INTRODUCTION

The diagnosis of posttraumatic stress disorder (PTSD) first appeared in 1980 in the third edition of Diagnostic and Statistical of Mental Disorders (DSM-III). It underwent some revision in 1987 in the revised third edition (SM-IV) defines it in six parts: (1) the person must have experienced, witnessed, or been confronted with an event involving death, serious injury, or a threat to the physical integrity of the self or others. (2) the traumatic event must be persistently reexperienced in the form of distressing images, thoughts, perceptions,dreams, or reliving; intense psychological or psychological reactivity may also be present since the trauma and numbing of responsiveness must be present since the trauma. (4) persistent symptoms of increased arousal should be present since the trauma. (5) duration should be at least four weks. (6) the disturbance should cause clinically significant distress in social, occupational, or other important areas functioning

Long-lasting states ad may adversely affect interpersonal relationships and development; exposure to the most extreme kinds of trauma (for example, pisoner-of-war and death camps) may result in partculary severe and persistent states of PTSD.

Group trauma and the loss of the community may complicate the course of PTSD, as may engagement in litigation and extensive media coverage. The media serve a constant and often uncontrolled reminders of the trauma and as evokers of negative affect. The nature of a particular trauma can be both of a pathological risk factor for PTSD and a determinant of symptom expression. For example, being extremely confined spaces, such as underground tunnels in wartime, can give rise to panic symptoms. Participation in abusive violence leads to a predominance of denial and numbing, whereas witnessin such acts as a nonparticipant result in a predominance of reexperining symptoms.

Social support consistently relates to the risk of developing PTSD. The presence of social support has a buffering affect; lack of support serve as a vulnerability factor. Lack of support can be a preexisting vulnerability fator, or it can develop when trauma victims become separated from their social support networks(for example, in a natural disaster or mass genocide).

Additional premorbid risk factors from epidemiological and treatment-seeking samples include a family history of psychiatric illness in general and of anxiety disorder in particular, previous psychiatric disorders, personality traits of high neuroicism and poor self-confidence, early separation of parents, parental proverty, behavioral misconduct in childhood, limited education, adverse life events before the trauma, being feamale, and the quantity of alcohol ingested.

Epidemiologic data identify the risk factors for exposure to trauma, as they are somewhat different from the risk factors for posttraumatic stress disorder once the trauma has occurred. One study found the six strongest predictors of exposure to trauma to be male sex, absence of a college education, extroversion, neuroticism, early misconduct, and family psychiatric illness. By contrast, the six strongest predictors for risk of PTSD are female sex, neuroticm, early separation for parents, prior anxiety or depression, familial anxiety, and familial anxiety, and familial antisocial personality disorder.

Knowledge of the causative and the risk factors of the disorder can guide the efforts at early recognition and prevention of the disorder.

The Clinical Picture of Post-Traumatic Stress Disorder

Symptoms experienced by individuals with post-traumatic stress disorder (PTSD) are identified in Figure 14-3. The three major features of PTSD are (1) re-experiencing the trauma through dreams and waking thoughts, (2) having emotional numbing to other life events and relationships, and (3) having symptoms of depression, poor concentration, and other cognitive difficulties.

PTSD has two subtypes: acute and chronic. The acute disorder is diagnosed when symptoms occur within six months of the trauma. The delayed or chronic type is diagnosed when the onset of symptoms is delayed at least six months. PTSD may occur following any psychologically traumatic event that is outside the range of usual experience. Such as military combat, natural disaster (e.g., floods or earthquakes), man-made disaster (e.g., car or airplane crashes, bombings, or torture), and crime-related events (e.g., assaults, muggings, robberies, rapes, or hostage-taking). After a devastating disaster, 50-80% of the survivors may experience PTSD (Kaplan and Sadock 1991)

Exposure to a highly traumatic event predisposes an individual to the development of PTSD and signals a potensial need for help in coming to terms with the experience. We learned all to well from the Korean and Vietnam wars that for combat veterans to resume a normal civilian life, they must come to terms with their war experiences. If resolution does not occur, PTSD can result. More recently, medical facilities are seeing more clients who have experienced sexual or physical abuse in childhood and are presenting with the same cluster of symptoms seen in PTSD (Schatzberg and Cole 1991). Particularly disturbing to clients are the intrusive symptoms, such as nightmares, flashbacks, an memories of traumatic events. Nightmares and flashbacks may be related to changes in catecholmine transmission, with the possibility existing that flashbacks are waking nightmares (Post-traumatic Stress: Part 1 1991).

