Heart Rate and Posttraumatic Stress in Injured Children FREE

Posttraumatic stress reactions are a common consequence of pediatric injury, with a significant minority of injured children going on to develop posttraumatic stress disorder (PTSD).^1- 6 Recent investigations have explored early predictors of persistent traumatic stress in order to identify, during acute medical care, those children in need of further assessment and possible intervention.^6- 7 For traumatically injured adults, several investigators have found an association between elevated heart rate during acute medical care and later development of PTSD.^8- 10 The relationship between early postinjury heart rate and later PTSD has not been examined in children.

The potential relationship between heart rate assessed in the first hours or days after a traumatic event and later PTSD outcome is of interest for several reasons. First, understanding the course and trajectory of physiological functioning and immediate responses to traumatic events may help elucidate the etiology of posttraumatic stress responses. A recent meta-analysis documents an association between chronic PTSD and elevated basal heart rate,¹¹ but our knowledge of the prospective course of this relationship is far more limited. Second, if heart rate data were shown to reliably aid in the prediction of later PTSD, this might serve as a fairly simple and straightforward marker of risk to identify those in need of further assessment after the occurrence of a traumatic event.

Although elevated heart rate in the immediate aftermath of a traumatic event has been related to later PTSD development in adults,^8- 10 to our knowledge, no published study has examined the relationship between acute heart rate and later PTSD outcome in children exposed to traumatic events. A challenge in studying this in children and adolescents is the developmental trend in normative resting heart rates across childhood. Resting heart rates are higher in younger children and decrease through early adolescence. For example, the mean heart rate for children aged 8 to 11 years is 91 beats per minute (BPM); between the ages of 12 and 15 years, children’s normative resting heart rates are similar to adults, at 85 BPM.¹² A further challenge for studying heart rate in recently injured children is the potential impact on heart rate from the injury itself, its physiological aftermath, and any emergency treatment procedures or medication. In addition, when heart rate is assessed at emergency department (ED) triage, the actual time elapsed since the occurrence of the injury may differ among patients. These variations (age, injury effects, timing) have the potential to create “noise” in the data that could obscure relationships between ED heart rate and posttraumatic stress outcomes. Nonetheless, the promise of a straightforward early risk marker for child posttraumatic stress that can be applied in a real-life setting makes the relationship between ED heart rate and later PTSD outcome a compelling research question.

The current prospective study examines the relationship between heart rate and PTSD in injured children. We hypothesized that (1) heart rate assessed at ED triage would be related to later PTSD outcome in traumatically injured children and that (2) the relationship between heart rate and PTSD outcome would remain significant after controlling for child age, sex, and the presence of a severe injury.

Children admitted to a level I pediatric trauma center were enrolled in a prospective study of posttraumatic stress after injury. Following an institutional review board–approved protocol, all children between the ages of 8 and 17 years admitted for treatment of traffic-related injuries sustained as a pedestrian, passenger, or bicyclist were eligible for inclusion. An ED triage nurse assessed the heart rate in a private triage area. Child posttraumatic stress was assessed at least 3 months’ postinjury in a follow-up assessment conducted in the child’s home.

Triage heart rate was assessed as part of standard clinical care within 5 minutes of the child’s arrival at the ED, using 1 of 3 methods: cardiac auscultation, radial pulse palpation, or an automated vital-signs monitoring device (Critikon Dinamap; Critikon, Tampa, Fla). Standard deviation scores (“heart rate z scores”) were calculated for heart rate compared with age and sex norms in order to have an alternate measure of heart rate that was not affected by normative age differences. Each child’s heart rate value in BPM was converted to a standard deviation score by using age-specific reference values. Skewness coefficients, medians, and coefficients of variation were obtained from a published sample of 1254 healthy children.¹³ Heart rate z score reflects the child’s heart rate in valid standard deviation units compared with the reference mean for his or her age and sex (for example, a score of 2.0 denotes a heart rate 2 SDs higher than the age and sex mean and a score of –1.0 denotes a heart rate 1 SD lower than this mean). For this study, elevated heart rate was defined as a heart rate z score greater than 2.0.

