Iliopsoas Abscess Infection

psoas anatomy

The iliacus and the psoas are the main hip flexors supplied by the femoral nerve which lies between the two muscles. The obturator nerve is medial to the psoas. The psoas arises from the transverse process of the lateral aspect of the vertebral bodies between the 12th thoracic vertebrae and the 5th lumbar vertebrae. The psoas runs downward across the pelvic brim and then passes deep to the ilioinguinal ligament bursawhere it then forms a tendon past the hip joint capsule which inserts into the lesser trochanter of the femur. The iliacus arises from the upper two-thirds of the iliac fossa and joins the psoas to insert in the same tendon as the posas muscle. Both muscles are in the extraperitoneal space, or referred to as the iliopsoas compartment. The iliopsoas tendon is separated from the hip joint capsule by the iliopsoas bursa.

What causes an abscess of the iliopsoas muscle?

A primary abscess is caused by a hematogenous spread of the infection. The infection starts in the muscle itself. In a secondary abscess, the infection spreads from another area to the psoas muscle. For example, the infection may travel from the spine when it is infected by tuberculosis (Pott’s disease). This historically is the cause of this abscess. It can also spread from the SI joint, kidneys, or bowels. The iliopsoas abscess may initially present with sign and symptoms in the buttock, hip, or thigh. Such signs and symptoms may be obscure, nonspecific, and misleading.

staphaurusStaph aureus is the cause of iliopsoas abscesses in 88% of primary types. Polymicrobial infections are usually the cause in the secondary types. CT scans are usually the CTENLARGEDdiagnostic modality of choice.


An abscess of the iliopsoas muscle is a diagnostic dilemma with a difficult diagnosis that is often delayed. The patient may be lying supine with the hip flexed and refuses to move, resisting any attempt for examination. With psoas involvement, the hip appears to be flexed, with limited and painful range of motion. This diverts attention away from the abdomen or pelvic source of the abscess. The patient may have a low grade fever and cannot straighten the leg. A high index of suspicion and performing the Psoas sign is necessary for diagnosis.

Psoas Sign

The patient is positioned on their side and the hip is extended to see if there is pain present in the iliopsoas region. The psoas sign is used in diagnosis of appendicitis but is also helpful in diagnosing a psoas abscess.

psoas sign

The iliopsoas abscess manifests itself as pain in the abdomen, flank, or groin area, as well as pain in the lower back. Flexion posture of the hip is also commonly noted. These abscesses are rare and present with vague clinical features.



Percutaneous drainage is done if the abscess is simple, small, and single. Otherwise, an open drainage is the procedure of choice. When performing an open drainage of the abscess, a splitting incision is made along the iliac crest for easy access to the iliacus, psoas, and SI joint. Other incisions may be needed such as the anterior approach in the front of the hip or the posterior approach. Other sites for drainage depend on the location and extension of the abscess.

Risk factors for developing an iliopsoas abscess:

  • Diabetes
  • Immunosuppression
  • Trauma
  • Renal failure
  • IV drug abuse
  • Older individuals and AIDS patients




General Trauma- Shock

There are different types of shock in regards to medical terminology. The first type of shock we will discuss is hypovolemic shock occurs due to low blood volume. Trauma patients with hypovolemic shock will need to be given fluids. The patient’s heart rate will be increased and the most reliable early clinical finding is tachycardia (fast heart rate). cardioThe patient will have an increased systemic vascular resistance. The patient will be cold and clammy. The patient should be given 2 liters of bolus Ringer’s lactate solution (RL), followed by a reevaluation of their vital signs.

Cardiogenic shock occurs as a result of poor pump function of the heart. There will be a decreased cardiac output and a decreased peripheral resistance. Obstructive shock is similar to cardiogenic shock as cardiac tamponade and pulmonary embolisms have the same features.

obshockAnother type of shock is known as septic shock and occurs during a decreased peripheral resistance and vasodilation. This is commonly seen in patients with septic neurogenicshock and necrotizing fasciitis.

Neurogenic shock occurs in patients with an acute spinal cord injury. There will be an impaired sympathetic response to the heart and blood vessels. Circulation will collapse with hypotension and bradycardia. The patient will have a decreased systemic vascular resistance and warm skin. Treatment is Swan-Ganz monitoring for careful fluid intake and giving pressor. Neurogenic shock is not a spinal shock with loss of all spinal cord function and reflexes below the level of the lesion. Neurogenic shock is hypotension and bradycardia.

