CHAPTER KEY WORDS
- Exercise-induced anaphylaxis
- Methicillin-resistant Staphylococcus aureus
CHAPTER SCENARIO
You are the athletic trainer for the Pine Hollow Fighting Bulldogs football team. The team is playing its archrival, the Sun Valley Raging Lions. The team is keyed up for this annual Saturday night event. The stands are filled on both sides, and the energy in the air can be palpated. It is a hot, humid night, and the team has been practicing all afternoon. By game time, the team has been at it for hours, with few breaks and little nourishment.
The game gets underway, and the players are energized. “Touchdown” Ted Turner, the star quarterback, is particularly hyped. With a good showing, his acceptance to State College is almost guaranteed. The game is going well for the Bulldogs, and Touchdown Ted is at the top of his game. Just prior to halftime, he is sacked on a failed third down conversion by a particularly hefty middle linebacker. As he is exiting the field, he collapses. Suddenly, you are the center of attention. The team and crowd look at you to react. What is your first response?
As you approach him, he is surrounded by his teammates yelling for you to do something. You notice that he is unresponsive. Primary assessment reveals that his airway is open, respirations are shallow and rapid, and his pulse is weak and rapid. His skin is cool and clammy. What is your diagnosis? What is your next action?
You turn him supine and elevate his legs. The ambulance crew comes out onto the field and administers oxygen. Vital signs show his pulse to be 140/min, respiratory rate is 40/min, and blood pressure is 70/palpation. They initiate intravenous fluid wide open. Secondary assessment reveals guarding when palpating his abdomen. Does this change your differential diagnosis? Does this change your treatment approach?
SCENARIO RESOLUTION
After 2 liters of intravenous fluids, he begins to respond. He complains of severe abdominal pain. Emergency medical services staff take him to the emergency department. They determine that his hemoglobin and hematocrit is low. He is taken for a computed tomography scan and is found to have a ruptured spleen. He is admitted for observation and potential surgery.
Discussion
Long, outdoor activity in a warm environment is suspicious for dehydration. This is heightened because the focus is on a rival game and not on fluid replacement. The quarterback is the star player, and his adrenalin is running high. After an hour or so playing in the warm, humid climate, he is likely dehydrated. However, during the last play, he is tackled by a hefty linebacker. This detail could easily be missed if the athletic trainer is not paying attention.
Regardless of the underlying etiology, this player is clearly in shock. The first-line treatment is the same. Maintain airway, breathing, and circulation. Placing him supine and elevating his feet assists in shunting blood from the periphery into the central circulation. Suspicion of cervical spine injury is low, as he was ambulating prior to collapse. It is clear that he requires fluid resuscitation; however, oral replacement is dangerous in a person with altered mental status because of the risk of aspiration. Therefore, intravenous fluid replacement is the preferred method of volume resuscitation. The key to making the correct diagnosis is in the history. Shock due to dehydration would be less likely to occur acutely. However, gathering history from the referee would add information to make the diagnosis clearer.
Other Considerations
Concussion/Closed Head Injury
Although this would explain the sudden loss of consciousness, it does not explain the hypotension or tachycardia.
Other Types of Shock
Septic shock would present with other prodromal symptoms such as fever and malaise prior to collapse. Neurogenic shock may present with sudden collapse; however, it would be accompanied by severe neurological symptoms such as paresthesia or paralysis. Cardiogenic shock would explain some of these symptoms but it would not explain the abdominal pain.
Anaphylaxis
This would explain the tachycardia and hypotension; however, it does not explain the sudden collapse and would be accompanied by wheezing, urticaria, or rash.
Shock
The textbook definition of shock is simply inadequate tissue perfusion; however, shock is a very complex syndrome. In its simplest terms, a state of shock arises when blood flow to vital tissues does not supply adequate nutrients, specifically glucose and oxygen, to the cells. Shock can be defined by the means of restriction, such as cardiogenic shock, which results from decreased cardiac output; hypovolemic shock, resulting from decreased circulatory volume leading to inadequate peripheral blood flow; neurogenic shock that results from vascular dilation and decreased systemic vascular resistance; and septic shock as a response to a pathogen, which causes vascular dilation, increased capillary permeability, and increased cellular metabolism. The result of these syndromes is nutritional and oxygen starvation of the body’s cells. This sets off a cascade of events that, if left unchecked, rapidly progresses to massive cellular death and the individual’s eventual demise. Although shock can rapidly progress, intervention by the athletic trainer can halt the process. The key is early recognition and intervention, with an adequate recovery period.
Shock on the Cellular Level
Shock is a cascade of events that can lead to cellular death. To survive, cells require 3 essential components: oxygen, glucose, and water, as shown in the following formula:
C6H12O6 + 6O2 → 6CO2 + 6H2O + Energy
In addition to receiving essential nutrients, cells must be able to excrete byproducts and waste. Normal, aerobic metabolism produces waste products such as CO2; ATP, or energy; and sulfates. When the body is in a state of homeostasis, these products are carried away by the circulation and excreted mainly by the liver and kidneys. However, in a state of low blood flow, these wastes and byproducts accumulate in the cells and interstitial fluid, causing electrolyte disturbances, fluid shifts, and acidosis.
