**3. Clinical evaluation**

The most important, and still very much essential, component of determining if a patient is in state of shock is the performance of an accurate clinical examination. There is no substitute for the judgment of an experienced clinician who is attuned to the most subtle manifestations of early (or compensated) shock.

The number one cause of death in the first hour after trauma is hemorrhage, and nearly 40% of all trauma related deaths are secondary to bleeding and its complications [8]. As such, hemorrhagic shock, a unique form of hypovolemic shock, has been the main focus of considerable trauma research and management applications, both in civilian and military settings. However, the astute and well-experienced clinician recognizes that trauma patients are not immune to other types of shock and that different types of shock are not mutually exclusive. Clinical manifestations of shock vary broadly and are based on the underlying etiology, the degree of organ perfusion, and previous organ dysfunction [9]. Understanding of the physical exam findings which may help differentiate between types of shock is a skill paramount to any clinician involved in trauma care. Proper attention to physical exam findings may guide initial therapy before other adjuncts such as imaging studies or laboratory measurements are available.

A complete, "head-to-toe" examination, such as is described for the secondary survey for trauma patients, will reveal multiple findings correlating with hypoperfusion of several organs. Altered mental status, manifesting as confusion, delirium, or coma, reveals decreased cerebral blood flow, most often at mean arterial pressures less than 50 mmHg [10, 11]. The differential diagnosis for any trauma patient who is altered must not only include traumatic brain injury or possible toxin ingestion but also take into account that this mental status change could be an initial presentation of shock. The cardiovascular system is one of the main players in the initial evaluation of shock. Sympathoadrenal stimulation typically causes an increase in heart rate. However, "misleading" heart rate might be present when managing high endurance athletes, geriatric patients, pregnant trauma victims, cardiovascular drug users, those with preexisting cardiovascular disease, or those in neurogenic shock [12–15]. Bradycardia, jugular venous distention, and new onset heart murmur might be present in cardiogenic shock [15, 16]. Distant/muffled heart sounds and pulsus paradoxus might be present in obstructive shock from cardiac tamponade [17]. Obstructive shock from tension hemothorax and/or pneumothorax might be evidenced by distant breath sounds, tracheal deviation, and hypotension [18, 19]. Dyspnea and hypoxia might clue the clinician in on a possible pulmonary embolus and obstructive shock.

**29**

*Resuscitation Endpoints in Traumatic Shock: A Focused Review with Emphasis on Point-of-Care…*

Classical teaching would presume that shock is associated to arterial hypotension. Although this might be prevalent in patients suffering from any etiology of shock, arterial hypotension may happen without shock, and hypoperfusion and organ ischemia may happen despite normal blood pressure. Increase in systemic vascular resistance, leading to pale or dusky skin, peripheral cyanosis, damage to small capillaries producing petechiae, decrease in temperature, and delayed capillary refill, is present in almost all forms of shock, except for distributive. Patients in "cold" shock almost universally have alterations in peripheral perfusion. Capillary refill, also termed peripheral perfusion status, can be an easy and rapid assessment of resuscitation status. Abnormal peripheral perfusion has been found to identify normotensive patients with more severe organ dysfunction and correlated with high lactate levels [20]. However, basing resuscitation solely on peripheral perfusion status would not be recommended as this was not found to improve mortality compared to lactate-based resuscitation in septic shock patients [21]. Initial respiratory alterations in shock include an increase in minute ventilation leading to hypocapnia and respiratory alkalosis. Increased work of breathing and attempted respiratory correction of metabolic acidosis, coupled with impaired respiratory muscle function from hypoperfusion, lead to respiratory failure. Although acute kidney injury is commonplace in patients suffering from shock, identifying oliguria requires insertion of a urinary catheter and measurement of output for at least 1 hour; both of these interventions are necessary yet timeconsuming. In the absence of prompt intervention, global hypoperfusion leads to failure of multiple organ systems and increases the morbidity and mortality