The hypervigilance experienced by most individuals with PTSD creates its own set problems. PTSD victims seem to be attempting to prepare themselves for another traumatic event by being overly alert to danger. As a result, their bodies are in an almost permanent state of physiological arousal.

Because the symptoms of disorder are not as well defined as those of other an anxiety disorders, the disorder may go undiagnosed. The individual may seek relief by developing additional symptoms, such as physiological complaints (e.g., headaches, ulcers, or hypertension) or phobias, or by developing chemical dependence and abuse. Suicide attempts and intermittent psychothic episodes may occur, and problems axisting before the traumatic event, such as impulsiveness or antisocial tendencies, may be intensified.

Difficulty in interpersonal relationships almost always occurs and may be manifested in many ways. The PTSD victim frequently states that he or she has turned off feelings and is empty inside. The psychic numbing protects the client from feelings associated with intense stress. Avoiding emotional attachment may become a learned response to protect the individual from experiencing the pain of multiple losses stemming from, for example, combat or natural disasters. Thrill-seeking behavior may also be noted. Thrill seeking allows feelings to surface and aggression to be mobilized. Spouse and child abuse may occur as part of PTSD. Struggles with bosses, family, and coworkers are frequent themes, as is having difficulty trusting others. The last is a recurrent theme among rape victims.

ETIOLOGY

PTSD is one of only a few disorders in DSM-IV that is defined by its cause. Without a stressor, the disorder cannot exist, but the trauma is not sufficient; many traumatized people do not have the disorder. The relative importance and the predisposing elements of the trauma are not clearly understood; the same is true for other causative factors. An interactive relation may exist between one even and one victim. At all events, no model of the cause of PTSD would be complete unless it took into account pretrauma (that is, personal vulnerability), trauma (stressor characteristics), and posttrauma variables.

A. STRESSOR
A consistent relation emerges between the magnitude of the stress exposure and the risk of PTSD. The relation holds true across several kinds of trauma, including combat, homicidal crime, and sexual trauma. No evidence suggests that a certain threshold of severity must be met, nor does good evidence suggest that low-magnitude stress (for example, divorce, loss of income, chronic illness in the family) gives rise to PTSD to any appreciable extent.
Besides the events involving actual or threatened death or injury or a threat to the physical integrity of the self or others, cognitive appraisal factors are probably important. For example, one study noted that a rape victim’s perception of being in a safe place at the time of the assault predicted high levels of symptoms. The experience of being intensely afraid, helpless, or horrified is a likely risk factors. Extreme shame or guilt may also be a risk factor, as in the participants in a brutal atrocity.

B. BIOLOGICAL FACTORS
Numerous psychophysiological and neurochemical systems appear to be implicated in PTSD. Although not proved, the assumption is that changes in those systems were absent before the trauma and that the trauma itself is the inciter of short-term and long-term functional and structural changes. Some indirect evidence supports the contention.

1. Sympathetic activity
Several studies show that enduring autonomic arousal exist in chronic PTSD arising from both civilian and military trauma. Elevated heart rate and elevated 24-hour urinary catecholamines both suggest increased sympathetic tone. Comparable with that interpretation are findings of lowered platelet monoamine oxidase (MAO) acticity and of α-adrenoreceptor activity. However, there is some debate as to whether tonic increases of catecholamines are present in PTSD once the duration of baseline is taken into account. Studies which employed longer baseline rest periods did not find an increase in norepinephrine.
Further evidence of abnormal noradrenergic functioning in PTSD comes from studies which show increased psychophysiological reactivity to yohimbine (Yocon), an α2 antagonist. Symptoms of PTSD are increased when yohimbine is given to patients with PTSD.
Heightened sympatethic arousal in combat veterans with PTSD is seen when they are exposed to reminders of their original trauma, as shown by heart rate, blood pressure, electromyography, and sweat activity. Enduring arousal in response to combat cues occurred in veterans with PTSD but not in combat veterans without PTSD but with other forms of anxiety. That finding confers a specificity to the diagnosis that allows the conclusion that cue-specific arousal in PTSD is more than a nonspecific index of anxiety-proneness. Recent studies have indicated a promising application of that paradigm to the diagnosis of PTSD as part of a multimodal assessment. Enduring arousal is accompanied not only by anxiety but also by anger and depression. The fact that those emotions may be primal can be taken to support the view that PTSD is best classified not as an anxiety disorder but in separate category.

