Pharmacodynamics
Scopolamine is a nonspecific muscarinic antagonist at all four muscarinic acetylcholine receptors (M1, M2, M3, and M4).,

Biosynthesis in plants
Scopolamine is among the secondary metabolites of plants from Solanaceae (nightshade) family of plants, such as henbane (Hyoscyamus niger), jimson weed (Datura), angels trumpets (Brugmansia), deadly nightshade (Belladonna), mandrake (Mandragora officinarum), and corkwood (Duboisia). The biosynthesis of scopolamine begins with the decarboxylation of L-ornithine to putrescine by ornithine decarboxylase. Putrescine is methylated to N-methylputrescine by putrescine N-methyltransferase.A putrescine oxidase that specifically recognizes methylated putrescine catalyzes the deamination of this compound to 4-methylaminobutanal, which then undergoes a spontaneous ring formation to N-methyl-pyrrolium cation. In the next step, the pyrrolium cation condenses with acetoacetic acid yielding hygrine. No enzymatic activity could be demonstrated to catalyze this reaction. Hygrine further rearranges to tropinone.Subsequently, tropinone reductase I converts tropinone to tropine, which condenses with phenylalanine-derived phenyllactate to littorine. A cytochrome P450 classified as Cyp80F1 oxidizes and rearranges littorine to hyoscyamine aldehyde. In the final step, hyoscyamine undergoes epoxidation catalyzed by 6beta-hydroxyhyoscyamine epoxidase yielding scopolamine. History
One of the earlier alkaloids isolated from plant sources, scopolamine has been in use in its purified forms (such as various salts, including hydrochloride, hydrobromide, hydroiodide, and sulfate), since its isolation by the German scientist Albert Ladenburg in 1880, and as various preparations from its plant-based form since antiquity and perhaps prehistoric times.
);
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].)