Acute stress reaction

Acute stress reaction
Classification and external resources
Specialty psychiatry
ICD-10 F43.0
ICD-9-CM 308
MeSH D040701

Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASD is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.[1]

Signs and symptoms

The DSM-IV specifies that ASD must be accompanied by the presence of dissociative symptoms, which largely differentiates it from PTSD.

Dissociative symptoms include a sense of numbing or detachment from emotional reactions, a sense of physical detachment, such as seeing oneself from another perspective, decreased awareness of one’s surroundings, the perception that one’s environment is unreal or dreamlike, and the inability to recall critical aspects of the traumatic event (dissociative amnesia).[2]

In addition to the characteristic dissociative symptoms, ASD shares many of the symptoms with PTSD, including:

History

The term ASR was first used to describe the symptoms of soldiers during World War I and II, and it was therefore also termed combat stress reaction (CSR). Approximately 20% of U.S. troops displayed symptoms of CSR during WW II, and it was assumed to be a temporary response of healthy individuals to witnessing or experiencing traumatic events. Symptoms include depression, anxiety, withdrawal, confusion, paranoia and sympathetic hyperactivity.[2]

The APA officially included the term ASD in the DSM-IV in 1994, and prior to that, symptomatic individuals within the first month of trauma were diagnosed with adjustment disorder. According to the DSM IV, ASR refers to the symptoms experienced right after exposure to a traumatic event, up until 48 hours after it. In contrast, ASD is defined by symptoms experienced after 48 hours of the event, up until one month past the event. Symptoms experienced for longer than one month are consistent with a diagnosis of PTSD.[2]

Causes

There are several theoretical perspectives on trauma response, including cognitive, biological, and psychobiological. While the theories are PTSD-specific, they are still useful in understanding ASD, as both share many symptoms.[2]

Acute stress disorder (abbreviated ASD, and not to be confused with autism spectrum disorder) is the result of a traumatic event in which the person experiences or witnesses an event that causes the victim/witness to experience extreme, disturbing, or unexpected fear, stress, or pain, and that involves or threatens serious injury, perceived serious injury, or death to themselves or someone else. A study of rescue personnel after exposure to a traumatic event showed no gender difference in acute stress reaction.[3] Acute stress reaction is a variation of post-traumatic stress disorder (PTSD).

A recent study found that a single stressful event may cause long-term consequences in the brain. This result calls the traditional distinction between the effects of acute vs chronic stress into question.[4]

Pathophysiology

Stress is characterized by specific physiological responses to aversive or noxious stimuli.

Hans Selye was the first to coin the term “general adaptation syndrome”, to suggest that stress induced physiological responses proceed through the stages of alarm, resistance, and exhaustion.[5]

The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses in response to physical or psychological stress. The body’s response to stress is also termed “fight-or-flight response”, and it is characterized by an increase in blood flow to skeletal muscles, the heart and brain, a rise in heart rate and blood pressure, as well as dilation of pupils, and an increase in the amount of glucose released by the liver.[6]

The onset of an acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and to a lesser extent noradrenaline from the medulla of the adrenal glands. These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviors often related to combat or escape.

Normally, when a person is in a serene, unstimulated state, the "firing" of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signaling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes alert and attentive to the environment.

If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system (Thase & Howland, 1995). The activation of the sympathetic nervous system leads to the release of norepinephrine from nerve endings acting on the heart, blood vessels, respiratory centers, and other sites. The ensuing physiological changes constitute a major part of the acute stress response. The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis.

The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aids in response to an acute stress reaction. These two subunits are the sympathetic nervous system and the parasympathetic nervous system. The sympathetic response is colloquially known as the "fight or flight" response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands. the norepinephrine and epinephrine strike the beta receptors of the heart in order to feed the heart sympathetic nerve fibers to increase the strength of heart muscle contraction. as a result more blood is being circulated increasing the heart rate and respiratory rate. The sympathetic nervous system also stimulates the skeletal system and muscular system in an effort to pump more blood to those areas to handle the acute stress. Simultaneously the sympathetic nervous system inhibits the digestive system and the urinary system in order to optimize blood flow to the heart, lungs, and skeletal muscles. This plays a role in the alarm reaction stage. The para-sympathetic response is colloquially known as the "rest and digest" response, indicated by reduced heart and respiration rates, and more obviously by a temporary loss of consciousness if the system is fired at a rapid rate. The parasympathetic nervous system stimulates the digestive system and urinary system in order to send more blood to those systems to increase the process of digestion. In order to do this, it must inhibit the cardiovascular system and respiratory system in an effort to optimize blood flow to the digestive tract causing low heart and respiratory rates. parasympathetic plays no role in acute stress response (VanPutte Regan Russo 2014).[7]

