Supracondylar Fractures of the Humerus in Children

Supracondylar fractures constitute approximately 50% of all elbow fractures. The supracondylar region is thin and weak and thus can fracture easily. These fractures are classified into two different types: extension and flexion.

fracture typesExtension type fractures are the most common type, occurring approximately 95% of the time. Extension fractures typically occur due to falling onto an outstretched hand. With extension fractures, the distal fragment of the humerus displaces posteriorly. Anterior interosseous neurapraxia is the most common nerve palsyOKsign occurring with supracondylar fractures. Injury to the anterior interosseous nerve will lead to weakness of the flexor digitorum profundus muscle to the index finger and the flexor pollicis longus muscle. The patient will not be able to make an “OK” sign or bend the tip of his index finger. Radial nerve neurapraxia is the second most common palsy and is evident by weakness in wrist and finger extension.

The second type of fractures, flexion type fractures are rare and occurs due to falling flexionfxdirectly on a flexed elbow. In flexion type fractures, the distal fragment is displaced anteriorly. This type of fracture may be accompanied with ulnar nerve neurapraxia. Injury to the ulnar nerve will lead to a loss of sensation along the little finger. Later on, the patient may also have weakness of the intrinsic hand muscles and clawing.


Gartland Classification System

gartland classificationThe Gartland Classification System provides physicians with a way to categorize supracondylar humerus fractures. There are four classifications and are as follows: Type I fractures are nondisplaced fractures; Type II are angulated with an intact posterior cortex; Type III are completely displaced; and Type IV has complete periosteal disruption with instability in both flexion and extension.


Plain AP and lateral x-rays should be obtained. A posterior fat pad sign seen on a anterior humeral linelateral view x-ray should increase your suspicion of an occult fracture around the elbow. On a lateral view x-ray, the anterior humeral line is drawn along the anterior border of the distal humerus. Normally, the anterior humeral line should run through the middle third of the capitellum. In extension type fractures, the capitellum will be displaced posteriorly, relative to the anterior humeral line.

The Baumann’s Angle is formed by a line perpendicular to the axis of the humerus and a line going through the physis of the capitellum. Normally, the Baumann’s angle should measure at least 11° (variable).


Physical Examination

It is important to assess the neurovascular structures. The anterior interosseous nerve is assessed by asking the patient to do the “OK” sign with their hand. The radial nerve is assessed by asking the patient to extend their wrist and fingers. Ulnar nerve damage is usually indicated by the loss of sensation along the little finger; however, later on the patient may have weakness of the intrinsic hand muscles and clawing.

finger extensionTreatment

Nonoperative treatment is usually indicated for type I fractures. This treatment usually consists of splinting or casting the elbow for a duration of 3-4 weeks. It is very important to remember not to flex the elbow in the splint or cast beyond 90° in order to avoid vascular compromise and compartment syndrome.

closed reductionOperative treatment is usually indicated for Types II and III, and are usually treated by a closed reduction and percutaneous pinning. During reduction, pronation of the forearm during elbow flexion helps to correct a varus deformity. After reduction, the surgeon will want to check for a gap in the fracture, as the neurovascular bundle may be trapped there. The surgeon will need to free the brachialis muscle from the fracture site if it is interpositioned there. Fixation is usually achieved with 2-3 ulnar nerve pinningdivergent lateral pins, depending on stability. Medial pins may also be added depending on stability; however, the surgeon will need to be aware of the ulnar nerve when placing the medial pin.

Open reductions are only performed when closed techniques are unable to achieve the appropriate reduction of the fracture. The surgeon will want to avoid posterior dissection in order to preserve the vascularity of the fractured segment. Fracture reduction and fixation should be done emergently in cases of vascular compromise.


Neurapraxia is a common complication of supracondylar fractures and usually resolves on its own—thus, treatment is observation only. A cubitus varus deformity may occur due to a malunion of the fracture. This only presents as a cosmetic problem since it does not affect the function of the arm or elbow. Additionally, this cubitus varusdeformity can be corrected later on by a supracondylar valgus osteotomy. Vascular problems, such as compartment syndrome, may also occur. Volkmann’s ischemic contracture may occur due to a compression of the brachial artery with then patient is placed in a cast with the arm in hyperflexion (more than 90°).

