Your hospital is closed for all appointments? I apologize that I don't know any other way for you to be checked by a doctor except to go to another hospital or clinic.
But I do have a bit of good news, since you said it has been at least 3 days without a visual sign. With wet (moist) gangrene, a sign shows up within 36-72 hours. So perhaps you pinched a nerve and/or sprained your toe, causing the "sleepy feeling" and discomfort when you "step on it funny".
Since websites are prohibited in these boards, I have cut and pasted the following on gangrene in general. If you want to skip the rest of the article to read up on "wet gangrene", just hit "control" + "f", enter "wet gangrene" and hit "Find Next" until you find the article:
Gangrene is defined as the gradual destruction of living tissue, due to an obstruction in the supply of blood and oxygen to an area of the body (Pipkin and Janelli, 2000). Any part of the body can be affected by gangrene, but it most frequently occurs in the hands, fingers, feet and toes, particularly as these acral parts of the body seem to be the most susceptible to trauma (Gibbs, 1974). “Gangrene of the skin is often called sphaceloderma” (Costello and Gibbs, 1967, pp. 404-406).
Gangrene can also occur internally and is extremely dangerous if abdominal organs are involved (Griffith, 1995). It does not generally discriminate between the sexes, although a predisposition to malnourished, elderly persons or those with Diabetes mellitus or serious vascular impairment is recognised (Pipkin and Janelli, 2000).
Gangrene can be divided into three categories:
1. Dry gangrene
2. Wet gangrene
3. Gas gangrene
Although the list of contributing factors causing each type of gangrene is “theoretically almost unlimited” (Gibbs, 1974, p. 133), some of the documented causes have been detailed by (Costello and Gibbs, 1967, pp. 404-406) who state that whilst “arteriosclerosis obliterans and thromboangitis obliterans account for 95% of all cases of pvd causing damage, additional causes of gangrene are:
Raynards disease or syndrome
vascular changes with diabetes mellitus
sickle cell anaemia
arterial or venous embolism
phlegmasia cerulea dolens
ergotism and frostbite
congenital anularia constrictions
keratosis hereditarium mutilans
severe and complicated cutaneous pyodermas
cryoglobulinemia and pyoderma gangrenosum
dermatitis nodularis necrotica,
various types of vasculitis
subacute bacterial endocarditis
erysipelas and surgical infections of the palms
Gangrene of the fingertips may also complicate meningitis, malaria, typhus fever, typhoid fever, diptheria and pneumonia. Anthrax or malignant pustule, which is characterized by a carbuncle or papule with black centre surrounded by a halo of vesicles and inflammation, may result in gangrene of the hand. Ulceration of the fingertips has been reported following MI”.
Smoking and excessive alcohol consumption have also been recognised as specific risk factors because of the possibility of arteriosclerosis and interference to the function of the blood vessels respectively (Pipkin and Janelli, 2000) and (Griffith, 1995).
Dry gangrene is caused by a gradual reduction in the blood supply to an area of tissue. The resultant obstruction usually only involves the arterial blood supply without interference to the venous return and is a type of “coagulation necrosis” (Porth, 1998, p. 42).
Unlike wet gangrene, dry gangrene is almost exclusively limited to the extremities (Porth, 1998). In the initial stages of dry gangrene, the affected area is extremely painful to palpate (Pipkin and Janelli, 2000). This area then becomes dry and wrinkled, with distinct colour changes occurring. The skin becomes dark brown at first and as the necrosis continues, turns a dark purplish-blue and then completely black. This process is very slow and a distinct “line of demarcation” is visible between the necrotic tissue of the gangrenous area and the surrounding healthy tissue. This line is one of the most important clinical features of dry gangrene and is the result of inflammation caused by irritation from the dead tissue (Porth, 1998, p. 42).
Good medical history and thorough examination
Tissue or blood cultures from affected site (Griffith, 1995).
As dry gangrene is rarely life threatening, regular monitoring of the progression of the disease is often all that is required. Eventually the area of dead tissue becomes autolytic and healing takes place at the demarcation line between the dead and living tissue (Pipkin and Janelli).
In its early stages however, extreme pain and a high fever are often present and the administering of analgesics may be required.
The prognosis for dry gangrene is very good in the absence of infection. If bacteria invade the necrotic tissue however, then systemic antibiotic therapy will be required as deeper tissues are likely to become infected (Noble, 1987).
Wet gangrene is caused by a bacterial infection in an area of tissue that has been denuded of blood and oxygen. Cells in the area surrounding the necrotizing tissue begin to lyse and release fluid. In the presence of this moist environment, bacteria flourish (Pipkin and Janelli, 2000). The bacteria most likely involved are Staphylococcus epidermidis (Haber and Shuman, 1984), Enterobacter, Kleibsiella and Streptococcus (Fishman and Bartolomei, 1986).
Where the cause of wet gangrene is the Streptococcus bacterium, there is usually evidence of infection (pain, erythema, swelling and heat), with an associated fever. Between 36-72 hours after infection, small vesicles or yellow bullae begin to surround the area, which may appear bluish-black. These blisters (which may exude a foul smelling discharge) (Griffith, 1995) burst and form a black eschar, “...which sloughs in 7-10 days” (Noble, 1987, p. 573).