2. Neuroendocrine functions
Several studies have examined hypothalamo-pituitary-adrenal (HPA) function in PTSD. Both reduced and elevated levels of 24-hour urinary cortisol have been reported, an inconsistency that has not been satisfactorily resolved. Possible explanation include (1) differences in the collection or assay procedure, (2) differences in the type of PTSD, and (3) differences in the symptomatic state (that is, acute exacerbation versus chronic stable symptoms). One study found basal plasma cortisol to correlate with increased PTSD severity; lowered cortisol may bespeaks a pattern of denial. Therefore, conceivable some people with the disorder have decreased guilt and relative lack of denial and, perhaps, increased urinary cortisol levels.
One study found a blunted adrenocorticotropic hormone (ACTH) response after a challenge with corticotrophin-releasing hormone (CRH). That finding was correlated with PTSD symptom severity but not with depression severity, suggesting a specific relation between PTSD symptoms and HPA axis dysfunction.
Recently, some researchers found a supersensitivity and an increase in glucocorticoid receptors in combat veterans with PTSD. Furthermore, a relation was found between HPA axis dysfunction and the disorder’s symptom severity.

3. Other biological factors
Opioid system abnormalities, including a naloxone (Narcan)-reversible analgesia in combat veterans who were exposed to remainders of trauma, have been seen. The degree of analgesia so induced was comparable to the analgesia produced by an 8 mg dose of morphine sulfate. The full relevance of such findings is unclear; perhaps the numbing and dissociative components of PTSD are mediated by changes in the opiate system.
Animal models and the clinical effects of fluoxetine (Prozac) in PTSD both suggest that serotonin is implicated. In further support is evidence that some serotonin agonists can evoke symptoms of PTSD in combat veterans with that diagnosis.
Abnormal event-related potential (ERP) indices of information processing have been found in PTSD, indicative of problems distinguishing target and distractor (that is, relevant and irrelevant) stimuli. Those may form the basis of concentration and memory impairment, and be reflective of an underlying noradrenergic fault.

4. Sleep studies
Studies of prisoners of war from Wolrd War II, 30 years after their exposure to trauma, and studies of Vietnam veterans with PTSD have revealed increased rapid eye movement (REM) sleep and decreased stage 2 sleep. Following treatment with doxepin (Adapin), REM sleep measures were reduced, while the restorative stages 3 and 4 sleep increased.
Of importance to the separation of PTSD from major depressive disorder is the fact that the REM alterations of PTSD do not share many of the characteristics found in major depressive disorder, such as shortened latency or increased early sleep REM.

C. PSYCHOLOGICAL FACTORS
Three relevant psychological models – based on psychodynamic, cognitive and information-processing, and behavioral theories – have been advanced.

1. Psychodynamic theory
Sigmund Freud and other early analysts made several attempts to explain the symptoms and the cause of traumatic neurosis. An early formulation contended that trauma revives the original childhood neurosis through regression. Later, an energy model was postulated in which a strong external trauma causes a disturbance in the organism’s energy. The stimulus barrier or protective shield is exceeded. Defensive mechanisms, such as repression of the event and undoing (in dreams and compulsive repetition of the trauma), are the ego’s attempts to cope with the event and to drain off excess energy. Fixation on the trauma is important to the theory. Severe trauma with a chronic course and a poor response to treatment may lead to two unmodifiable ego changes: ego exhaustion and changes in the ego-superego boundary as a result of overwhelming guilt and shame.
Other analysts revised the concept of a stimulus barrier, changing it from a passive shield to an active attempt by the ego to protect itself against traumatization: The trauma must be understood in terms of the person’s psychic reality and how the person interprets and the reacts to the experience. Psychic trauma may result in the person’s being overwhelmed with emotion and becoming terrified of the emotion’s uncontrollable elements. The central role of affect in the theory explains such phenomena as affective blocking, alexithymia, and chronic depression.

