Dose-response changes in plasma cortisol and lymphocyte glucocorticoid receptors following dexamethasone administration in combat veterans with and without posttraumatic stress disorder.

BACKGROUND: Our previous studies have suggested that combat veterans with posttraumatic stress disorder (PTSD) have alterations in hypothalamic-pituitary-adrenal axis functioning that are different from the well-documented biological changes observed in major depressive disorder and following exposure to stress. METHODS: In the present study, we examined cortisol and lymphocyte glucocorticoid receptor number before and after the administration of 0.50 and 0.25 mg of dexamethasone in 14 combat veterans with PTSD, 12 combat veterans without PTSD, and 14 nonpsychiatric healthy men. All subjects were medication free at the time of testing and none met diagnostic criteria for major depression or substance dependence. RESULTS: Combat veterans with PTSD suppressed cortisol to a greater extent than did combat veterans without PTSD and normal controls in response to both doses of dexamethasone. Differences in cortisol suppression could not be attributed to substance dependence history or differences in dexamethasone bioavailability. Combat veterans with PTSD showed a larger number of baseline glucocorticoid receptors compared with normal men. Combat veterans without PTSD also had a larger number of baseline glucocorticoid receptors compared with normal men and in fact were comparable to combat veterans with PTSD on this measure. However, only veterans with PTSD showed a decrease in lymphocyte glucocorticoid receptor number following dexamethasone administration. CONCLUSION: The data support the hypothesis of an enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal axis in PTSD.

Prolactin response to low-dose dexamethasone challenge in combat-exposed veterans with and without posttraumatic stress disorder and normal controls.

The prolactin and cortisol responses to dexamethasone (0.5 mg) were studied in combat veterans with (n = 18) and without (n = 12) posttraumatic stress disorder (PTSD) and normal controls (n = 18). Both veteran groups demonstrated greater prolactin suppression than the normals. In contrast, only veterans with PTSD showed an enhanced cortisol suppression in response to dexamethasone. These findings suggest that the prolactin response to dexamethasone may reflect a feature of combat exposure rather than PTSD per se.

Glucocorticoid receptor number and cortisol excretion in mood, anxiety, and psychotic disorders.

In the present study, we measured cytosolic lymphocyte glucocorticoid receptor and 24-hour urinary cortisol excretion in patients with major depressive disorder, bipolar mania, posttraumatic stress disorder, panic disorder, and schizophrenia. Patients with major depression had the smallest, and posttraumatic stress disordered patients the largest, mean number of glucocorticoid receptors per cell compared to patients in the other groups. Bipolar manic and panic patients did not differ from each other in regard to the number of lymphocyte glucocorticoid receptors. Bipolar manic and panic patients did have significantly more glucocorticoid receptors/cell than schizophrenic patients. The mean 24-hour urinary cortisol excretion was significantly higher in patients with major depression and bipolar mania than in those in the other diagnostic groups. Lymphocyte glucocorticoid receptor number and cortisol excretion tended to be inversely related, when the entire sample was considered as a whole, but this effect did not reach statistical significance. It is concluded that lymphocyte glucocorticoid receptors may be modulated by multiple influences, not just ambient cortisol levels. These preliminary data suggest that the assessment of lymphocyte glucocorticoid receptor number in tandem with cortisol levels may provide a more meaningful estimate of hypothalamic-pituitary-adrenal axis activity than is achieved using cortisol alone.

The quantity of cause-of-injury information documented on the medical record: an appeal for injury prevention.

OBJECTIVE: To determine how much information about the cause of injury (available at the time of ED treatment) is documented on the medical record. This information is used by medical records coders to assign e-codes. METHODS: Quantitative "stages of information" were defined: stage 1 = the maximum amount of information available from the patient, as collected by a trained research assistant; stage 2 = the amount of information obtained by the care provider during the patient interview; and stage 3 = the amount of information the care provider documented in the medical record. Comparisons were made between the three stages; subgroup analyses compared amounts of information loss between the stages for levels of care provider and cause-of-injury information categories. RESULTS: Information was obtained from 109 patients. Only 46% of the cause-of-injury information available during the ED visit was recorded on the medical record. Incomplete history taking (obtaining 68% of the available information) and failure to document (writing 67% of the information obtained during the patient interview) contributed equally to the loss of information. The most information was obtained about who had received the injury (72%) and the least amount of information was in the category of where the injury had occurred (14%). Attending physicians collected the most information (74%) but documented significantly less (65%) than did physician assistants (70%) or medical students (81%). Medical students collected the least (65%) but documented the most, resulting in the students' medical records' being the most complete (52%) for cause-of-injury information. CONCLUSION: Emergency providers obtain significantly less cause-of-injury information than is available from the patient. Also, these providers' handwritten medical records contain significantly less cause-of-injury information than was obtained during the patient interview.

Accuracy of e-codes assigned to emergency department records.

OBJECTIVE: To determine the accuracy of ICD-9-CM external-cause-of-injury codes (e-codes) assigned to the medical records of injured patients treated in an ED and released. METHODS: A comparison was made of routine coding and expert recoding of medical records generated in the ED for a convenience sample of patients treated for injuries within 24 hours of injury occurrence and subsequently released from the ED. The medical record was handwritten and subsequently coded by three medical records coders (MRCs). The e-coded charts were sent to an external medical record consultant (expert), who was blinded to the codes previously assigned. The expert reading was used as the criterion standard. Accuracy was measured using a kappa statistic, and errors were described. RESULTS: Of 126 available patient charts, 108 (85.7%) were assigned e-codes by MRCs. The expert assigned two codes to (double-coded) 67 patients, while the MRCs double-coded only one patient. The additional code was usually a "place of occurrence code." In 60 cases (55.6%), the expert code exactly matched the MRC code; kappa = 0.462. Of the 48 mismatches (44.4%), 20 (41.7%) were e-coded in the wrong category, 20 (41.7%) were e-coded in the correct category but with incorrect specificity of information, either too specific or not specific enough, and eight (16.6%) had combined coding errors. CONCLUSION: The accuracy of e-codes assigned to ED records was moderate in this single institution analysis. Errors were predominantly related to the specificity of the code, but some e-codes were in the wrong category. There are implications for injury surveillance and research. E-code assignment must be standardized and applied uniformly to obtain accurate codes. Automation of e-coding could improve accuracy and consistency of codes. National and international epidemiologic studies of cause of injury among ED patients will be severely hampered until e-code assignment can be better standardized.