Hemorrhage and Shock

• Shock is a state of inadequate tissue perfusion, representing a critical transitional stage between homeostasis and death and a common cause of mortality in trauma and medical patients.

Types of Hemorrhage

• Capillary hemorrhage: slow oozing from a wound, typically caused by minor injuries, characterized by bright red, well-oxygenated blood, and usually stops quickly.
• Venous hemorrhage involves a quicker flow of dark, oxygen-depleted blood, generally stopping within minutes, but can be extensive due to the size and number of vessels.
• Arterial hemorrhage: rapid spurting of bright red, oxygenated blood from a wound, posing a significant risk of blood volume loss due to pressure and vessel size.

Hemostasis

• Vascular phase: blood vessel damage causes smooth muscle contraction, reducing blood flow by withdrawing the vessel into the wound, thickening the vessel wall, and decreasing the lumen size.
• Platelet phase: platelets aggregate and adhere to the injury site, rapidly slowing hemorrhage from capillaries and small vessels, though the resulting clot is unstable.
• Coagulation phase: clotting factors activate and release into the bloodstream, triggering a series of chemical reactions that form strong protein fibers (fibrin), creating a stable mesh that entraps red blood cells.

Factors Affecting Hemostasis

• Immediate immobilization of the wound site, such as splinting, aids the clotting process.
• Aggressive fluid therapy can negatively affect hemostasis.
• Hypothermia slows down and reduces the effectiveness of hemostasis.
• Certain medications, like aspirin, NSAIDs, clopidogrel, heparin, enoxaparin, warfarin, and dabigatran, can slow clot formation, increasing the risk of hemorrhage.

Hemorrhage Control: Internal Hemorrhage

• Internal hemorrhage can result from blunt and penetrating trauma, leading to capillary, venous, or arterial blood loss, with blood accumulating in interstitial spaces (contusion) or forming pockets (hematoma) between tissue layers.
• Large body cavities (chest, abdomen, pelvis) do not offer resistance to ongoing blood loss.
• Indicators of internal hemorrhage include localized injury signs/symptoms and early signs/symptoms of blood loss/shock.
• Tranexamic acid (TXA) is an antifibrinolytic that can reduce trauma mortality by mitigating fibrinolysis in patients with trauma-induced coagulopathy.
• Signs of internal hemorrhage may be present at body orifices.
  • Epistaxis, or mild to moderate hemorrhage within the nasal cavity.
  • Bright red blood vomited shortly after ingestion.
  • Coffee ground-like emesis indicates blood has been in the gastrointestinal tract for a while.
  • Hemoptysis is when bright red blood is coughed up, indicating lower respiratory injuries.
  • Potential accumulation of blood in the stomach results from upper digestive system injuries.

Classes of Hemorrhage

• Critical considerations include time elapsed since injury, the suspected class of hemorrhage upon initial contact, and the rate at which shock appears to be worsening.
• Class 1: up to 15% blood loss; compensated by healthy patients, maintaining constant blood pressure, pulse pressure, respiratory rate, and urine output.
• Class 2: 15-30% blood loss, compensatory responses are insufficient, leading to tachycardia, narrowed pulse pressure, diminished pulse strength, increased peripheral vascular resistance, and normal renal output.
• Class 3: 30-40% blood loss, compensatory mechanisms fail, resulting in pronounced tachycardia, falling blood pressure, barely palpable pulse, dyspnea/tachypnea, anxiety, restlessness, thirst, altered mental status, pale, cool, diaphoretic skin, declining urinary output.
• Class 4: more than 40% blood loss; pulse barely palpable in central arteries, rapid, shallow, ineffective respirations, extreme lethargy/confusion, progression towards unconsciousness, very cool, clammy, extremely pale skin, cessation of urinary output; survival is unlikely even with aggressive interventions.

Stages of Shock

• Compensated shock is the initial stage where the body progressively compensates for blood loss via increased pulse rate, decreased pulse strength, cool and clammy skin, anxiety, restlessness, combativeness, thirst, weakness, and air hunger.
• Decompensated shock begins when compensatory mechanisms fail, leading to an un-palpable pulse, precipitously dropping blood pressure, unconsciousness, and slowed/ceased respirations.
• Irreversible shock occurs shortly after decompensation, causing irreversible damage to cells, tissues, and organs, leading to patient death.

Etiology of Shock

• Hypovolemic shock results from a significant reduction in the cardiovascular system's volume, with hemorrhage being a common cause, but also fluid loss from other pathologies.
• Hemorrhagic shock is a specific type of hypovolemia caused by blood loss.
• Cardiogenic shock: impaireds cardiac function, which may present with MI or pulmonary edema signs/symptoms, as well as cool, pale skin; has a poor prognosis with an 80% mortality rate.
• Distributive shock includes:
  • Neurogenic shock: disruption in communication between the central nervous system and body; spinal/head injury; may not present with expected shock signs (tachycardia/rising diastolic BP), with warm, pink skin below the injury site and pallor, coolness, clamminess above it.
  • Anaphylactic shock: introduces histamine which results in drop in BP and High HR.
  • Septic shock: massive infection that releases toxins which impair blood vessels and blood distribution.
• Obstructive shock results from diminished lung sounds and spontaneous Pneumothorax.

Shock Management: Fluid Resuscitation

• The goal is to restore organ perfusion, not just blood pressure.
• Hemodynamically stable may involve patients with tachycardia, tachypnea, and decreased urine output and still be in shock.
• Normal hemodynamics do not always equate to adequate tissue perfusion.
• Patients in hypovolemic shock respond to IV fluids in one of three ways: rapid, transient, or minimal/no response.
• Use the largest catheter possible, inserted into a vein using a large-bore trauma or blood administration set, with catheter length and fluid pressure influencing fluid flow.
• The objective in the field is to stabilize vital signs for transport to a trauma center.
• Cautious monitoring of fluid volume is essential.

Temperature Control

• Hypothermia reduces the effectiveness of the clotting mechanism and exacerbate hemorrhage.
• Cover the patient with a blanket and keep the ambulance warm.
• Ensure infused fluids are well above room temperature.