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Traumatic Shock: the Fifth Shock Maighdlin W ADVANCED PRACTICE Traumatic Shock: The Fifth Shock Maighdlin W. Anderson , MSN, ACNP-BC, CCRN ■ Gregory A. Watson , MD, FACS based primarily upon its etiology—obstructive, cardio- ABSTRACT genic, hypovolemic, or distributive ( Table 1 ). 2 ,3 Although, historically, shock associated with traumatic injury has been evaluated through knowledge of the 4 recognized SHOCK TYPES shock patterns—cardiogenic, obstructive, distributive, and hypovolemic—many trauma practitioners view traumatic Hypovolemic Shock shock as a unique ffth shock pattern. Although secondary This is the most common type of shock present in trauma to a systemic infammatory response syndrome triggered patients and is generally due to acute blood loss. 2 by endogenous danger signals, traumatic shock represents a unique pathological condition that begins with multiple, Obstructive Shock usually blunt, trauma and may conclude with multiple organ In this type of shock, there is a physical obstruction pre- dysfunction syndrome and death. While varying mecha- venting blood from f owing into or out of the thoracic nisms of injury may lead to different presentations of shock vasculature from or to the rest of the body. Classic causes and cardiovascular decompensation, a unifying theme of in the trauma patient include tension pneumothorax and traumatic shock is an overwhelming inf ammatory response pericardial tamponade, while pulmonary embolus is the driven by proinfammatory cytokines, and the downstream prototype in noninjured patients. 2 results of this cytokine storm including, but not limited to, acute respiratory distress syndrome, coagulopathy, sepsis, Cardiogenic Shock and multiple organ dysfunction syndrome. Treatment is pri- This may appear very similar to obstructive shock, but it marily supportive; however, research into novel therapeutics is caused by mechanical cardiac dysfunction leading to an for traumatic shock is ongoing and promises some direction acute and signifcant decrease in cardiac output. The heart for future care. does not pump blood effciently, leading to a decrease in the mean arterial pressure as blood pools in the precardi- Key Words ac spaces (right atrium and periphery). 2 Myocardial infarc- MODS , SIRS , Traumatic shock tion and severe blunt cardiac injury are potential causes. Distributive Shock imply stated, shock is defned as a state of inad- This type of shock state results from widespread vasodi- equate oxygen delivery relative to the metabolic latation and encompasses septic, anaphylactic, and neu- needs of the host. This may result from either a rogenic shock. Unlike the other types defned earlier, dis- decrease in the amount of delivered components tributive shock does not present with decreased cardiac S(red blood cells, hemoglobin, and oxygen) or from output and is commonly referred to as “warm shock,” es- altered distribution of fow (depressed cardiac output and pecially in the early stages before compensatory functions vasodilatory states). Left untreated, this can lead to wide- fail. 2 Spinal cord injury and sepsis are classic examples. spread ischemia, and a systemic effort to compensate that Common causes of shock in trauma patients are listed often causes additional harm to the patient ( Figure 1 ). in Table 2 . In most cases, patients in shock can be de- The nature of the shock state stems directly from its etiol- scribed by one of the classic syndromes discussed earlier. ogy, and characteristic patterns of dysfunction and com- However, some trauma patients (particularly the multi- pensation may reveal the type of shock that is present. 2 ply injured) will display components of more than one Historically shock has been classifed into 1 of the 4 types if not all of these syndromes. Traumatic shock, the “f fth shock,” is increasingly recognized as a distinct syndrome Author Affi liations: School of Nursing (Ms Anderson) and School of with features overlapping many of the classic syndromes Medicine (Dr Watson), University of Pittsburgh, Pittsburgh, Pennsylvania . def ned earlier. 