Reaksi Stres Akut
Published on September 10, 2026
Risk Factors
Prior psychiatric vulnerability, poor coping mechanisms, physical exhaustion, extremes of age, pre-existing organic conditions (e.g., head injury), social isolation, repeated prior trauma exposure
Etiology
Exposure to an extraordinary physical or mental stressor (natural disaster, accident, assault, rape, combat, sudden bereavement, fire)
Presentation
A patient who was functioning normally, then experienced an overwhelming stressor and within minutes to immediately after develops a "dazed" state with fluctuating emotional and autonomic symptoms
Classic Exam
Initial daze (narrowed attention, inability to process stimuli, disorientation), tachycardia, diaphoresis, hyperventilation, tremor, facial flushing or pallor; rapidly shifting affect between anxiety, anger, withdrawal, and overactivity
Diagnostics
Clinical diagnosis only. No confirmatory lab or imaging test. Diagnosis rests on: (1) clear temporal link to stressor, (2) onset within minutes, (3) symptom resolution within hours if removed from stressor, or within 3 days maximum if not
Management
Psychological first aid, removal from stressor environment, brief supportive psychotherapy, short-term low-dose benzodiazepines only if severe autonomic or agitation symptoms; no long-term pharmacotherapy indicated
Keywords
"Extraordinary stressor," "onset within minutes," "daze/terpaku," "mixed fluctuating symptoms," "resolves within 3 days," "no single symptom dominates"
01Pathophysiology
Acute Stress Reaction is the mind's immediate, transient response to an overwhelming stressor that exceeds normal adaptive capacity. The PPDGJ-III emphasizes that the stressor must be "luar biasa" (extraordinary), meaning it is not a routine life difficulty but rather an event of exceptional severity such as a natural disaster, serious accident, or violent assault.
When an individual encounters such a threat, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic-adrenal-medullary system activate simultaneously. The hypothalamus releases corticotropin-releasing hormone (CRH), which triggers ACTH secretion from the anterior pituitary, ultimately driving a surge of cortisol from the adrenal cortex. In parallel, the sympathetic nervous system stimulates the adrenal medulla to release epinephrine and norepinephrine, producing the classic fight-or-flight response: tachycardia, diaphoresis, tremor, and hyperventilation.
The initial "daze" (terpaku) state described in PPDGJ-III reflects a dissociative narrowing of consciousness. The prefrontal cortex, overwhelmed by amygdala-driven threat signaling, temporarily loses its capacity for integrative processing. This explains why the patient appears stunned, has narrowed attention, and cannot fully comprehend the surrounding environment. This is not confusion from an organic cause but rather a protective psychological mechanism.
The mixed, fluctuating symptom picture (depression, anxiety, anger, disappointment, overactivity, withdrawal) occurs because the limbic system is in a state of dysregulated arousal. No single emotional circuit dominates for a prolonged period, which is why the PPDGJ-III explicitly states that no one symptom should dominate the clinical picture for long. This fluctuation is itself a diagnostic feature.
The rapid resolution (hours to a maximum of 3 days) occurs because the stressor is acute and self-limited. Once the threat is removed, cortisol feedback loops normalize HPA axis output, parasympathetic tone is restored, and the prefrontal cortex regains executive control. Individual vulnerability and coping capacity (kerentanan individual dan kemampuan menyesuaikan diri) directly influence how quickly this normalization occurs.