The PTSD symptoms and diagnostic status were evaluated using the Clinician-Administered PTSD Scale for Children and Adolescents (CAPS-CA), a semistructured interview with established reliability and validity for assessment of child PTSD¹⁴ that yields scores for both continuous symptom severity (CAPS-CA total score) and categorical diagnostic outcome. Three levels of categorical PTSD outcome were defined: (1) “full PTSD”: meeting DSM-IV¹⁵ symptom criteria for PTSD, (2) “partial PTSD”¹⁶ : at least 1 moderate to severe posttraumatic stress symptom in each of the 3 PTSD symptom categories (reexperiencing, avoidance, and hyperarousal) and functional impairment from these symptoms, and (3) “no PTSD”: did not meet either of these standards. Partial PTSD has been shown to be clinically meaningful and associated with significant distress,^16- 18 and investigators have found partial PTSD in a significant minority of children following traumatic injury.⁵

Information regarding demographics, hospital admission, and the child’s injuries was abstracted from the medical record and the hospital’s trauma registry. Injury information included Abbreviated Injury Scale scores and the Injury Severity Score.^19- 20 The Abbreviated Injury Scale and Injury Severity Score are widely used to classify injury severity in terms of threat to life; both have proved reliable and valid as measures of injury severity in children.²¹ The Abbreviated Injury Scale rates the severity of an anatomical injury from 1 (minor injury) to 6 (fatal injury) for each of 6 body regions. An Abbreviated Injury Scale score of 2 or greater is considered clinically important (eg, concussion, fracture, or abdominal organ injury). The Injury Severity Score is a well-recognized measure of overall injury severity; Injury Severity Scores higher than 19 generally represent severe injury.

Demographics, injury characteristics, and heart rate of participants completing vs not completing follow-up assessment were compared using t tests or Wilcoxon rank sum tests for continuous variables and χ² or Fisher exact tests for categorical variables.

Heart rate data were examined in 2 different ways. First, we compared mean ED triage heart rate (BPM) between the no PTSD, partial PTSD, and full PTSD groups with analysis of variance followed by post hoc tests for group differences. Second, Fisher exact test, χ², or t tests were used to examine the association of elevated heart rate at ED triage with dichotomous, categorical, and continuous PTSD outcome measures, respectively. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for elevated heart rate as a predictor of PTSD status. The PPV is the probability that a child with an elevated heart rate will develop posttraumatic stress. The NPV is the probability that a child without an elevated heart rate will not develop posttraumatic stress.

Relationships among potential predictors (age, sex, presence of significant injury, and elevated heart rate) and PTSD outcome were examined, and 2 regression models were used. A multivariable regression model with CAPS-CA total score as the dependent measure was used to test the independent contribution of age, sex, presence of significant injury, and presence of elevated heart rate to the prediction of PTSD symptom severity. A parallel analysis used multiple logistic regression analysis to assess the independent contribution of each of these variables to the prediction of categorical PTSD outcome (partial or full PTSD); odds ratios and the area under the curve were calculated. Statistical significance was defined as a P value <.05. All tests were 2-tailed.

Two hundred eighty-three children were enrolled in the study and had their heart rate recorded in the ED. Of these children, 190 (67%) completed a follow-up assessment, 78 (28%) could not be contacted or were unable to schedule a follow-up CAPS-CA interview, and 15 (5%) refused participation at follow-up. No differences were found in demographic characteristics (sex, Fisher exact test, P = .88; age, t test, P = .93), proportion with an elevated heart rate (Fisher exact test, P = .10), mechanism of injury (χ², P = .82), admission to the intensive care unit (Fisher exact test, P = .76), or severity of injury (Wilcoxon rank sum test, P = .83) between those completing the study and those lost to follow-up. Table 1 presents demographic and clinical characteristics of the final sample of 190 children. Presence of a moderate to severe injury was not related to child age or sex. Mean time from injury to follow-up assessment was 6.4 months; 90% of follow-up assessments were within 8.7 months of injury.

Thirty-two percent of the children had an elevated heart rate at triage. The mean heart rate z score in this sample was 1.25 (SD 2.0), indicating that on average this group of children had a higher than normal heart rate (for their age and sex) when they arrived at the ED. Younger children (aged 8 to 11 years), girls, and those with at least 1 moderate to severe injury had a higher mean heart rate (BPM), but presence of an elevated heart rate (z score >2.0) did not differ by age group, sex, or injury (Table 2).