Important Scenerios

A patient may present with a Displaced Type III fracture and a pulseless hand. He may have adequate circulation—which is evident by the normal temperature and color of the hand—or he may have inadequate circulation—indicated by a cold blue hand. In both cases, an urgent closed reduction and percutaneous pinning is required. Once this has been performed and the circulation is adequate, the surgeon can observe the patient and place them in a splint that is at a 45° angle. However, if the patient continues to have inadequate circulation after the closed reduction, then the patient will require a vascular exploration and repair.


Differential Diagnosis of SI Joint Pain

Sacroiliac Joint pain can often be inappropriately treated or mistaken as lower back pain. There are several conditions that simulate sacroiliac joint pain.

1. Myofascial Painmyofacial pain

This is a chronic pain caused by multiple trigger points and fascial constrictions. This particular condition involves the muscles and fascial areas of the back. The patient may feel knots or hardening of the muscle with weakness and tenderness. Myofascial pain syndrome and fibromyalgia may present the same clinical picture but, they are different problems. The site location is close to the SI joint and can be confused with SI joint pain.

2. Trochanteric Bursitis

Inflammation of the greater trochanter bursa. This condition causes tenderness and pain bursapiriin the hip. Trochanteric bursitis occurs in middle aged women. The area of pain may overlap with the SI joint area of pain and can radiate close to the sacroiliac joint. The pain from this condition is sometimes severe and associated with iliotibial band syndrome. Trochanteric Bursitis is occasionally overlooked. This condition may present with arthritis of the hip and low back pain and other conditions.


3. Piriformis Syndrome

This condition occurs when the sciatic nerve is compressed by the piriformis muscle in the buttocks. Piriformis Syndrome may be associated with lower lumbar radiculopathy similar to spine pathology. It occasionally develops due to blunt trauma to the buttocks. Localized buttocks pain will increase with sitting or driving. Tenderness is commonly found in the sciatic notch.


4. Cluneal Nerve Entrapment

cluneal nerve entrapThe superior cluneal nerve has three branches. The medial branch of this nerve is confined within a tunnel which may cause impingement of the nerve producing pain close to the SI joint.

5. Lumbosacral Disc Herniation or Bulge

The disc may move out of place (herniate) or break open (rupture) from injury or strain. Disc herniation of the lumbosacral region could involve the nerve roots, creating lower back pain. The pain is usually found in the midline and can go down the leg.


6. Lumbosacral Facet Syndrome

facetThe facet provides stability for the spine and contain a joint. This joint may be affected by inflammations or degeneration which causes pain that can be mistaken for SI joint pain.


7. Lumbar Radiculopathy

Lumbar Radiculopathy is a major source of back pain. This condition occurs from inflammation, irritation, or impingement of the nerve root. It is commonly confused for SI joint pain.lumbarradi




Osteonecrosis of the Hip

Osteonecrosis or Avascular Necrosis of the hip is death of a segment of bone in the femoral head due to disruption of the blood supply. The etiology of this condition is not fully understood. There are several risk factors associated with osteonecrosis of the hip. The condition occurs bilaterally in about 80% of patients. It is important for the physician to check both hips, even if one is asymptomatic. An early diagnosis is important because during the early stages of osteonecrosis, a femoral head preserving procedure can be done. In the late stages of osteonecrosis, the femoral head collapses and cannot be saved. The femoral head may need to be replaced. Obtain AP and Frog Leg Lateral views of the hip. The Frog Leg Lateral view will show the crescent sign.

An MRI is the imaging of choice, especially when the patient has persistent hip pain, the radiographs are negative, and the diagnosis of osteonecrosis is suspected.

osteonoThe Ficat Classification is a commonly used system to stage osteonecrosis of the hip. Stage I classifications will have a normal appearing x-ray and an MRI will detect the lesion; changes in the marrow. Stage II classifications are identified by sclerosis and cyst formation. Characteristics of the Stage III classifications are a subchondral fracture and the appearance of a crescent sign and flattening of the femoral head. Stage IV classifications will show advanced lesions with arthritis, osteophyte formation, and a loss of the joint space.