Rapid yet thorough physical examination can lead the clinician to institute therapy to alleviate different causes of shock. Cessation of hemorrhage and volume repletion are the most common maneuvers needed in the trauma bay. However, other culprits of shock are alleviated by, for example, prompt decompression of a tension pneumothorax or cardiac tamponade, rapid administration of fibrinolytic in massive pulmonary embolus, quick activation of the catheterization lab for myocardial ischemia, and fast initiation of vasoactive medications in the setting of heart failure, among others. Adjuncts to the physical exam, such as imaging studies and laboratory values, are valuable assets in the race against time during the manage-

In a study of over 2800 patients, a comparison of four different fundamental serum markers of acidosis was conducted (**Figure 1**) [23]. Although not the first published report of lactate being superior to other well-established serum markers, the authors were able to perform a unique side-by-side comparison of serum lactate versus three other common markers of metabolic acidosis—base deficit, anion gap, and serum bicarbonate [23]. The study demonstrated superiority of lactic acid (AUC, 0.75) and base deficit (AUC, 0.72) over the other indicators (bicarbonate

At-risk populations, including the geriatric patients and those with elevated comorbidity-polypharmacy scores (CPS), are at elevated risk of poor outcomes, including morbidity, mortality, and readmissions [24–27]. More specific to the context of trauma, patients with end-stage renal disease, severe peripheral vascular disease, and chronic respiratory failure may present with physiologically misleading vital signs, as evidenced by a study of >30,000 patients examining post-injury vital signs across various age groups [14]. In such setting,

*DOI: http://dx.doi.org/10.5772/intechopen.90686*

associated to shock [22].

ment of the patient in shock.

AUC, 0.68, and anion gap AUC, 0.66) [23].

**4. Serum lactate**

#### *Resuscitation Endpoints in Traumatic Shock: A Focused Review with Emphasis on Point-of-Care… DOI: http://dx.doi.org/10.5772/intechopen.90686*

Classical teaching would presume that shock is associated to arterial hypotension. Although this might be prevalent in patients suffering from any etiology of shock, arterial hypotension may happen without shock, and hypoperfusion and organ ischemia may happen despite normal blood pressure. Increase in systemic vascular resistance, leading to pale or dusky skin, peripheral cyanosis, damage to small capillaries producing petechiae, decrease in temperature, and delayed capillary refill, is present in almost all forms of shock, except for distributive. Patients in "cold" shock almost universally have alterations in peripheral perfusion. Capillary refill, also termed peripheral perfusion status, can be an easy and rapid assessment of resuscitation status. Abnormal peripheral perfusion has been found to identify normotensive patients with more severe organ dysfunction and correlated with high lactate levels [20]. However, basing resuscitation solely on peripheral perfusion status would not be recommended as this was not found to improve mortality compared to lactate-based resuscitation in septic shock patients [21]. Initial respiratory alterations in shock include an increase in minute ventilation leading to hypocapnia and respiratory alkalosis. Increased work of breathing and attempted respiratory correction of metabolic acidosis, coupled with impaired respiratory muscle function from hypoperfusion, lead to respiratory failure. Although acute kidney injury is commonplace in patients suffering from shock, identifying oliguria requires insertion of a urinary catheter and measurement of output for at least 1 hour; both of these interventions are necessary yet timeconsuming. In the absence of prompt intervention, global hypoperfusion leads to failure of multiple organ systems and increases the morbidity and mortality associated to shock [22].

Rapid yet thorough physical examination can lead the clinician to institute therapy to alleviate different causes of shock. Cessation of hemorrhage and volume repletion are the most common maneuvers needed in the trauma bay. However, other culprits of shock are alleviated by, for example, prompt decompression of a tension pneumothorax or cardiac tamponade, rapid administration of fibrinolytic in massive pulmonary embolus, quick activation of the catheterization lab for myocardial ischemia, and fast initiation of vasoactive medications in the setting of heart failure, among others. Adjuncts to the physical exam, such as imaging studies and laboratory values, are valuable assets in the race against time during the management of the patient in shock.
