Lesions of the Shoulder—Hill-Sachs Lesion

hillsachs

The Hill-Sachs lesions is a dent in the posterior aspect of the humeral head, which occurs during an anterior shoulder dislocation. The humeral head impacts against the front of the glenoid cavity of the scapula. A Hill-Sachs lesion is usually associated with a Bankart lesion. A Bankart lesion is the most common lesion of anterior shoulder instability following dislocation. It involves an avulsion of the anterior inferior labrum. The Hill-Sachs lesion can range from a small to large indentation and the size of the lesion can affect the treatment given to the patient. The larger the Hill-Sachs lesion, the more likely that the shoulder will be unstable and the more likely to

bankart lesiondislocate again (recurrent dislocations). The larger the Hill-Sachs lesion is, the more likely that the glenoid labrum and joint capsule have a significant tear.

Treatment for a small sized Hill-Sachs lesion of less than 20% can usually be treated nonoperatively. A medium sized Hill-Sachs lesion—a defect greater than 25%– may require an arthroscopic or open remplissage procedure (may be performed in combination with Bankart repair). The defect is “filled in” with the posterior capsule and rotator cuff. Larger sized Hill-Sachs lesions are rare. Lesions greater than 40% are usually filled with bone or metal.

lesion

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Thoracic Disc Herniation

thoracic regionThere are 12 vertebrae in the thoracic region. The spinal canal in the thoracic region is relatively small, however, the spinal cord could be easily compressed or injured in this area. Pain in the thoracic region can occur from cardiovascular origin, tumors, infection, compression fractures, and mediastinal structures. A point of consideration is thoracic disc herniation. It occurs more in the lower thoracic region, usually during the fifth decade of life. This disc herniation causes pain to radiate to the ribs and anteriorly at the same level. A thoracic disc herniation is uncommon and most are asymptomatic.

Clinically, a thoracic disc herniation will present itself as a radicular pain, anteriorly towards the rib (nerradicular painve root irritation).Myelopathy can occur from spinal cord compression. The patient could have a gait disturbance, leg weakness, as well as bladder and bowel dysfunction. Myelopathic findings are usually subtle. The physician should look for upper motor neuron signs such as hyperreflexia, clonus, and Babinski. A diagnosis is usually determined with magnetic resonance imaging (MRI). MRIs will help in ruling out the presence of fractures, tumors, or infections. Although an MRI is the study of choice, it has a high false positive rate. Asymptomatic patients may show a thoracic disc abnormality in their MRI.

Treatment

Conservative treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy. Surgery is indicated when the patient has pain that is not responding to conservative treatment for 6 months or if the patient has a thoracic disc herniation with myelopathy. Most surgeries are performed with an anterior approach with or without fusion. Fusion is done for spine instability and significant chronic pain. A laminectomy is contraindicated. thoracic disc

 

 

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.

Treatment

treatment

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.