Studies have shown that patients with ASD have overactive right amygdalae and pre-frontal cortices, both structures that are involved in the fear-processing pathway.[1]

Diagnosis

There must be a clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes or days but may occur up to one month after the stressor. In addition, the symptoms show a mixed and usually changing picture; in addition to the initial state of "daze," depression, anxiety, anger, despair, overactivity, and withdrawal may all be seen, but no one type of symptom predominates for long; the symptoms usually resolve rapidly in those cases where removal from the stressful environment is possible; in cases where the stress continues or cannot by its nature be reversed, the symptoms usually begin to diminish after 24–48 hours and are usually minimal after about 3 days.[8]

Treatment

This disorder may resolve itself with time or may develop into a more severe disorder such as PTSD. However, results of Creamer, O'Donnell, and Pattison's (2004) study of 363 patients suggests that a diagnosis of acute stress disorder had only limited predictive validity for PTSD. Creamer et al. did find that re-experiences of the traumatic event and arousal were better predictors of PTSD.[9] Medication can be used for a short duration (up to four weeks).

Studies have been conducted to assess the efficacy of counselling and psychotherapy for people with ASD. Cognitive behavioral therapy which included exposure and cognitive restructuring was found to be effective in preventing PTSD in patients diagnosed with ASD with clinically significant results at 6 months follow-up. A combination of relaxation, cognitive restructuring, imaginal exposure, and in vivo exposure was superior to supportive counseling.[10] Mindfulness based stress reduction programs also appear to be effective for stress management.[11]

In a wilderness context where counseling, psychotherapy, and cognitive behavioral therapy is unlikely to be available, the treatment for acute stress reaction is very similar for the treatment of cardiogenic shock, vascular shock, and hypovolemic shock; that is, allowing the patient to lie down, providing reassurance, and removing the stimulus for the occurrence of the reaction. In traditional shock cases, this is generally the relieving of pain from injuries or the stopping of blood loss. In an acute stress reaction, this may be pulling a rescuer away from the emergency to calm down, or blocking the sight of an injured friend from a patient.[7]

References

  1. 1 2 Reynaud, Emmanuelle; Guedj, Eric (2015). "Acute Stress Disorder Modifies Cerebral Activity of Amygdala and Prefrontal Cortex". Cognitive Neuroscience. 6: 39–43.
  2. 1 2 3 4 5 Bryant, R.; Harvey, A. (2000). Acute Stress Disorder: A Handbook Of Theory, Assessment, And Treatment. Washington, D.C.: American Psychological Association. pp. 3–40, 87–134.
  3. ↑ Ben-Ezra M.; Essar N.; Saar R. (2006). "Gender Differences and Acute Stress Reactions Among Rescue Personnel 36 to 48 Hours After Exposure to Traumatic Event". Traumatology. 12 (2): 139–142. doi:10.1177/1534765606294557.
  4. ↑ Musazzi L, Tornese P, Sala N, Popoli M (2016). "Acute stress is not acute: sustained enhancement of glutamate release after acute stress involves readily releasable pool size and synapsin I activation.". Mol Psychiatry. PMID 27698433. doi:10.1038/mp.2016.175. Lay summary.
  5. ↑ Butler, G. (1993). "Definitions of stress". Occasional Paper Royal College of General this is true. Practitioners. 61: 1–5.
  6. ↑ Widmaier, Eric P., (2015). Vander's Human Physiology: The Mechanisms Of Body Function. Boston: McGraw-Hill Education. p. 182. ISBN 9781259607790.
  7. 1 2 Isaac, Jeffrey E.; Johnson, David E. (2013). Wilderness and Rescue Medicine. Burlington, MA: Jones & Bartlett Learning. pp. 27–28. ISBN 978-0-7637-8920-6.
  8. ↑ Acute Stress Disorder
  9. ↑ Creamer M.; O'Donnell M.L.; Pattison P. (2004). "The relationship between acute stress disorder and posttraumatic stress disorder in severely injured trauma survivors". Behavior Research and Therapy. 42: 315–328. PMID 14975772. doi:10.1016/s0005-7967(03)00141-4.
  10. ↑ Lambert, M.J., (Ed.). (2004). Bergin and Garfield's Handbook of Psychotherapy and Behavioral Change. New York: Wiley
  11. ↑ Sharma M, Rush SE (Jul 2014). "Mindfulness-based stress reduction as a stress management intervention for healthy individuals: a systematic review". J Evid Based Complementary Altern Med. 19 (4): 271–86. PMID 25053754. doi:10.1177/2156587214543143.
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