Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
Mary D. Nettleman, MD, MS, MACP is the Chair of the Department of Medicine at Michigan State University. She is a graduate of Vanderbilt Medical School, and completed her residency in Internal Medicine and a fellowship in Infectious Diseases at Indiana University.
Your body works to stay alive first, and to stay functioning second.
In conditions of prolonged cold exposure, your body sends signals to the blood vessels in your arms and legs telling them to constrict (narrow). By slowing blood flow to the skin, your body is able to send more blood to the vital organs, supplying them with critical nutrients, while also preventing a further decrease in internal body temperature by exposing less blood to the outside cold.
As this process continues and your extremities (the parts farthest from your heart) become colder and colder, a condition called the hunter's response is initiated. Your blood vessels are dilated (widened) for a period of time and then constricted again. Periods of dilatation are cycled with times of constriction in order to preserve as much function in your extremities as possible. However, when your brain senses that you are in danger of hypothermia (when your body temperature drops significantly below 98.6 F), it permanently constricts these blood vessels in order to prevent them from returning cold blood to the internal organs. When this happens, frostbite has begun.
Frostbite is caused by two different means: cell death at the time of exposure and further cell deterioration and death because of a lack of oxygen.
In the first, ice crystals form in the space outside of the cells. Water is lost from the cell's interior, and dehydration promotes the destruction of the cell.
In the second, the damaged lining of the blood vessels is the main culprit. As blood flow returns to the extremities upon rewarming, it finds that the blood vessels themselves are injured, also by the cold. Holes appear in vessel walls and blood leaks out into the tissues. Flow is impeded and turbulent and small clots form in the smallest vessels of the extremities. Because of these blood flow problems, complicated interactions occur, and inflammation causes further tissue damage. This injury is the primary determinant of the amount of tissue damage
that occurs in the end.
It is rare for the inside of the cells themselves to be frozen. This phenomenon is only seen in very rapid freezing injuries, such as those produced by frozen metals.