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Emergency Medical Services


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department, hypotension may be treated with boluses of phenylephrine or epinephrine [69]. Prehospital “push dose” vasopressors increase blood pressure but may increase mortality [70, 71]. Further research is necessary to identify the appropriate patient population, agent, and dose for prehospital push dose vasopressors.

      Other Medications

      Other agents used for shock resuscitation include corticosteroids, antibiotics, and inotropic agents [72–74]. The role of these agents in out‐of‐hospital shock management remains unclear. It would be reasonable to administer steroids to shock victims with known adrenal insufficiency or chronic steroid use and refractory hypotension.

      Shock Science

      The lack of definitive studies on the treatment of shock by EMS clinicians leaves the medical director without clear guidelines for treating these patients. As a result, considerable controversy exists with respect to many areas of the treatment of shock (especially traumatic shock) in the prehospital setting.

      The benefit of an EMS procedure must be weighed against potential risks. A major pitfall associated with shock treatment is that resuscitative interventions may delay definitive care. Pantridge and Geddes demonstrated that some aspects of definitive care, such as defibrillation and arrhythmia management, should be delivered in the field [75]. However, for trauma victims with uncontrolled internal hemorrhage, definitive care can only be provided in the hospital. Any field procedure that significantly delays delivery of definitive care must have proven value. For example, pneumatic anti‐shock garments were implemented in clinical EMS practice without supporting evidence, and then a formal assessment revealed that they actually worsened patient outcome in certain circumstances, particularly thoracic injury [76].

      Sepsis

      There are multiple challenges associated with identifying sepsis in the prehospital setting. EMS clinician knowledge and understanding of the condition is the first barrier [83]. EMS protocols may include the presence of hypotension, respiratory distress, and altered mental status as criteria for invoking sepsis protocols. However, these findings may be missing in the prehospital patient with sepsis [79, 84, 85]. While hypotension and fever are typical findings in septic patients, their presence is often missed in the prehospital setting [79, 86]. In addition, patients with alterations in physiological variables identified in the emergency department may have had normal vital signs in the field [79]. The lack of diagnostic tools in the field (e.g., point‐of‐care lactate, white blood cell count, urinalysis, chest x‐ray) makes the diagnosis of sepsis and determining a potential source of infection more challenging in the field. Of note, ETCO2 has been proposed as a surrogate for serum lactate levels. Inversely correlating with serum lactate, lower ETCO2 levels have been identified in patients with serious penetrating trauma and sepsis [32,87–89]. Finally, attempts at developing prehospital scores or tools to identify patients with sepsis have had mixed results [82,90–92]. In general, there is considerable variation in the sensitivity for EMS identification of sepsis, and EMS clinician impression alone is poor in the identification of these patients [93].

      The emergency department care of the septic patient includes the early initiation of goal‐directed volume resuscitation and early antibiotics [30, 81]. Vasopressors are initiated for fluid refractory hypotension or in patients with fluid overload, to maintain a mean arterial pressure of 65‐70 mmHg. The role of empiric antibiotics in the field for presumed sepsis has yet to be defined and antibiotic administration is not in the scope of practice for many EMS clinicians. Fluids, vasopressors, and hemodynamic monitoring (vital signs) are generally achievable in the prehospital setting.

      A prehospital protocol for the treatment of patients with suspected sepsis not in congestive heart failure may include repeat fluid boluses of 500 mL, with reassessment between each bolus for blood pressure responsiveness and signs of respiratory distress secondary to fluid overload [85, 87]. While crystalloids are the fluid of choice for the initial resuscitation of the septic patient, balanced salt solutions (e.g., lactated Ringer’s) may be preferred over normal saline [94]. The solution used for resuscitation will often be directed by what is carried on the ambulance. Prehospital fluid administration of any volume and even IV placement alone have been associated with decreased odds of in‐hospital mortality [95]. In patients with hypotension secondary to sepsis, prehospital administration of fluids resulted in a lower in‐hospital mortality as compared to those without hypotension, but longer scene times resulted [93].

      Vasopressors are an important part of the treatment of sepsis. Norepinephrine, epinephrine, and vasopressin can be used as single agents or in combination [96]. However, the use of dopamine is associated with increased mortality in septic shock [96]. Unfortunately, the administration of these vasoactive agents is best done via medication pumps. These pumps are expensive, require additional training for EMS clinicians, and are not in the scope of practice for some.

      Despite the many challenges, patients identified with sepsis in the prehospital setting have a decreased mortality compared with patients diagnosed later in the hospital [78, 82, 97]. There are three key steps for EMS to improve sepsis‐related outcomes: 1) Maintain high suspicion and recognize the potential for sepsis; 2) Initiate resuscitation with IV fluids; and 3) Provide a prehospital sepsis alert to the receiving hospital well before arrival. Improving identification of patients with serious infections may include a combination of EMS clinician impression along with physiological factors. Simply identifying potential patients with sepsis and alerting and transporting to the most appropriate facility – analogous to the care of myocardial infarction, trauma, and stroke – can improve survival.

      Hemorrhagic Shock

      Hemorrhage is a common cause of shock among trauma victims. Field clinical trials have suggested that volume resuscitation before controlling hemorrhage may be detrimental [36, 49,56–58, 60]. Possible mechanisms for worse outcomes include dislodgement of clot, dilution of clotting factors, decreased oxygen‐carrying capacity of blood, hyperchloremic metabolic acidosis, and exacerbation of bleeding from injured vessels in the thorax or abdomen.

      Controlling external hemorrhage is essential for maintaining vascular volume. Direct pressure is usually sufficient to control external bleeding. Military and civilian experience suggests that tourniquets should be used early and liberally [98]. An assortment of topical hemostatic materials to be placed directly on the bleeding wound also exists [98–101] (see Chapter 35).

      Studies in Houston and San Diego suggest that mortality following traumatic hemorrhage is not influenced by prehospital administration of fluid [57, 59]. Survival to hospital discharge rates were not significantly different for patients receiving fluids versus patients not receiving fluids in the field. Both studies were performed in systems with relatively short scene and transport times.

      As discussed above, currently EMS clinicians are taught to administer only enough IV or IO fluids to restore a peripheral pulse or to reach a systolic blood pressure of 80–90 mmHg. However, the optimum target blood pressure for these patients remains undefined. Trauma victims with isolated head injuries who receive excessive fluids may develop worsened cerebral swelling. In addition, excess fluids may precipitate congestive heart failure in