Physiology, Trauma


Article Author:
Jenna Dumovich


Article Editor:
Paramvir Singh


Editors In Chief:
Jasleen Jhajj
Cliff Caudill
Evan Kaufman


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
2/12/2019 10:21:29 PM

Introduction

Although there are several different mechanisms of injury, trauma can be categorized broadly into three groups: penetrating, blunt, and deceleration trauma. There is a significant overlap in the causes, outcomes, and body’s response to the different types of injury. However, a common theme is the body’s activation of the autonomic nervous system. It is also important to note that each person responds differently to trauma and underlying chronic medical conditions can alter normal physiologic responses. There is another entity, trauma-induced coagulopathy which presents in trauma patients.

Cellular

Multiple complex pathways activate in response to damaged DNA, cellular stress, or infections. Here we will focus on the cellular response to mechanical trauma. Although there may be many mechanisms of traumatic injury to cells (physical damage or extreme temperature changes), the ultimate consequence is a loss of cellular integrity and function, eventually leading to cell death. Necroptosis is one mechanism in which cell death due to injury can occur and is the most studied. The pathway begins with TNF alpha binding to its receptor and subsequently leads to the "RIPotosome" formation. 

After TNF binding to its corresponding receptor, TRAF2 (TNF receptor-associated factor 2) and TRADD (TNF associated death domain protein) are signaled, which leads to the ligation of RIPK1 and RIPK3's recruitment.[1]  Of note, the "RIPotosome" can also spontaneously form without TNF alpha binding in response to trauma.[2] Once RIPK3 gets phosphorylated by RIPK1, it causes oligomerization of MLKL. The exact mechanism of MLKL remains someone of a mystery, but research proposes that MLKL disrupts the plasma membrane integrity via ion channels. The "RIPotosome" can be turned off via ubiquitination of RIPK1.[2]

Mechanism

  1. Penetrating trauma
  2. Blunt trauma
  3. Deceleration trauma 

Related Testing

When a patient arrives at the trauma center, it is vital to rule out life-threatening injuries as soon as possible and initiate necessary treatment. Commonly the preferred method of evaluation is the "ABCDE rule."

(1) Airway – ensure the patient has a patent airway while maintaining cervical spine stability

(2) Breathing

(3) Circulation and control of hemorrhage if applicable 

(4) Disability – evaluation of the patients mental status

(5) Exposure – removing all clothing items from the patient to obtain a full assessment.[3] 

Another exam modality commonly implemented in the emergency department when assessing a trauma patient is the focused abdominal sonogram for trauma or FAST exam. This exam uses ultrasound to identify free fluid in the abdomen. This exam is preferred over a CT initially due to time, feasibility, and accessibility. If the FAST exam is positive, then a CT is generally obtained.[4] Blood type and cross are also necessary in case a blood transfusion is warranted. Depending on the patient's initial evaluation and assessment further testing may be warranted.

Pathophysiology

Penetrating Trauma

A hypovolemic shock from penetrating trauma is one of the most feared consequences because if not treated promptly it can result in death. A patient in hypovolemic shock typically presents with hypotension, tachycardia, tachypnea, and cold skin. Acute blood loss means less circulating volume leading to decreased organ perfusion, which is dependent on arterial pressure. The most vulnerable organs of decreased perfusion are the kidneys, brain, heart, liver, and colon. In an attempt to maintain adequate oxygenation to the previously mentioned organs the body implements several processes. All of which, the mainstay is the autonomic nervous system. One goal is to maintain cardiac output (CO) defined by heart rate x stroke volume, which is achieved by activation of the SNS causing release of plasma catecholamines, such as vasopressin and norepinephrine, increasing the heart rate and thus CO. Another goal is to increase systemic vascular resistance (SVR); via the renin-angiotensin-aldosterone system. Renin is released by juxtaglomerular cells in response to a decrease in systemic blood pressure and a decrease in NaCl delivery to the macula densa. From there, renin subsequently converts to angiotensin I, angiotensin II, and aldosterone. In regards to hypovolemia, angiotensin II acts on blood vessels causing vasoconstriction, and on the hypothalamus to cause the release of anti-diuretic hormone leading to water reabsorption at the collecting ducts. Additionally, angiotensin II limits baroreceptor reflex bradycardia further aiding in the maintenance of CO.[5]  Each of these cascades are a component of the body’s response to hemorrhage to avoid shock.

