Signs of septic shock include:
Abnormal heart rhythms, often a fast heart rate
Reduced blood pressure
Decreased urine output
Altered mental status
Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen, antigen, drug, or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability. Signs typically occur after exposure to an allergen and may include:
Skin changes, such as hives, itching, flushing, and swelling. Wheezing and shortness of breath. Abdominal pain, diarrhea, and vomiting. Lightheadedness, confusion, headaches, loss of consciousness. High spinal injuries may cause neurogenic shock, which is commonly classified as a subset of distributive shock. The classic symptoms include a slow heart rate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels. (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the hemodynamic instability.) Endocrine
Although not officially classified as a subcategory of shock, many endocrinology disturbances in their severe form can result in shock. Hypothyroidism (can be considered a form of cardiogenic shock) in people who are critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency. Thyrotoxicosis (cardiogenic shock) may induce a reversible cardiomyopathy. Acute adrenal insufficiency (distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.
And the action of sulfur mustard on tumors in laboratory animals was investigated for the first time.After the U.S. entry into the Second World War the nitrogen mustards were candidate chemical warfare agents and research on them was initiated by the Office of Scientific Research and Development (OSRD). The OSRD let contracts to study them to two universities—Yale University and the University of Chicago. Inspired perhaps by the preliminary research in 1935, independently both groups thought to test whether a medically useful differential toxicity between animals and animal tumors existed. The Yale pharmacologists Louis Goodman and Alfred Gilman were the first to conduct a clinical trial, on 27 August 1942, using the agent HN3 (tris(2-chloroethyl)amine) on a patient known as J.D.The next year the Chicago group, led by Leon O. Jacobson, conducted trials with HN2 (chlormethine) which was the only agent in this group to see eventual clinical use. Wartime secrecy prevented any of this ground-breaking work on chemotherapy from being published, but papers were released once wartime secrecy ended, in 1946.Further clinical trials after the war, led by Cornelius P. Rhoads at Memorial Sloan-Kettering, helped establish the medical utility of the drug for Hodgkins disease and several other lymphomas and leukemia. Chemistry
Chlormethine is combustible and becomes explosive under extreme conditions. It can react with metals to form gaseous hydrogen. See also
Nitrogen mustards
HN1
HN3

References
External links
British Columbia Cancer Agency profile
"Chlormethine". Drug Information Portal. U.S. National Library of Medicine.