02Classification and Clinical Manifestation
The PPDGJ-III does not subdivide Acute Stress Reaction into formal subtypes, but the symptom domains and their temporal course can be organized as follows:
Initial phase (Daze)
Timing
Within minutes of stressor
Predominant Features
Narrowed consciousness, reduced attention, inability to comprehend stimuli, disorientation, psychomotor retardation or stupor
Mixed affective phase
Timing
Minutes to hours
Predominant Features
Fluctuating symptoms: depression, anxiety, anger, irritability, disappointment, despair; no single symptom dominates
Autonomic arousal phase
Timing
Concurrent with affective symptoms
Predominant Features
Tachycardia, diaphoresis, tremor, hyperventilation, facial flushing/pallor, nausea, dry mouth
Behavioral phase
Timing
Variable
Predominant Features
Either withdrawal (social isolation, mutism, immobility) or overactivity (agitation, purposeless motor activity, flight reaction)
Resolution phase
Timing
Hours (if removed from stressor) to maximum 3 days (if stressor persists)
Predominant Features
Gradual return to baseline; symptoms begin to diminish after 24-48 hours if stressor is ongoing
Phase | Timing | Predominant Features |
|---|---|---|
Initial phase (Daze) | Within minutes of stressor | Narrowed consciousness, reduced attention, inability to comprehend stimuli, disorientation, psychomotor retardation or stupor |
Mixed affective phase | Minutes to hours | Fluctuating symptoms: depression, anxiety, anger, irritability, disappointment, despair; no single symptom dominates |
Autonomic arousal phase | Concurrent with affective symptoms | Tachycardia, diaphoresis, tremor, hyperventilation, facial flushing/pallor, nausea, dry mouth |
Behavioral phase | Variable | Either withdrawal (social isolation, mutism, immobility) or overactivity (agitation, purposeless motor activity, flight reaction) |
Resolution phase | Hours (if removed from stressor) to maximum 3 days (if stressor persists) | Gradual return to baseline; symptoms begin to diminish after 24-48 hours if stressor is ongoing |
Severity Spectrum
Severity | Description |
|---|---|
Mild | Criteria for daze state met but only autonomic symptoms are prominent (tachycardia, diaphoresis); functional impairment is minimal |
Moderate | Daze plus at least two additional symptoms from the mixed affective/behavioral domain (e.g., anxiety + withdrawal); social functioning clearly impaired |
Severe | Marked dissociative stupor or severe agitation/flight reaction; patient may be unresponsive or dangerously hyperactive; autonomic symptoms are prominent |
03Diagnostic Workup
Structured clinical interview
Role
Best initial and confirmatory "test"
Expected Finding
Clear temporal link between extraordinary stressor and symptom onset within minutes; mixed fluctuating symptoms; no single dominant symptom; resolution trajectory within 3 days
Mental Status Examination (MSE)
Role
Core assessment
Expected Finding
Altered consciousness (daze), labile affect, variable psychomotor activity, intact orientation once daze clears
Physical examination
Role
Rule out organic cause
Expected Finding
Autonomic hyperarousal signs (tachycardia, elevated BP, diaphoresis) without evidence of head trauma, intoxication, or medical illness explaining the presentation
Basic labs (CBC, glucose, electrolytes, toxicology screen)
Role
Exclusion of organic causes
Expected Finding
Expected to be normal; ordered to rule out hypoglycemia, intoxication, metabolic derangement, or thyrotoxicosis
CT/MRI head
Role
Only if trauma suspected
Expected Finding
Ordered only to exclude intracranial pathology if mechanism of injury suggests head trauma
Test | Role | Expected Finding |
|---|---|---|
Structured clinical interview | Best initial and confirmatory "test" | Clear temporal link between extraordinary stressor and symptom onset within minutes; mixed fluctuating symptoms; no single dominant symptom; resolution trajectory within 3 days |
Mental Status Examination (MSE) | Core assessment | Altered consciousness (daze), labile affect, variable psychomotor activity, intact orientation once daze clears |
Physical examination | Rule out organic cause | Autonomic hyperarousal signs (tachycardia, elevated BP, diaphoresis) without evidence of head trauma, intoxication, or medical illness explaining the presentation |
Basic labs (CBC, glucose, electrolytes, toxicology screen) | Exclusion of organic causes | Expected to be normal; ordered to rule out hypoglycemia, intoxication, metabolic derangement, or thyrotoxicosis |
CT/MRI head | Only if trauma suspected | Ordered only to exclude intracranial pathology if mechanism of injury suggests head trauma |
This is a purely clinical diagnosis. There is no biomarker, lab test, or imaging study that confirms it. The diagnosis is made at the bedside by satisfying the PPDGJ-III criteria:
Criterion 1: Temporal link. There must be a clear and unambiguous temporal connection between the extraordinary stressor and the onset of symptoms. The onset must occur within minutes or immediately ("segera") after the event. If symptoms appear days or weeks later, this diagnosis does not apply.