Blunt Trauma

Blunt trauma is classified as a force striking the body, and its consequences are dependent on the location of the trauma. The most common cause and location of blunt force trauma in adults are abdomens after motor vehicle accidents. Solid organ blunt abdominal trauma includes the most commonly the liver, but also the spleen, and kidneys. Blunt trauma to the liver usually results in venous hemorrhage versus arterial and is managed conservatively. Pathophysiologic effects of hemorrhage are similar to penetrating trauma. Of note, the most common cause of traumatic injury to the spleen is blunt trauma.[6]

Internal hemorrhage is an obvious concern with blunt abdominal trauma, but inflammation accompanied by edema is a common underlying effect. There are four cardinal signs of inflammation mediated by different factors: redness, swelling, pain, and loss of function. In response to the traumatic injury mast cells are signaled to release histamine and bradykinin. Both of these mediators cause vasodilation and increased blood flow. Bradykinin also sensitizes nerve endings leading to pain The edema associated with acute inflammation occurs due to endothelial contraction and endothelial damage. The disruption of the endothelial lining of the vessels makes them “leaky” allowing a shift of fluid from postcapillary venules into the interstitial space.[7]

Neurologic injury can also be sustained by blunt trauma. Epidural hematomas, secondary to skull fractures, are caused by arterial rupture, most commonly the middle meningeal artery. The middle meningeal artery is located behind the pterion, which is thin, making it susceptible to injury. Since arteries are under high pressure, expansion of the hemorrhage occurs quickly versus a subdural hematoma which is under venous pressure. Expansion of the hemorrhage can eventually lead to an uncal herniation.[8] CN III palsy or a “blown” pupil is a common outcome of an uncal herniation and therefore an important clinical clue in diagnosis. Subdural hematomas also caused by traumatic injury are different from epidural hematomas in that it is due to rupture of the bridging veins.  

Deceleration Trauma

Deceleration trauma is an injury caused by a sudden stop in motion. Like the two previously discussed categories of trauma, deceleration trauma also affects different organ systems. Acceleration-deceleration injury to the brain resulting from the motion of the brain hitting one area of the skull and bouncing back hitting the direct opposite side of the brain on the other side of the skull.[9] This movement can result from both direct forces like direct head impact on the steering wheel in a motor vehicle accident or by non-contact forces like the shaken baby. After such an injury large amounts of neurochemicals and prostaglandins are released further exacerbating the deleterious effects. The aorta is also a potential site for deceleration injury causing traumatic aortic rupture; this most commonly occurs at the aortic isthmus due to its mobility, unlike the aortic arch which is relatively held in place by the brachiocephalic vessels to the thoracic inlet.[10]

Clinical Significance

It is essential to recognize the clinical signs as a result of trauma. For example, recognizing signs of blood loss such as tachycardia and hypotension as precursors for potential hypovolemic shock. Another warning sign would be single pupillary palsy post head trauma. The physical exam along with the patient’s history is pertinent to initiating the correct treatment. Missing these clinical clues can delay patient treatment and can lead to adverse outcomes including death.


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Physiology, Trauma - Questions

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A patient arrives at the emergency department. The patient was found on the sidewalk unresponsive. The patient has a blood pressure of 103/60 mmHg and is tachycardic. FAST exam is positive for free fluid, and he is started on IV fluids. Which is most likely to be elevated in this patient?



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A 16-year-old male hit his knee on the corner of his desk. Within seconds the area becomes erythematous, warm, and sensitive to the touch. What cell releases the cytokines responsible for the symptoms?



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A 28-year-old female presents to have sutures removed. The patient cut her hand while making dinner seven days ago. The wound appears to be healing well. There are no signs of infection. What initiated the pathway involved in the death of cells involved in the initial cut?



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A 38-year-old male is brought to the emergency department by his friend after being stabbed in the lower left leg. The patient is alert and oriented x 4 in moderate distress secondary to pain. The patient’s vitals are stable, and he is sent for a lower extremity radiograph. His cells that were affected directly by the trauma have undergone necroptosis. What structure is ultimately responsible for the ion changes seen within the plasma membrane?



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Physiology, Trauma - References

References

Martin JG,Shah J,Robinson C,Dariushnia S, Evaluation and Management of Blunt Solid Organ Trauma. Techniques in vascular and interventional radiology. 2017 Dec;     [PubMed]
Shrestha R,Khadka SK,Thapa S,Shrestha B,Shrestha SK,Ranjit S,Pradhan BB,Shakya YR,Lama D,Shrestha J, Improving Knowledge, Skill and Confidence of Novice Medical Doctors in Trauma Management with Principles of ABCDE. Kathmandu University medical journal (KUMJ). 2018 Jan.-Mar;     [PubMed]
Bloom BA,Gibbons RC, Focused Assessment with Sonography for Trauma (FAST) 2018 Jan;     [PubMed]
Kelley DM, Hypovolemic shock: an overview. Critical care nursing quarterly. 2005 Jan-Mar;     [PubMed]
Gabay C,Kushner I, Acute-phase proteins and other systemic responses to inflammation. The New England journal of medicine. 1999 Feb 11;     [PubMed]
Stienen M,Abdulazim A,Hildebrandt G,Gautschi O, [Emergency scenario: epidural hematoma - evaluation and management]. Praxis. 2013 Jan 30;     [PubMed]
Martin GT, Acute brain trauma. Annals of the Royal College of Surgeons of England. 2016 Jan;     [PubMed]
Balm R,Hoornweg LL, Traumatic aortic ruptures. The Journal of cardiovascular surgery. 2005 Apr;     [PubMed]
Grootjans S,Vanden Berghe T,Vandenabeele P, Initiation and execution mechanisms of necroptosis: an overview. Cell death and differentiation. 2017 Jul     [PubMed]
    [PubMed]

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