During anaerobic metabolism, ATP is generated at an accelerated rate. This inefficient use of resources produces lactate and causes the blood pH to fall. The resulting metabolic acidosis causes peripheral vasoconstriction, precapillary sphincter failure, increased capillary permeability, and peripheral pooling of blood. A drop in cellular pH also causes membrane dysfunction and sodium pump failure; therefore, extracellular potassium and intracellular sodium increase. With a higher intracellular sodium concentration, water is drawn into the cell by osmosis, causing intravascular dehydration and cellular edema. Cells begin to lyse, and intracellular enzymes leak into the extracellular fluid. These enzymes erode the capillary endothelium, worsening peripheral edema. This further depletes the intravascular volume, and the shock response cycle continues (Figure 8-1).
As the cascade escalates, oxygen use by the cells becomes increasingly tedious, further shifting to anaerobic metabolism and acidosis. The body activates neurohumoral, negative feedback mechanisms in an attempt to correct the hypotension. Decreased circulatory volume further limits the compromised flow of oxygen to the cells. In septic, anaphylactic, and neurogenic shocks, the resultant vasodilation exacerbates the already-depleted intravascular volume. Profound hypotension ensues, and vital organs begin to fail. The extreme shift in electrolytes inhibits the function of intracellular enzymes. Cells begin to lose their ability to absorb nutrients and rid themselves of waste. Moreover, capillary flow becomes sluggish due to increased permeability and increased vascular viscosity. This, in turn, activates the clotting cascade, resulting in disseminated intravascular coagulation, which not only clots many smaller vessels, but also depletes circulating clotting components, producing even more uncontrolled hemorrhage. Finally, the deluge of enzymes exiting the cells destroys the cell membrane and the surrounding tissues. Anaerobic metabolism is used as a final effort for cellular survival but produces even more lactic acid and electrolyte shifts. The cycle continues until the environment becomes too hostile for the cells to survive. The victim becomes unconscious and, without rapid intervention, death is imminent.
Figure 8-1. Biologic pathology of shock syndrome.
Much as when cells are oxygen deprived, the inability to use glucose initiates a catastrophic set of events in cells. Glucose delivery is inhibited by the same mechanisms as oxygen delivery: low volume and low flow. Further, most tissues have limited, readily available glucose stores. Shock states, such as sepsis, increase cellular metabolism, thus exacerbating an already-broken system. When glucose stores are consumed, cells will revert to proteins, lipids, and other nontraditional sources for energy. Use of these is highly inefficient and produces toxic byproducts such as lactic acid, uric acid, and ammonia.
Classifications of Shock
Shock can be classified in a variety of ways; often, it is classified via etiology (Table 8-1). However, within any classification system, more than one shock state can exist simultaneously in the human body.
Hypovolemic Shock
Hypovolemic shock is one of the most frequent types of shock that an athletic trainer may encounter. Hypovolemic shock can be either hemorrhagic or non-hemorrhagic. Hemorrhagic, as the name implies, is the loss of whole blood. This is frequently the result of a traumatic insult, causing either external or internal bleeding. External hemorrhage results from lacerations, open fractures, or other types of external traumas that disrupt major vessels and create an external pathway for blood to escape. Internal hemorrhage is often due to blunt trauma. Detecting external hemorrhage is more subtle and more difficult. Unfortunately, internal injuries can be erroneously dismissed as bruises or contusions. Common sites of internal hemorrhage include solid organs, such as the pancreas and liver; large bones, such as the femur or pelvis; and hollow organs, such as lungs or bowel. When hemorrhagic events occur in sports, the quick recognition and treatment by the athletic trainer can turn a potential tragedy into a manageable event with a good outcome (Box 8-1).
Although hemorrhagic shock is frequently due to a loss of whole blood, it can also be the result of loss of plasma or other fluids. Burn injury can result in acute fluid loss. When a thermal burn occurs, the epidermis is disrupted, allowing massive loss of plasma externally. A similar example, not foreign to athletes, is dehydration, whereby fluid loss via the skin’s sweating is not replenished.
In addition to blood volume loss resulting in a reduction in perfusion pressure, there is also a loss of oxygen-carrying capacity due to a loss of erythrocytes. As the body’s defenses attempt to combat the hypovolemic state, fluid shifts from intracellular and interstitial spaces into the vasculature. Although this may partially or completely replace the lost blood volume, it does not replace the lost erythrocytes, and therefore does not restore the oxygen-carrying capacity. For example, individuals with coronary artery disease may not be able to adapt to this reduction-relative anemia and myocardial infarction may result. A myocardial infarction causes cardiogenic shock, further decreasing the circulating blood volume and exacerbating the shock state. The patient now suffers from hypovolemic shock and cardiogenic shock. Treatment for these may include volume replacement via fluids, blood, or blood products, and a combination of alpha- and beta-adrenergic agents.
TABLE 8-1. CLASSIFICATIONS OF SHOCK
ETIOLOGY | TYPE OF SHOCK |
| Hypovolemic |
|
| Distributive |
|
| Cardiogenic |
|
| Obstructive |
|
BOX 8-1. HEMORRHAGIC EVENTS IN SPORTS
On March 22, 1989, Clint Malarchuck, the goalie for the Buffalo Sabres, was struck in the neck by the skate of opponent Steve Tuttle, slicing his jugular vein. He lost an estimated 1.5 L of blood before athletic trainer Jim Pizzutelli was able to apply pressure to the wound and stop the bleeding. He required 300 sutures and was back to playing in 10 days.
On February 10, 2008, Richard Zednik of the Florida Panthers was playing against the Buffalo Sabres when his teammate Olli Jokinen collided with Saber player Clarke MacArther. During the collision, Zednik’s carotid artery was severed by Jokinen’s skate. Zednik lost an estimated 2 L of blood. The team’s athletic trainer, Dave Zenobi, applied pressure to stop the bleeding until they arrived at DeRay Medical Center.
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