When A Patient Presents With A Painful Red Toe
- Volume 22 - Issue 10 - October 2009
- 112313 reads
- 0 comments
A vascular reaction occurs under the frozen superficial tissues and consists of damage to the wall of the blood vessels and leakage of plasma into the tissues (forming blisters). Red blood cells and platelets start to stick together, causing clots, ischemic damage and an increased viscosity of the remaining intravascular blood. The blood flow then stops via the action of the precapillary sphincters and the arteriovenous shunts open up and blood bypasses the frozen area. The diseased part is sacrificed for survival of the whole organism.
The second reaction is the freezing and crystallizing of fluids in the interstitial and cellular spaces due to prolonged exposure to freezing temperatures. The intracellular osmotic pressure rises and enzyme mechanisms are disturbed with subsequent cell death.
The toes contain multiple arteriovenous anastomoses that allow shunting of blood in order to preserve core temperature at the expense of peripheral tissue circulation. This leads to cold injuries.
The normal cutaneous flow is 200 to 250 mL/min. Maximal vasoconstriction occurs at 15°C (59ºF) with blood flow measured at 20 to 50 mL/min.
Below 15°C, vasoconstriction is interrupted by rhythmic bursts of vasodilation occurring three to five times per hour and lasting five to 10 minutes. At 10°C (50ºF), neurapraxia occurs and results in loss of cutaneous sensation. Below 0°C (32ºF), negligible cutaneous blood flow allows the skin to freeze.
Frostbite injury may be classified into a cascade and includes four phases: prefreeze, freeze, vascular stasis and late progressive ischemia. These all may overlap.
• The prefreeze phase consists of superficial tissue cooling.
• The freeze phase consists of ice crystal formation in the extracellular space more than the intracellular space.
• The vascular stasis phase consists of arteriovenous shunting at the margin between injured and uninjured tissue. This phase causes progressive microvasculature erythrocyte sludging, leading to stasis, coagulation and thrombus formation.
• The late progressive ischemia phase consists of thrombus-induced inflammation, hypoxia and anaerobic metabolism, leading to tissue necrosis.
A Closer Look At Injury Staging And Sequelae
The initial appearance of frostbite does not accurately predict the eventual extent and depth of tissue damage. Signs and symptoms vary according to severity of the frostbite injury. Frostbite is classified into four degrees of progressive injury identified by physical signs and the following sequelae.
A first-degree injury is characterized by epidermal involvement, which causes erythma, mild edema and subsequent desquamation and cold sensitivity.
A second-degree injury is full thickness skin freezing with substantial edema and formation of clear blisters. These blisters contract and dry within two to three weeks, forming a dark eschar.
A third-degree injury is characterized by the formation of hemorrhagic blisters, blue-grey discoloration of the skin, deep burning pain or rewarming, thick gangrene and eschar formation.
In a fourth-degree injury, muscle, bone and tendons are involved.
Long-term sequelae include the following:
• cold insensitivity;
• peeling skin;
• loss of fingernails or toenails;
• hyperhidrosis or anhidrosis;
• muscle atrophy;
• premature closure of epiphyses;
• decreased mineralization of bone; and
• joint stiffness.