Flexor Tenosynovitis of the Hand—Kanavel’s Signs

Flexor tenosynovitis is an infection of the synovial sheath around the tendons of the flexorfingers and hand. The affected finger is red, swollen, and painful due to infection occurring with deep puncture wounds, such as a splinter. Pain is located in the finger at the flexor tendon sheath. Signs of infection of the tendon sheath are called Kanavel’s Signs. There are four Kavanel’s Signs to support the presence of flexor tenosynovitis.

Flexor Tenosynovitis (Kanavel’s Signs)

  1. Uniform swelling of entire finger
  2. The finger is flexed
  3. Intense pain when attempting to straighten the finger
    1. Occurs early
  4. Tenderness along the tendon sheath is the most specific sign.

Treatment consists of antibiotics and surgery may be performed by incision and drainage of the infection.

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.

 

Unbelievable Bacteria- Part II

Why do open fractures have increased risk for infection?

The presence of bacteria within an open wound increases the risk of colonization when hardware is used. Once the hardware is colonized, the bacteria grows rapidly. During the rapid growth phase, the bacteria secretes a polysaccharide sugar layer, called a “biofilm”, or slime layer that encases the bacteria. This biofilm provides protection to the bacteria against the body’s defenses and antibiotics.

biooo

Within the biofilm, there are channels that allow the bacteria to pass nutrients, messaging signals, and even DNA to each other. The bacteria pass on their DNA by:

passDNA

  1. Transformation
  2. Transduction
  3. Conjugation

Transformation is when a bacterial cell ruptures, releasing its DNA, which is then taken in by another bacteria. Transduction occurs when DNA is transferred from one bacterium to another by a virus. Phage DNA and proteins are made and bacterial chromosomes are broken up, completing the gene transfer. The phage release themselves from the host, carrying either bacterial or phage DNA. Conjugation occurs when two bacteria attach themselves together with a sex pilus and exchange their DNA.

How does the bacteria become resistant to antibiotics?

beta

The bacteria can alter the genes they express by as much as 50-60%. By doing this, the bacteria can produce enzymes such as beta-lactamases, which destroy certain antibiotics before they can reach their target site. They can also make Efflux pumps which expel antibacterial agents from the cell before it can reach its target site. Finally, by expressing different genes, the bacterial cell wall can be altered to no longer contain the binding site of the antibiotic agent. Because the antibiotics cannot break through the biofilm and access the bacteria, the bacterium in the biofilm can become up to a thousand times more resistant to the antibiotics by the different mechanisms previously discussed.

If there is biofilm on the hardware, what can the physician do?

xfix

The only proven treatment, is to remove the hardware and wash the wound. However, removal of the hardware is a problem if the fracture is not healed and the fixation is needed. The physician may decide to suppress the infection, leaving the hardware until the fracture has improved. Or, the physician may decide the remove the hardware and seek an alternative method for stabilizing the fracture, such as an external fixator, and then using a biological material to help heal the fracture.

These are the issues that make infection with hardware so complex!

Antibiotics: Mechanism of Action

The mechanism of antibiotics and how they work on bacteria is an important topic, especially on exams. Antibiotics are grouped together and work on a specific part of the bacteria. Some antibiotics such as penicillin, cephalosporin, and vancomycin work on the cell wall. Antibiotics, such as polymyxin, work in the cell membrane. Trimethoprim, sulfonamides and Bactrim will affect folic acid synthesis. Two antibiotics that affect Nucleic Acid Synthesis include: Ciprofloxacin and Metronidazole (flagyl)—which works on DNA gyrase, and rifampin, which works on the RNA polymerase.

cellparts

Antibiotics that work on protein synthesis are Tetracyclines such as Doxycycline and Aminoglycosides —both of which are 30S. Another subunit of antibiotics that affect protein synthesis classified as 50s are Clindamycin, Macrolides such as Erythromycin, and Zyvox.

protein synthesis