Criterion 2: Symptom profile. The initial presentation is typically a daze state (terpaku), followed by a mixed and fluctuating picture that can include depression, anxiety, anger, disappointment, overactivity, and withdrawal. The critical rule is that no single symptom dominates the clinical picture for a prolonged period. If one symptom (e.g., depressed mood) persists and dominates, consider an alternative diagnosis.
Criterion 3: Resolution timeline. If the patient is removed from the stressor, symptoms should resolve rapidly, within hours. If the stressor persists or cannot be avoided, symptoms should begin to subside after 24-48 hours and be largely gone by 3 days. Symptoms persisting beyond 3 days should prompt reconsideration of the diagnosis.
Exclusion criteria. Per PPDGJ-III, this diagnosis must not be applied to an acute exacerbation of symptoms in someone who already carries another psychiatric diagnosis. If a patient with known generalized anxiety disorder decompensates after a stressor, that is a flare of the underlying condition, not an Acute Stress Reaction.
04Management & Treatment
Psychological first aid (PFA)
Timing
Immediate
Details
Ensure safety, provide calm presence, orient to surroundings, meet basic needs (water, warmth, shelter), facilitate contact with social support
Remove from stressor
Timing
Immediate
Details
Physical removal from the threatening environment is the single most effective intervention; correlates directly with rapid symptom resolution
Brief supportive psychotherapy
Timing
Acute (hours to days)
Details
Active listening, normalization of the stress response, psychoeducation that symptoms are expected and self-limiting; avoid forced debriefing
Short-term benzodiazepine
Timing
Only if severe agitation/autonomic distress
Details
Diazepam 5-10 mg orally or Lorazepam 1-2 mg orally/IM; single dose or for a maximum of 2-3 days; avoid routine prescribing
Follow-up assessment
Timing
48-72 hours
Details
Re-evaluate to confirm symptom resolution; if symptoms persist beyond 3 days, reassess diagnosis (consider Acute Stress Disorder or Adjustment Disorder)
Intervention | Timing | Details |
|---|---|---|
Psychological first aid (PFA) | Immediate | Ensure safety, provide calm presence, orient to surroundings, meet basic needs (water, warmth, shelter), facilitate contact with social support |
Remove from stressor | Immediate | Physical removal from the threatening environment is the single most effective intervention; correlates directly with rapid symptom resolution |
Brief supportive psychotherapy | Acute (hours to days) | Active listening, normalization of the stress response, psychoeducation that symptoms are expected and self-limiting; avoid forced debriefing |
Short-term benzodiazepine | Only if severe agitation/autonomic distress | Diazepam 5-10 mg orally or Lorazepam 1-2 mg orally/IM; single dose or for a maximum of 2-3 days; avoid routine prescribing |
Follow-up assessment | 48-72 hours | Re-evaluate to confirm symptom resolution; if symptoms persist beyond 3 days, reassess diagnosis (consider Acute Stress Disorder or Adjustment Disorder) |
Step 1: Immediate stabilization. The first priority is ensuring the patient's physical safety and removing them from the stressor environment. This alone is often sufficient for resolution. Provide psychological first aid, which involves a calm, non-intrusive presence, orienting the patient to safety, and meeting immediate physical needs.