Based on results of the follow-up CAPS-CA interview, 21 (11%) of the children were classified as having partial PTSD and another 12 children (6%) as having full PTSD. Mean heart rate (BPM) for those children with no PTSD, partial PTSD, or full PTSD is shown in Table 3. Post hoc tests showed that those in the partial PTSD and the full PTSD groups had a higher heart rate at ED triage than the no PTSD group and that the partial and full PTSD groups did not differ from each other. Presence of an elevated heart rate was also associated with PTSD status at follow-up (Table 4).

Based on prior literature^5,16- 18 regarding the clinical salience of partial PTSD and the current results suggesting that the groups did not differ significantly in ED heart rate, the partial PTSD and full PTSD groups were combined for subsequent analyses. The combined partial/full PTSD group, with 33 (17%) of the children in the sample, had a higher mean ± SD heart rate (BPM) at ED triage than the no PTSD group (109.6 ± 22.3 vs 99.7 ± 18.0 BPM; t₁₈₈ = 2.75; P = .007). Triage heart rate in the partial/full PTSD group ranged from 74 to 172 BPM (median, 105). For the no PTSD group, this range was 59 to 170 BPM (median, 99.0). The Figure shows the distribution of heart rate (BPM) at ED triage for children who later met criteria for partial or full PTSD and for those who did not.

Children with an elevated heart rate at ED triage were more likely to meet criteria for partial or full PTSD at follow-up compared with children without an elevated acute heart rate (28% vs 12%; Fisher exact test, P = .01; odds ratio, 2.73 [95% confidence interval, 1.27-5.87]). Elevated heart rate as a predictor of later partial or full PTSD had a sensitivity of 52% and a specificity of 72%. The PPV was 28%, and the NPV was 88%. Alternatively, the useof a cut-off score of 1 SD higher than the age and sex mean (heart rate z score≥1.0) would increase sensitivity to 70% and lower specificity to 53% (PPV = 24%; NPV = 89%). Examining the 3 core symptom categories that compose the PTSD diagnosis, children with an elevated heart rate at ED triage were more likely to later meet DSM-IV diagnostic criteria for hyperarousal (30% vs 16%; Fisher exact test, P = .04) but not for reexperiencing (44% vs 31%; Fisher exact test, P = .09) or avoidance (13% vs 9%; Fisher exact test, P = .52).

Regression analyses estimated the effects of sex, age, presence of a severe injury, and presence of an elevated heart rate on continuous PTSD severity or dichotomous PTSD outcome. Results from the multivariable linear regression analysis to estimate the effects of these predictors on PTSD severity (continuous CAPS-CA total score) showed that only sex (P = .01) and elevated heart rate (P = .05) were statistically significant (R² = 0.07). To facilitate comparison of this study’s findings with prior adult studies,^8- 10 a multiple logistic regression model was fitted to estimate the effects of the same set of predictors on a dichotomous PTSD outcome (presence of partial or full PTSD). After adjusting for the other predictors, children with an elevated heart rate at ED triage had a higher probability of developing partial or full PTSD than children who displayed a lower heart rate in the ED; the adjusted odds ratio was 2.4 (95% confidence interval, 1.1-5.4). In this regression analysis, sex also predicted development of partial or full PTSD with an adjusted odds ratio for girls of 2.6 (95% confidence interval, 1.1-5.8). The area under the curve was 0.68. There is an independent sex effect controlling for heart rate level. In other words, independent of their heart rate, girls were more likely to develop posttraumatic stress than boys.

By documenting a relationship between acute posttrauma heart rate and later PTSD symptoms in a sample of injured children and adolescents, this study replicates the central findings from several studies of injured adults. Heart rate after injury was associated with child PTSD outcome assessed an average of 6 months later. Children with an elevated heart rate at ED triage assessment were 2.4 times more likely to develop partial or full PTSD, even after controlling for child age and sex and the presence of a severe injury.

The current investigation examined heart rates normalized for age in order to explore the relationship between acute physiological arousal and PTSD outcome in children. Prior analyses from this prospective study included heart rate, in conjunction with other factors assessed in the acute care setting, in the creation of a screening tool to help identify children or adolescents at higher risk for persistent and distressing PTSD symptoms.⁷ The current results indicate that as a single predictor, the presence of elevated heart rate demonstrated only moderate sensitivity but better specificity for the presence of persistent traumatic stress symptoms, and normal heart rate demonstrated a high NPV (88%). These results also suggest that the presence of elevated heart rate was able to predict a small (but statistically significant) portion of the variance in PTSD symptom severity.