3 - 12 The authors declare no confict of interest. Correspondence: Maighdlin W. Anderson, MSN, ACNP-BC, CCRN, Department of Critical Care Medicine, University of Pittsburgh, 3550 CASE PRESENTATION Terrace St, Pittsburgh, PA 15261 ( [email protected] ). Mr Doe, a 15-year-old white adolescent boy, presented DOI: 10.1097/JTN.0b013e318286620a to emergency department via air ambulance following an JOURNAL OF TRAUMA NURSING WWW.JOURNALOFTRAUMANURSING.COM 37 Copyright © 2013 Society of Trauma Nurses. Unauthorized reproduction of this article is prohibited. JTN200200.indd 37 25/02/13 2:02 PM hemorrhage, multiple rib fractures, and a large pelvic he- matoma with active contrast extravasation. He was placed in a pelvic binder and taken emergently to interventional angiography where a completely disrupted right hypo- gastric artery was identif ed and treated with coil and Gel- foam embolization. He later became hemodynamically unstable after being transferred to the intensive care unit (ICU) and was transfused with several units of packed red blood cells as well as fresh frozen plasma, platelets, and cryoprecipitate for a developing coagulopathy. Repeat angiography failed to identify additional hemorrhage. He subsequently suffered a cardiac arrest, and an emergent left anterolateral throracotomy was performed, reveal- ing only a small amount of blood in the left chest and no pericardial tamponade. After internal compressions and defbrillation, he regained a perfusing rhythm and was taken to the operating room. At laparotomy, 400 to 500 cc of blood was evacuated from the peritoneal cavity. A minor hepatic laceration was noted but was not actively bleeding. A large retroperitoneal hematoma was identi- f ed but did not appear to be signifcantly larger than on Figure 1. Compensatory mechanism in shock often leads to fur- ther organ hypoperfusion and ischemia. From Ref. 1. Used with the initial computed tomographic scan. Mr Doe's abdo- permission from Striped Giraffe Press. CNS indicates central men was packed, and he was taken back to the ICU. nervous system. Over the next 17 days, he remained severely ill, and despite intensive support, he died from multiple organ all-terrain vehicle collision with a coal truck. He had been dysfunction syndrome (MODS). intubated in the feld. Initial hemodynamic instability was treated with fuids and uncrossmatched packed red blood BACKGROUND cells. Bilateral chest tubes were inserted, and there was What is striking about the clinical picture is the speed of no large hemo-/pneumothorax. The Focused Assessment onset and the apparent disconnect between clinical symp- With Sonography for Trauma examination result was neg- toms and root cause. A sharp drop in blood pressure may ative. Plain radiographs showed a right iliac wing and look exactly like acute hemorrhage, but diagnostics may bilateral rami fractures as well as an open (grade IIIb) show limited or no areas of bleeding. Systemic vasodila- tibia fracture with no active bleeding. His hemodynam- tation seems to signal the onset of sepsis, but no source ics normalized, and computed tomographic scans were of infection can be located, and the early onset follow- performed. Injuries included a traumatic subarachnoid ing injury makes infection less likely. There is no single TABLE 1 Nonunique Hemodynamic Pattern Associated With Traumatic Shocka Distributive Traumatic Hypovolemic Cardiogenic Obstructive CO MAP CVP PA PAOP ••• SVRI Warm/cold Warm Cold/warm Cold Cold Cold PP •• Abbreviations: CO, cardiac output; CVP, central venous pressure; MAP, mean arterial pressure; PA, pulmonary artery (pressure); PAOP, pulmonary artery occlusion pressure; PP, pulse pressure; SVRI, systemic vascular resistance index. aElements may mimic distributive and/or hypovolemic patterns during the evolution of the syndrome and depending on the primary etiology of the syndrome. 38 WWW.JOURNALOFTRAUMANURSING.COM Volume 20 | Number 1 | January–March 2013 Copyright © 2013 Society of Trauma Nurses. Unauthorized reproduction of this article is prohibited. JTN200200.indd 38 25/02/13 2:02 PM associated molecular patterns that drive the immune re- TABLE 2 Causes of Shock in the Trauma 14 - 16 a sponse. Patient Cause Pathophysiology PATHOPHYSIOLOGY AND CLINICAL MANIFESTATIONS Lost airway or pulmonary Inability of O2 to reach the injury circulation Systemic Inflammatory Response Syndrome Tension pneumothorax Diminished blood return to heart in Trauma The systemic inf ammatory response syndrome (SIRS) is Cardiac tamponade Diminished blood return to heart an innate response of the immune system to tissue injury and infection. Blunt tissue trauma leads to adenosine tri- Hemorrhage Inadequate oxygen-carrying capacity phosphate release from damaged epithelium, which in turn activates the complement system, resulting in a f ood Cardiac injury Inadequate pump function of proinf ammatory cytokines that, among other things, Spinal cord injury Inappropriate vasodilatation leads directly to systemic vasodilatation and oxygen-use 7,11,14,15,17 Inadequate pump function abnormalities. A secondary hypovolemic state en- sues, and hypoperfusion of end organs leads to further Poisoning Direct failure of cellular me- tabolism ischemia, pushing the body into anaerobic metabolism and increasing the lactic acid byproduct. Monocytes are Inappropriate vasodilatation considered the expression engines of a large number of Sepsis Inappropriate vasodilatation immunomodulators, including the proinf ammatory
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