Unlike dry gangrene, there is no line of demarcation between normal tissue and infected tissue in wet gangrene and the spread is rapid.
Good medical history and thorough examination
Blood and tissue cultures of the area affected
X-rays (Griffith, 1995)
Wet gangrene is usually curable in the early stages with antibiotic therapy and excision of dead tissue (Griffith, 1995). (McCabe, 1998) describes the use of Hyperbaric Oxygen (H2O2) Therapy in the treatment of vascular diseases. This treatment is used to infuse oxygen back into depleted tissues and prevent the proliferation of anaerobic bacteria. Patients are placed into a hyperbaric chamber “...for 1 to 3 hours every 6 to 8 hours...” (Norris, 1995, p. 170).
The spread of infection is very fast and death may occur unless the condition can be prevented from becoming systemic (Porth, 1998).
Gas gangrene is often associated or confused with wet gangrene. (Porth, 1998) however, considers it an individual disease state because infection occuring in devitalized tissues is usually caused by one of the Clostridium bacteria (C. perfringens in about 80-90% of cases, C. novyi or C. septicum) (Black, 1993).
Clostridium perfringens normally resides in the gastrointestinal tract, female genitalia and in soil. It is an anaerobic bacterium, which can invade traumatized tissue, particularly around deep necrotic wounds. Where infection occurs, it produces “...thrombosis of regional blood vessels, tissue necrosis and localized oedema.” (Norris, 1995, p. 169). A release of hydrogen and carbon dioxide subcutaneously from the necrotic tissue produces interstitial gas bubbles. Spores flourish in the anaerobic environment, which multiply and destroy cells in the surrounding tissue.
The onset of gas gangrene occurs rapidly within 12 to 48 hours, with most clinical signs apparent within the first 72 hours post surgery or trauma. The most significant feature of gas gangrene is the audible cracking sound made by the “crepitant tissue” (Black, 1993, p. 567), which can be heard whenever the patient is moved. This is a result of the ongoing metabolic processes in the necrotic tissue.
Other signs include extreme pain, a low fever, ischaemia, loss of pulses, pallor, inflammation and a red or dusky brown discolouration of the area. Within 36 hours after the presentation of symptoms, a bullous eruption may occur, revealing dark red necrotic tissue, with an odorous watery discharge. Anaerobic cellulitis may occur because of blood vessel thrombosis, spreading the infection quickly.
As the infection progresses, the patient becomes pale and limp, exhibiting “...signs of toxemia and hypovolemia (tachycardia, tachypnea and hypotension)...” (Norris, 1995, p.169).
Diagnosis is usually determined by the presenting clinical features and by affirming a recent history of trauma or surgery. Cultures from the wound confirm the diagnosis by recording findings of C. perfringens, with a presentation of gram positive bacillus bacteria. X-rays of the area show black spots within the tissue, synonymous with gas bubbles. Blood tests may reveal leukocytosis and hemolysis in later stages (Norris, 1995).
Debridement of necrotic tissue is carried out prior to the administering of high doses of intravenous penicillin. If signs of myositis or cellulitis appear, then a wide surgical excision of the affected area is carried out. If available, hyperbaric treatment should then be commenced (Norris, 1995).
In severe cases, where treatment has not been administered in time, delirium, coma and circulatory shutdown usually precede death. Where the disease has been diagnosed in its early stages, wide debridement of the area and possible amputation usually precipitate a successful recovery (Norris, 1995).
Black, J.G. 1993. Microbiology: principles and applications. Prentice Hall, Englewood Cliffs.
Costello, M.J. and Gibbs, R.C. 1967. The palms and soles in medicine. Charles C. Thomas, Springfield.
Gibbs, R.C. 1974. Skin diseases of the feet. Warren H. Green, St. Louis.
Griffith, H.W. 1995. Complete guide to symptoms, illness and surgery. The Putnam Berkley Group Inc., Berkley.
Fishman, S.A. and Bartolomei, F.J. 1986. Digital amputation following trauma induced gangrene. Journal of the American Podiatric Medical Association, 76, (6), pp. 351-353.
Haber, G. and Shuman, C. 1984. Diabetic gangrenous ulcerative disease with an ectopic finding. Journal of the American Podiatry Association, 74, (10), pp. 516-517.
McCabe, E. 2000. Oxygen (hyperbaric oxygen) therapy, [http://www.sechristind.com/faq_hbo.html#whatisthedefinition ].
Med Web. [http://medweb.bham.ac.uk/http/mod/3/1/a/appearance.html].
Noble, J. 1987. Textbook of general medicine and primary care. Little, Brown and Company, Boston.
Norris, J. 1995. Professional guide to disease. Springhouse Corporation, Springhouse.
Pipkin, D. and Janelli, A. 2000.Gangrene, [http://brooks.pvt.k12.ma.us/~bheun/gg.html]
Porth, C.M. 1998. Pathophysiology: concepts of altered health. Lippincott, Philadelphia.
Hope this helps and that things get better. I apologize for scaring you into paranoia. Gangrene was only an assumption given by your initial post. Hopefully, what you're experiencing is not a serious case.
I wish you luck and send you prayers.
[This message has been edited by Valhalla (edited 09-28-2002).]