associated with osteonecrosis or nonunion. The effect of the anterior approach on osteonecrosis is not known. Stress fractures should be pinned before displacement occurs. Displacement will have a bad result. Osteonecrosis can be clinically significant when followed by lateral segmental collapse. The more vertical the fracture line, the greater the chance of AVN occurring. In acetabular fracture fixation, during intraoperative dissection for acetabular fracture reduction and fixation, avoid injury to the ascending branch of the Medial Femoral Circumflex Artery (MFCA). Fractures of the hip in children are associated with a high rate of osteonecrosis.



Tibial Plafond Fracture Classifications

The pilon fracture has two classifications that are commonly used. The first classification is the Ruedi-Allgower Classification, which is an old classification, and the second is known as the AO/OTA Classification.


The Ruedi-Allgower Classification is separated into three types. Type I fractures are cleavage fractures with no significant joint incongruity and no displacement of the fractured fragments. Type II fractures have a significant articular incongruity with minimal metaphyseal comminution or impaction. Type III fractures have significant articular comminution and a metaphyseal impaction; this is a very bad injury.

You will find three types of AO/OTA classifications and they are as follows: Extra-articular, partial articular, and complete articular. The extra-articular fractures are further broken down into simple (A1), metaphyseal wedge (A2), and metaphyseal complex fractures (A3). All of these extra-articular fractures are named “A”, followed by a number based on the complexity of the fracture. Partial-articular fractures are classified further with the letter “B” and are identified as Pure Split (B1), Split Depression (B2), and Multi-fragmentary depression (B3).


Split Depression fractures are a supination/adduction fracture of the ankle which is identified as a vertical fracture of the medial malleolus. The anteromedial portion of the plafond may also be impacted. The impaction or depression unique to this fracture is commonly missed, making this fracture a classic question on orthopaedic examinations. If the surgeon misses the impaction fracture after fracture fixation, they will need to revise the fixation and be sure to elevate the impaction or depression; additionally, they will need to restore the joint congruity before fixing the fracture. The surgeon will need to fix the fracture with a plate or screws. If screws are used, they have to be parallel to the joint in order to compress the fracture. If a plate is used, it should be an anti-glide plate.


The “C” fractures are Complete Articular fractures and have complete joint involvement. The Complete Articular fractures are broken down into Articular Simple/Metaphysis Simple (C1), Articular Simple Metaphysis Multi-fragmentary (C2), and Articular Multi-fragmentary/Metaphysis Multi-fragmentary (C3). C3 fractures are a very difficult fracture and probably has the worst prognosis.


Classically, there is a typical pilon fracture fragment. Usually there are three main joint fragments. The Three fragments are the:

  1. Medial Malleolus
    1. Attached to the deltoid ligament
  2. Anterolateral Fragment
    1. Chaput Fragment- attached to the anterior inferior tibiofibular ligament
  3. Volkmann Fragment
    1. Posterolateral fragment attached to the posterior inferior tibiofibular ligament

When the fibula is intact, the lateral collateral ligament of the ankle may rupture (fibula is intact in 20% of the cases).