PTSD can also occur after childbirth and the risk increases if a woman has experienced trauma prior to the pregnancy. Prevalence of PTSD following normal childbirth (that is, excluding stillbirth or major complications) is estimated to be between 2.8 and 5.6% at six weeks postpartum, with rates dropping to 1.5% at six months postpartum. Symptoms of PTSD are common following childbirth, with prevalence of 24–30.1% at six weeks, dropping to 13.6% at six months. Emergency childbirth is also associated with PTSD. Genetics
There is evidence that susceptibility to PTSD is hereditary. Approximately 30% of the variance in PTSD is caused from genetics alone. For twin pairs exposed to combat in Vietnam, having a monozygotic (identical) twin with PTSD was associated with an increased risk of the co-twins having PTSD compared to twins that were dizygotic (non-identical twins). Women with a smaller hippocampus might be more likely to develop PTSD following a traumatic event based on preliminary findings. Research has also found that PTSD shares many genetic influences common to other psychiatric disorders. Panic and generalized anxiety disorders and PTSD share 60% of the same genetic variance. Alcohol, nicotine, and drug dependence share greater than 40% genetic similarities.Several biological indicators have been identified that are related to later PTSD development. Heightened startle responses and, with only preliminary results, a smaller hippocampal volume have been identified as possible biomarkers for heightened risk of developing PTSD. Additionally, one study found that soldiers whose leukocytes had greater numbers of glucocorticoid receptors were more prone to developing PTSD after experiencing trauma.
);
tumor (e.g., laryngeal papillomatosis, squamous cell carcinoma of larynx, trachea or esophagus);
ALL (T-cell ALL can present with mediastinal mass that compresses the trachea and causes inspiratory stridor)

Diagnosis
Stridor is mainly diagnosed on the basis of history and physical examination, with a view to revealing the underlying problem or condition. Chest and neck x-rays, bronchoscopy, CT-scans, and/or MRIs may reveal structural pathology. Flexible fiberoptic bronchoscopy can also be very helpful, especially in assessing vocal cord function or in looking for signs of compression or infection. Treatments
The first issue of clinical concern in the setting of stridor is whether or not tracheal intubation or tracheostomy is immediately necessary. A reduction in oxygen saturation is considered a late sign of airway obstruction, particularly in a child with healthy lungs and normal gas exchange. Some patients will need immediate tracheal intubation. If intubation can be delayed for a period, a number of other potential options can be considered, depending on the severity of the situation and other clinical details. These include:

Expectant management with full monitoring, oxygen by face mask, and positioning the head on the bed for optimum conditions (e.g., 45 - 90 degrees). Use of nebulized racemic adrenaline epinephrine (0.5 to 0.75 ml of 2.25% racemic epinephrine added to 2.5 to 3 ml of normal saline) in cases where airway edema may be the cause of the stridor. (Nebulized Codeine in a dose not exceeding 3 mg/kg may also be used, but not together with racemic adrenaline [because of the risk of ventricular arrhythmias].)