2. Cognitive and information-processing theory
After severe stress some persons are unable to process and assimilate the event adequately or to deal affectively with its effects. Because trauma may require its victims to make unaccustomed changes in their plans, satisfactory assimilation of the experience may be difficult, prolonged, and sometimes incomplete. Unfortunately, the experience is kept alive as an active memory and repeatedly intrudes into awareness. Because such experiences are painful, the person attempts to deny or to avoid the experience; by such avoidance, levels of anxiety may be reduced. In PTSD, those intrusive and avoidance phases alternate. The degree of distress, the impact of the event, can be measured by a 15-item self-rating scale.
Information-processing models have been invoked to account for the development of the disorder. Fear may be stored as a memory network that contains information about danger-related stimuli. Because life-threatening trauma evokes a powerful response, that particular fear structure remains intense and easily activated. Distinctions between what is safe and what is dangerous are unclear, and persons who are strongly influenced by such fear structures may feel both lack of control and lack of predictability with respect to their environments.

3. Behavior theory
Behavior theory posits a two-factor learning process in PTSD. In the first phase, persons exposed to a trauma (the unconditioned stimulus) learn by association to be upset by central events, images, thoughts, or situations that occur in proximity to the trauma (the conditioned stimulus).
Instrumental learning leads to the second factor, avoidance of both the unconditioned stimulus and the conditioned stimulus; that process is sustained because it leads to a decrease in anxiety. High-order conditioning occurs; ultimately, a wide range of stimuli elicit arousal (stimulus generalization). Although the two-factor theory has been criticized, it provides a theoretical basis for treating PTSD by means of direct therapeutic exposure to cues of the original trauma, an approach that may be beneficial.

NURSING PROCESS FOR CLIENT WITH POST TRAUMATIC DISORDER

Focus:
For the client who develops fear, terror, dread, or helplessness following exposure to a traumatic event (rape, war, natural disaster, abuse, experiencing or witnessing serious trauma or violence). Symptoms range from emotional “numbness” to vivid nightmares in which the traumatic even is recalled.
NOC:
Suicide self-restraint, Anxiety level, Fear level, Abuse recovery, Emotional, Physical or Sexual, Coping, Depression level, Impulse self-control.
NIC:
Suicide prevention, Anxiety reduction, Anger control assistance, Simple relaxation therapy, Coping enhancement, Mood management, Support system enhancement.

ASSESMENT DATA

Related factors (Etiology)

· Overwhelming anxiety secondary to:

o War experiences/military combat

o Natural disaster (earthquake, hurricane, tornado, flood)

o Personal assault (rape, incest, molestation, beatings, abuse)

o Kidnap of self or significant others

o Catastrophic illness or accident

o Prisoner of war death camp hostage experiences

o Learning of a loved one’s serious accident, injury, or maiming

o Destruction of home or valued resources

o Witnessing a serious accident or act(s) of violence (car crash, building collapse, mother being beaten, killing of family member)

o Viewing a scene in which there are dead and/or maimed bodies (aftermath of war, plane or train crash, earthquake)

o Threat to physical and emotional integrity (all of the above)

Defining Characteristics

· Client relates frequent intrusive recollection of past traumatic experience.

· States that recollections are accompanied by feelings of dread, terror, helplessness, powerlessness, cardiac palpitations, shortness of breath, and other symptoms of emotional physical reactivity.

o “I feel out of control and terrified when I recall the event”

o “I get out of breath and my heart beats faster and faster”

o “I have a sense of doom, as if something terrible is going to happen”

· Describes recurrent dreams or nightmares in which vivid details of traumatic event are relived or reenacted.

o “I had another horrible nightmare last night and went through the same trauma and anxiety all over again”

· Express feelings of “numbness” detachment, or loss of interest toward people and the environment (generally occurs immediately after the traumatic event)

· Demonstrates avoidance or lack of responsiveness toward stimuli associated with the traumatic event (in rare instances, may experience psychogenic amnesia)

o A war veteran avoids hospitals, injured persons, bandages, and blood.

o An accident victim demonstrates a flat affect while listening to a news report describing a traumatic event.

· Demonstrates symptom of psychogenic reactivity (anxiety symptom) when exposed to events that resemble or symbolize the original trauma.

o A young woman develops fear, dread, or terror when she attempt sexual intimacy with her partner because it reminds her of when she was raped.

o A prison camp victim experiences sympathetic nervous system stimulation (rapid heart rate, shortness of breath, nausea, diarrhea) while sitting in a cell-sized room.

o A war veteran who fought in a hot, humid climate experiences dread or terror when exposed to similar weather many years later.