In Hemorrhagic shock, the initiation of resuscitation is based on the degree of hemorrhage. The physician should start by giving 2 liters of crystalloid fluids (usually Ringer’s Lactate) with two lines. Then, the physician will want to reevaluate the vital signs. The patient may have a rapid response, transient response, or no response. If the patient has a transient response, then the patient is considered to be a class 3 or 4. Type O- blood should be given immediately. Type specific blood transfusions will take about ten minutes. Cross-matching the blood transfusion will take 60 minutes. So, if the patient is in shock and bleeding, the patient should be given O-blood. The blood ratio will be: Packed RBC-1, fresh frozen plasma-1, and platelets-1 (1:1:1). This will avoid dilution thrombocytopenia. Hepatitis B carries the highest risk of viral transition with the blood transfusion.

hemorrhage classThe class of Hemorrhage is as seen in the graph above. The patient has to lose about 30% of the blood volume in order to have hypotension. Patients in class 3 and 4 may not respond to fluid resuscitation and will require blood transfusions. There must be adequate fluid resuscitation. If the physician relies on the hemodynamic perimeters alone, they will miss the subclinical hypotension. Hemodynamic perimeters alone is an inadequate assessment tool for resuscitation.

Additionally, the physician will need to correct the hypothermia and coagulopathy. The terrible trauma triad is:

  1. Hypothermia
  2. Coagulopathy
  3. Acidosis

These are the life threatening conditions that may become worse by surgery and/or anesthesia.

head injuryAnother injury which commonly causes hypotension, are head injuries. Patients with head injuries can run into the problem of episodic hypotension intraoperatively which causes a significant increase in mortality. All efforts should be made to avoid hypotension during surgery. Patients with an AP pelvis, the physician can place a pelvic binder and “close the book” to help with the hypotension and hemorrhage. If the patient has lateral compression, look for another source of the bleeding if the patient continues to be unstable despite any effort for resuscitation (probably not from the pelvis). If you give the patient four units of blood because they have a pelvic fracture and is in shock, and the patient is not improving, the physician should order an angiography and embolization for a possible major arterial bleed in the pelvis (such as the superior gluteal artery).

How will the physician know if the patient is resuscitated?
There are several ways that this can be assessed, however there are two ways that are commonly seen on Orthopaedic Exams. The physician can assess resuscitation by the base deficit (from -2 to +2) or by the serum lactate level (normal is less than 2.5—some sources say less than 2). The blood lactate is the end point of anaerobic metabolism. The blood level of lactate reflects a global hypoperfusion that is directly proportionate to the oxygen deficiency. The base deficit is a direct measure of metabolic acidosis and an indirect measure of the blood lactate level. Both of these measure correlate well with organ dysfunction, mortality, and the adequacy of resuscitation.

For exam purposes, you will need to measure:

  1. Blood lactate
  2. Base deficit

In order to find the adequacy of resuscitation.

glucose chartNormally, the body utilizes energy from the breakdown of glucose. Each molecule will give us 2 pyruvate molecules and 2 ATP. This occurs when oxygen is present. If oxygen is not present, the pyruvate will attach to the protons and produce lactic acid. Lactic acid is a pyruvate that is holding onto protons. Lactate gives away the protons, the protons attach to the bicarbonate, and then you will find the base deficit. When the patient is acidotic, this means that the body is experiencing an inadequate tissue perfusion. Then, it undergoes anaerobic metabolism to create energy and lactate. The greater the lactate level, the greater the base deficit.

The physician needs to be aware of the under resuscitated patient and the compensated IL6shock. The patient can be under-resuscitated with normal vital signs. This patient will be at an increased risk for huge, exacerbated systemic inflammatory response. Interleukin 6 (IL-6) plays a major role in the inflammatory response. IL-6 is secreted by the T-cells and by the macrophages. This stimulates the immune response, especially during infection and trauma. The interleukins are a group of cytokines which are secreted proteins and signal molecules. IL-6 warns the body and the immune system against the source of infection or inflammation. This response is similar to “sounding the alarm” or raising attention that there is something wrong.