Step 2: Supportive care. Brief supportive psychotherapy should focus on normalizing the reaction. The clinician should explain that what the patient is experiencing is a normal response to an abnormal situation. Psychoeducation about the expected self-limiting course (resolution within hours to 3 days) can significantly reduce the patient's secondary anxiety about their own symptoms. Avoid critical incident stress debriefing (CISD), as evidence suggests forced retelling of the traumatic event in the acute phase can worsen outcomes.
Step 3: Pharmacotherapy (only when indicated). Medications are not routinely required. If the patient has severe agitation, panic, or autonomic distress that is functionally disabling, a short-acting benzodiazepine may be given: Lorazepam 1-2 mg orally or intramuscularly, or Diazepam 5-10 mg orally. This should be a single dose or used for no more than 2-3 days. Benzodiazepines are contraindicated in patients with respiratory depression, known substance abuse history, or severe hepatic impairment. Antidepressants, antipsychotics, and long-term anxiolytics have no role in this condition.
Step 4: Follow-up. All patients should be reassessed at 48-72 hours. If symptoms have resolved, no further psychiatric intervention is needed. If symptoms persist beyond 3 days, the diagnosis must be reconsidered. Persistent symptoms with prominent re-experiencing, avoidance, and hyperarousal suggest evolution toward Acute Stress Disorder (if within 1 month) or Post-Traumatic Stress Disorder (if beyond 1 month).
05Differential Diagnosis & Distractors
Acute Stress Disorder
Why It Looks Similar
Also follows a traumatic stressor; also involves dissociative and anxiety symptoms
Key Discriminator
Acute Stress Reaction resolves within 3 days; Acute Stress Disorder persists from 3 days to 1 month and requires prominent dissociative symptoms (numbing, depersonalization, derealization, dissociative amnesia)
Post-Traumatic Stress Disorder (PTSD)
Why It Looks Similar
Same type of triggering stressor; overlapping anxiety and hyperarousal symptoms
Key Discriminator
PTSD requires symptoms lasting more than 1 month and includes a distinct triad of re-experiencing, avoidance, and hyperarousal that is not required for Acute Stress Reaction
Adjustment Disorder
Why It Looks Similar
Follows a stressor; produces emotional and behavioral symptoms
Key Discriminator
In Adjustment Disorder, the stressor is not necessarily extraordinary (can be divorce, job loss, illness); onset is within 1 month (per ICD-10) but symptoms can persist up to 6 months; the symptom pattern is more stable, not the mixed fluctuating picture seen in Acute Stress Reaction
Panic Disorder / Panic Attack
Why It Looks Similar
Autonomic hyperarousal: tachycardia, diaphoresis, tremor, hyperventilation, sense of impending doom
Key Discriminator
Panic attacks are not tied to a clear external extraordinary stressor; they arise spontaneously or from internal cues; there is no preceding traumatic event and no daze state
Brief Psychotic Disorder
Why It Looks Similar
Acute onset, can follow a stressor, dramatic behavioral disturbance
Key Discriminator
Brief Psychotic Disorder involves psychotic symptoms (hallucinations, delusions, disorganized speech) that are not part of Acute Stress Reaction; the daze in ASR is dissociative, not psychotic
Dissociative (Conversion) Disorder
Why It Looks Similar
Dissociative features overlap with the daze/stupor of Acute Stress Reaction
Key Discriminator
In Dissociative Disorder, symptoms are often more persistent, may not follow an extraordinary stressor, and typically involve more prominent motor or sensory conversion symptoms (paralysis, blindness, seizures)
Organic causes (hypoglycemia, intoxication, head injury)
Why It Looks Similar
Altered mental status, autonomic signs, behavioral changes
Key Discriminator
History and basic labs/imaging distinguish organic causes; the daze of Acute Stress Reaction clears with reorientation and removal from the stressor, while organic causes persist until the underlying condition is treated
Differential | Why It Looks Similar | Key Discriminator |
|---|---|---|