· Demonstrates symptom of increased arousal (inability to fall asleep or remain asleep, hypervigilance, exaggregated startle response).

· Manifest unpredictable episodes of explosive anger or aggression.

· Verbalize inability to concentrate or complete task.

o “I’m too distracted to make my bed or go to an activity”

o “I can’t concentrate on my craft”

o “I can barely shower and groom myself”

· Relates inability to express angry feelings.

o “I feel as if I might explode, but I can’t let it out”

o “I can’t begin to express my anger”

· Expresses thoughts of self-blame and guilt regarding a traumatic event.

o “If only I had locked the door, it wouldn’t have happened”

o “If I had been there on time, it wouldn’t have occurred”

· Verbalizes anger at others for perceived role in traumatic event.

o “If they had helped more, he wouldn’t have lived”

o “If they have called for help right away, I wouldn’t be so badly injured”

DIAGNOSIS AND CLINICAL FEATURES

In the immediate aftermath of trauma, a polymorphic symptom picture may emerge; the full complex of PTSD may not appear until several weeks later. A marked level of dissociation may be seen within the first few days of exposure to an extreme trauma, giving rise to the clinical diagnosis of acute stress disorder, which was introduced in DSM-IV for the first time. In other instances no clear-cut symptoms may emerge until some later time, when PTSD appears as a delayed response. Yet other manifestations may develop in which only some elements of PTSD appear, such as intrusive and arousal symptoms.

The stressor must meet two criteria : (1) be life-threatening or associated with serious injury or threat in physical integrity; and (2) evoke intense fear, helpness, or horror in the victim.

Symptoms are grouped into three categories (1) intrusive, painful, persistent, and recurrent reexperiencing of the trauma (the B criteria); (2) persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (the C criteria); and (3) persistent increased arousal that was not present before the trauma (the D criteria). Besides being conversant with the symptoms themselves, an assessor of PSTD must pay attention to the qualifying adjectives: “persistent,” “recurent,” and “distressing.” The assessor must also decide whether or not numbed responsiveness and hyperarousal occurred subsequent to teh taruma. In cases of chronic PSTD and in cases of early traumatization, ariving at such judgments is not easy; indeed, the validity of such a construct can be questioned when traumatic events like incest and childhood abuse were the causes of PSTD. Unless proper attentions is given to those points, PSTD may be overdiagnosised.

At least one of five possible intrusive symptomps is quired for B criteria, which represent the essential and distinctive set of symptomps by which represent the essential and distinctive set of symptomps by which represrnt the essential and distinctive set of symptomps by which PSTD is distinguished from all other forms of anxiety and depression.

At least three of seven possible avoidance (C criteria) symptomps are required. The first three criteria – (1) avoiding throughts or feelings associated with the trauma; (2) avoiding activities, situations, or play associated with the trauma; and (3) inability to recall an important aspect of trauma- specifically relate to the trauma. Teh remaining four criteria are not specific to PSTD and may be found in other disorders, such as depression. Both avoidance and numbing are required for the diagnosis.

At least two of five possible hyperarousal symptomps (D criteria) are requide. Those symptomps may also be seen in other disorder, such as generalized anxiety disorder.

On the basis of literatur surveys, no compelling reason lead one to believe that the symptomps picture differs substantially according to teh age, sex, or ethicity of the patient or teh type of trauma. However, somatic expressions of PSTD may be seen more commonly in populations from others cultures, as well as in children. A number of associated symptomps can occur and may prove important in the tretment of individual patients. Those symptomps include survival and teh behavioral guilt, somatic distress, paranoia, interpersonal alienation alienation, and the vegetative changes of depression. Victimes of prologed interpersonal abuse can inhibite impaired modulation of affect, impulsivebehavior, and feelings of ineed on studies of combat veterans.ffectiveness and hopelessness.

Outcome Criteria

· Clients verbalizes awareness of psychologic, and psychologic symptom of anxiety that accompany recollections of a past-traumatic event.

· Identifies situation/event/images that trigger recollections and accompanying responses of past traumatic experiences (small or enclosed spaces, hot or cold climate, argument or fight, sexual intimacy)

· Communicates and interacts within the milieu to control and manage anger and relieve thoughts of self-blame and guilt.

o Communicates thoughts/feelings to a trusted person.

o Problem solves source of thoughts/feelings.

o Participates in group activities.

o Engages in physical activities/exercise.