For these patients, we do damage control orthopaedics. For managing these patients, we should always do emergency procedures such as: a pelvic binder, angiography, fasciotomy (even bedside), consult with vascular surgery, prevent further injury to the spine by immobilizing the neck, reduce a knee or hip dislocation, reduce fractures thatfasciotomy will cause soft tissue compromise (like ankle or pilon fractures). The physician will deal with open fractures by doing debridement, splint, and improve the alignment of the fractures. The patient should be given antibiotics and a tetanus vaccination if needed. The physician will probably need to do traction or external fixation for femur fractures. The timing of debridement of open fractures does not really affect the infection rate. An early administration of antibiotics will decrease the rate of infection. The patient should be taken to the operating room as soon as possible after the life threatening condition is treated and stabilized (debatable). If the patient is adequately resuscitated, take the patient to the operating room and fix the fracture or convert the fractures which are stabilized by external fixation to an IM rod fixation.


Bursae around the Hip

bursaeThere are multiple bursae located around the hip joint. These bursae are present where friction normally occurs between the muscles, tendons, and bones. A bursa is a thin sack containing minimal fluid which lubricates the tissue to decrease friction.

There are three different types of bursae located around the hip area:

  1. The Greater Trochanter group of bursa
  2. Iliopsoas bursa
  3. Ischial bursa

Three main bursae surround the greater trochanter of the femur:

Greater Trochanter Group of Bursa

  1. Subgluteus medius bursa: smaller bursa between the gluteus medius muscle and greater trochanter groupthe greater trochanter, just medial to the trochanteric bursa.
  2. Trochanteric Bursa: located just superficial to the greater trochanter and the attachments of the gluteal muscles. If the trochanteric bursa becomes irritated and inflamed, this can lead to trochanteric bursitis.
  3. Subgluteus Minimus Bursa: lies beneath the gluteus minimus tendon at the anterosuperior edge of the greater trochanter.

Some people believe that there are over twenty bursas around the greater trochanter of the femur. Needling of the bursa in different directions may be helpful when the physician injects steroids into the bursa. Trochanteric bursitis is often associated with iliotibial band syndrome.

ITBSSSSSThe iliopsoas bursa lies between the iliopsoas muscle at the front of the hip joint and the underlying bone. The bursa may become irritated and inflamed due to friction from the iliopsoas muscle where it crosses the hip joint.

iliop bursaThe Ischial bursa is also called “weaver’s bottom” or “tailor’s seat”. This bursa prevents friction between the gluteus maximus and the ischial tuberosity. The bursa is located on the posterior side of the ischium. Bursitis of the ischial bursa may be caused by prolonged sitting on a hard surface, which aggravates the bursa. The patient will complain of tenderness and pain in the buttock area during sitting.ischial bursae


The Accessory Navicular Bone

What is an accessory Navicular Bone?

accessoryAn Accessory Navicular Bone is an extra bone that may be attached or detached from the navicular bone. It is considered a normal variant and is present in approximately 10% of people. This accessory bone is usually located under the plantar medial aspect of the navicular and is often associated with a pes planus (flatfoot) deformity. Ossification of the navicular bone occurs at three years of age in females and five years of age in males. However, the accessory navicular bone does not begin ossification before eight years of age.


The majority of patients are asymptomatic but, females tend to be more symptomatic. The patient may present with an activity related limp and pain in the arch area. The condition may also be bilateral. During examination, there may be swelling, tenderness, warmth, or redness in the plantar medial aspect of the arch. Relative to a normal foot, a plain x-ray AP view can detect the accessory navicular. An external oblique view is considered to be the best imaging position to detect an accessory navicular bone. An MRI may also be obtained in order to determine the size and type of the accessory navicular as well as assess the posterior tibial tendon.

radiologyThe accessory navicular is classified into three types. In Type I classifications, the accessory ossicle is mainly in the substance of the posterior tibial tendon and is not attached to the navicular. In Type II, the accessory bone resides very close to the navicular tubercle and is connected to the navicular by a thick layer of cartilage. In Type III classifications, the accessory bone is considered an enlarged navicular tubercle. Type IIIs are essentially a type II that is fused with the navicular by a bony bridge.

accessory typesIn regards to prognosis, when skeletal maturity has been reached, almost all patients become asymptomatic.


Nonoperative treatment usually consists of activity modification, orthotics, or a short leg walking cast. Surgical excision is indicated only after all conservative treatment options have failed.