Prospective cohort studies of injured adults have found elevated, acute heart rate to be associated with later PTSD. Comparing injured adults who later went on to meet diagnostic criteria for PTSD with those who did not go on to have the disorder, Shalev et al¹⁰ found that injured adults who went on to meet diagnostic criteria for PTSD months later were more likely to have higher ED heart rates than those adults who did not later meet criteria for PTSD. This difference persisted on subsequent evaluation of heart rate assessed 1 week postinjury but not for heart rate assessed 1 month or 4 months’ postinjury. Similarly, Bryant et al^8- 9 found that adults injured in motor-vehicle crashes who later met criteria for PTSD had higher resting heart rates at the time of hospital discharge compared with those who did not meet PTSD criteria. One exception to these findings in the adult injury literature is a study²² of adults injured in motor-vehicle crashes who were seeking treatment for posttraumatic stress symptoms an average of 13 months’ postinjury. In this sample, lower ED heart rate was associated with later diagnosis of PTSD. Methodological differences (particularly regarding sample selection) may account for this disparate finding. The results reported herein regarding a prospective cohort of injured children are quite consistent with the findings of similar prospective cohort studies of injured adults in the direction and degree of difference in mean ED heart rate for the PTSD vs non-PTSD groups.

Adult studies have not reported the relationship of acute heart rate to subsyndromal levels of PTSD symptoms or to specific categories of PTSD symptoms. In the current study, children who went on to have either full PTSD or partial PTSD had an elevated, acute heart rate. In addition, the results suggest a connection between acute physiological arousal and persistent psychological arousal, in that children with an elevated heart rate were more likely to go on to meet DSM-IV PTSD symptom criteria for hyperarousal (but not reexperiencing or avoidance) at follow-up. The similarity in acute heart rate findings between children with full PTSD and partial PTSD supports the notion that early posttrauma physiological arousal may mark a trajectory toward persistent and distressing posttraumatic stress reactions. The finding that children with an elevated, acute heart rate were more likely to later meet criteria for psychological arousal symptoms suggests 1 pathway through which this may occur. In the absence of information regarding preinjury baseline heart rate, we also cannot rule out the alternate explanation that children with trait high arousal are more likely to demonstrate physiological and psychological arousal in the aftermath of injury and are at higher risk for developing partial or full PTSD.

This study highlights the importance of considering early postinjury heart rate as a factor in any prospective investigation of acute stress reactions in injured children. Future studies of injured children might also include assessment of heart rate at multiple points across the first few weeks or months after injury to shed light on the course and trajectory of physiological responses in the development of posttraumatic stress.

The heart rate data analyzed in this study came from a single assessment collected in the course of normal emergency medical care (at the time of the patient’s arrival to the ED) rather than via a standardized research assessment. Participants were not excluded from the study based on injury type or severity, course of prehospital treatment, or medication status at the time of ED triage. The use of clinically assessed heart rate allowed us to examine the extent to which heart rate assessed as usual, in a busy emergency medical setting for patients with a range of injury types and severity, might still serve as a predictor for PTSD risk. Despite potential noise in the heart rate data, we were able to observe a relationship with PTSD outcome. Other limitations of this study were that we did not have information regarding pretrauma heart rate in these children and that we were not able to examine the effects of treatment, medication status, or time elapsed from injury to ED arrival on the relationship between acute child heart rate and later PTSD. These might be fruitful areas for future investigations.

This initial investigation of the relationship of heart rate and PTSD in injured children suggests an association between early physiological arousal and the development or persistence of PTSD symptoms in children. In the context of similar findings in several studies of injured adults, and a recent meta-analysis documenting an association between chronic PTSD and elevated basal heart rate,¹¹ these results point to the importance of better understanding the interplay among physiological and psychological responses to traumatic stressors.

Correspondence: Nancy Kassam-Adams, PhD, TraumaLink 3535, 10th floor, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104 (nlkaphd@mail.med.upenn.edu).

Submitted for Publication: March 31, 2004; final revision received September 10, 2004; accepted September 24, 2004.

Funding/Support: This work was supported by grant R40 MC 00138 from the Maternal and Child Health Bureau, Rockville, Md.