Acute Stress Disorder | Also follows a traumatic stressor; also involves dissociative and anxiety symptoms | Acute Stress Reaction resolves within 3 days; Acute Stress Disorder persists from 3 days to 1 month and requires prominent dissociative symptoms (numbing, depersonalization, derealization, dissociative amnesia) |
Post-Traumatic Stress Disorder (PTSD) | Same type of triggering stressor; overlapping anxiety and hyperarousal symptoms | PTSD requires symptoms lasting more than 1 month and includes a distinct triad of re-experiencing, avoidance, and hyperarousal that is not required for Acute Stress Reaction |
Adjustment Disorder | Follows a stressor; produces emotional and behavioral symptoms | In Adjustment Disorder, the stressor is not necessarily extraordinary (can be divorce, job loss, illness); onset is within 1 month (per ICD-10) but symptoms can persist up to 6 months; the symptom pattern is more stable, not the mixed fluctuating picture seen in Acute Stress Reaction |
Panic Disorder / Panic Attack | Autonomic hyperarousal: tachycardia, diaphoresis, tremor, hyperventilation, sense of impending doom | Panic attacks are not tied to a clear external extraordinary stressor; they arise spontaneously or from internal cues; there is no preceding traumatic event and no daze state |
Brief Psychotic Disorder | Acute onset, can follow a stressor, dramatic behavioral disturbance | Brief Psychotic Disorder involves psychotic symptoms (hallucinations, delusions, disorganized speech) that are not part of Acute Stress Reaction; the daze in ASR is dissociative, not psychotic |
Dissociative (Conversion) Disorder | Dissociative features overlap with the daze/stupor of Acute Stress Reaction | In Dissociative Disorder, symptoms are often more persistent, may not follow an extraordinary stressor, and typically involve more prominent motor or sensory conversion symptoms (paralysis, blindness, seizures) |
Organic causes (hypoglycemia, intoxication, head injury) | Altered mental status, autonomic signs, behavioral changes | History and basic labs/imaging distinguish organic causes; the daze of Acute Stress Reaction clears with reorientation and removal from the stressor, while organic causes persist until the underlying condition is treated |
06Traps & High-Yield Pearls
The most common way students lose points on this topic is by confusing the temporal boundaries between Acute Stress Reaction, Acute Stress Disorder, and PTSD. The exam often presents a vignette of a patient who experienced a traumatic event and now shows anxiety and dissociative symptoms. The question then hinges entirely on how much time has passed. If symptoms developed within minutes and resolved within 3 days, the answer is Acute Stress Reaction. If symptoms persist from 3 days to 1 month, the answer shifts to Acute Stress Disorder. Beyond 1 month, PTSD becomes the correct answer. Students who do not track the timeline in the stem will consistently pick the wrong option.
A second trap involves the nature of the stressor. The PPDGJ-III requires the stressor to be extraordinary ("luar biasa"). If the vignette describes a common life difficulty (failing an exam, a breakup, job loss), then Adjustment Disorder is the correct diagnosis, not Acute Stress Reaction, regardless of how dramatic the patient's symptoms appear.
The third trap is the "no single symptom dominates" rule. If a vignette shows a patient with persistent, dominant depressed mood after a stressor, students may reflexively pick Acute Stress Reaction because of the temporal link. However, the dominant depressive picture violates the diagnostic criterion of mixed, fluctuating symptoms. The correct answer in that scenario would be a Depressive Episode or Adjustment Disorder with depressed mood.
Finally, students must remember the exclusion rule: Acute Stress Reaction cannot be diagnosed in a patient who already has an established psychiatric disorder experiencing an acute flare. The vignette will often mention a psychiatric history in the stem to test whether the student catches this exclusion.
The core competency being tested is the ability to recognize a time-limited, self-resolving stress response in the context of extraordinary trauma and to distinguish it from conditions that share overlapping features but differ in duration, symptom dominance, and stressor severity.