For early stages of osteonecrosis of the hip, initial trial of nonsurgical treatment is usually done. Surgery may be needed if nonsurgical methods are not successful. Nonoperative treatment typically consists of bisphosphonates.

femoral head collapsedThese drugs may be used before the femoral head collapses and are still in the experimental stages. In regards to traditional surgical treatment, when the lesion is small a head preserving procedure can be done. For stages I & II, a core decompression is used. The surgeon can make a single large hole or multiple small holes in the femoral head. It decompresses the head and stimulates a healing response. The lesion is done anteriorly and superiorly.

bonegraft222If the surgeon chooses to perform a core decompression with bone graft, they will debride the necrotic area and insert the bone graft into the open space. Vascularized Fibular Grafts are done in younger patients. Complications include: donor site pain and leg dysfunction as well as tibial stress fractures on the side the graft was taken. Stages III and IV will require a total hip arthroplasty (cementless cup and stem) or total hip resurfacing; however, resurfacing is not commonly used. A total hip replacement is considered to be the traditional procedure for advanced stages of osteonecrosis of the hip. Total hip resurfacing is considered to be controversial because the patient will need adequate bone stock to support the femoral component. The result is not as good when compared with a patient with osteoarthritis.totalhip


AVN Causes and Risk Factors

AVN femoralAvascular Necrosis or osteonecrosis is death of a segment of bone due to disruption of the blood supply. The causes of avascular necrosis are numerous as there are several different ways that could interrupt the blood supply.

AVN may occur due to trauma, such as with a dislocation or fracture of the femoral neck. These injuries may interrupt the blood supply to the hip. Avascular necrosis may occur due to an occlusion of the arterial blood supply by a fat embolism; nitrogen bubbles in the blood stream (Caisson disease) or with Sickle Cell disease. fat embolism

Due to the low oxygen levels of the cells in patients with Sickle Cell Anemia, the cells become sickle shaped and are unable to pass through the vessels. This results in a diminished blood flow, which could lead to AVN. A patient with sickle cell disease and asymptomatic AVN diagnosed by an MRI will have a higher incidence of progression to collapse the AVN and pain (75%). Deterioration of the AVN will be rapid and can be bilateral, so it is important for the physician to screen the other hip at the same time and periodically. The physician will also want to watch the humeral head for AVN.

sickle obstructionAn obstruction of the venous outflow is another cause of avascular necrosis. With an increase in interosseous pressure, an obstruction can limit the blood flow. Injury or pressure on the blood vessel wall can also cause AVN. An excellent example of this would be Gaucher’s Disease, an increase in fat cell size may prevent the arterial inflow and lead to ischemia. Fatty substances can accumulate in the cells and certain organs. Marrow gauchersdiseases such as lymphoma and leukemia may also cause AVN. Radiation, vasculitis, and cytotoxins are also risk factors for AVN. Avascular necrosis may be associated with hypercoagulable states such as decreased anticoagulants, protein S and protein C.

Other common causes of AVN:

  • Steroid use
  • Alcohol
  • Idiopathic (no cause)
  • Metabolic and genetic factors
  • Systemic lupus erythematosus (SLE)
  • Rental failure
  • Organ transplant
  • Hemophilia

All of these conditions may cause loss of the vascular supply, marrow necrosis, and osteocyte death. An important condition related to AVN is steroid use. High doses for 2-3 weeks or low doses for long durations may cause AVN. There is a direct connection between the dose and duration of steroid use in the development of AVN. Joint injections are not proven to cause AVN. Additionally, avascular necrosis of the femoral head is a complication in HIV infected patients. The increased incidence of AVN may be caused by an increased prevalence of predisposing factors for osteonecrosis, including protease inhibitors, hyperlipidemia, corticosteroid use, alcohol, and intravenous drug use. Protease inhibitors play a role in the development of osteonecrosis through a tendency to cause hyperlipidemia. An easy mnemonic tool to remember the causes of AVN is “ASEPTIC”: Alcoholism/AIDS, Sickle Cell Disease/SLE, Erlenmyer Flask (Gaucher’s), Pancreatitis/Pregnancy, Trauma, Idiopathic/Infection, Caisson’s (the bends).

resorpThe anterosuperior segment of the femoral head is the area usually affected by AVN. Resorption of some of the dead bone is done by the osteoclasts, while osteoblasts lay down new woven bone. Dead trabecular bone is resorbed, ready to be remodeled. This process is repeated and the bone becomes weak. At the weakest stage, the AVN will result in collapse. Remodeling is not enough to support the bone. Progressive collapse due to bone death, resorption, remodeling and microfracture will occur. Avascular necrosis ends by final collapse, joint changes, and arthritis.