Calcinosis ?

Here at FFLC, we are asked to see a multitude of varied pathologies by surrounding physicians, and we will on occasion recieve difficult wounds which are otherwise well treated, but still fail to heal. This is something that may require advanced care and a more thorough diagnostic approach.

Sometimes wounds will not heal for more obvious reasons, such as too much pressure on the area or underlying bone infections that are present which will preclude closure of the site. But we will also see underlying metabolic pathology which can go unrecognized and lead to failure of wound healing; such as in the case of underlying calcinosis cutis.

What is this?

This can be seen sometimes on plain radiographic images, where one may see some abnormality in the soft tissue which can look like a bone, or bone densities within the soft tissue. This is somewhat rare, but may lead to wound healing delays, and even pain.

Other times this may be found only on skin biopsies of the ulcer may find the calcifications on a microscopic level, and in my opinion any peculiar skin lesion should have a biopsy done to check for cancer or any other pathology that may otherwise not be detected.  In fact, in the case of any non healing ulcer that is present for more than 4 weeks, a biopsy should always be done to further assess and treat the site along with bacterial culture and even CBC and C-reactive protein with BMP labwork.

Basically, there are varieties of presentations of calcinosis cutis, but the main concept here is that it may cause wound healing delays or preclude any healing from the site. This may require systemic treatment and evaluation from renal specialists, rheumatology specialists, and even vascular surgeons to some extent. Regardless, extensive workup must be entertained in any wound care patient in order to identify reasons for nonhealing. This also potentiates the need for aggressive debridement, as the tissue itself may be too compromised for any reasonable healing to occur, and with an aggressive debridement the tissue may be allowed to "reset" and build the scaffolding for dermal/epidermal cells again from "scratch".

OSTEOPOROSIS is a real risk for bone healing.


Two major factors that influence the risk of development of
osteoporosis are the level of bone mass achieved at skeletal
maturity (peak bone mass) and the rate at which bone loss
occurs in later years. The more bone mass available before
age-related bone loss ensues, the less likely it will decrease to
a level at which fractures occur.
Research studies point to a number of risk factors that
may have a strong influence on peak bone mass and the rate
of bone loss, and thus the development of osteoporosis
Some of these factors include: inadequate nutritional
intake, lack of physical activity, smoking, excessive alcohol
consumption, and prolonged use of corticosteroids.
In addition to diet and lifestyle factors, genetic and
ethnic factors significantly influence many aspects of
calcium and skeletal metabolism. Caucasian and Asian
women tend to have lower bone density than African and
Hispanic women and, consequently, are more likely to suffer
from osteoporotic fractures. The same holds true for thin,
smaller boned women. Evidence also suggests there may
be a link between mother and daughter; mothers with
low bone mineral content tend to have daughters with low
bone mineral content. Whether this link is a function of
heredity or the influence of the mother’s habits, or both,
remains uncertain.

HOW MUCH AND WHAT DO WE NEED FOR OUR BONES?

The Recommended Daily Allowance (RDA) for

calcium is currently set at 800 mg for individuals 1-10 years
old and 25 years and older and 1,200 mg for those 11-24
years old and for pregnant or lactating women. However,
these levels are well below the level of intake that many
experts recommend. The authors of a study of recent
intervention trials of calcium supplementation recommended that
the RDA during childhood should be 1,250 mg and 1,450 mg
during adolescence, while others have recommended a
calcium intake of up to 1,800 mg/day during adolescence.
Such an increase in calcium intake during adolescence could
play an important role in the attainment of optimal peak
bone mass.
Regarding the calcium intake for older individuals, many
experts recommend an intake of 1,500 to 2,000 mg/day to
minimize bone loss in some patients. The National
Institutes of Health (NIH) Consensus Conference on Optimal
Calcium Intake recommends calcium intakes of 1,200 to
1,500 mg for 11-24 year olds, 1,000 mg for those 25-50 years,
and 1,500 mg for those over 65.3 In addition, the NIH recommends
a calcium intake of 1,500 mg/day for women over 50
years who are not receiving hormone replacement.
While the RDA levels of calcium may be a source of
debate, the real issue is the fact that a large proportion of the
population isn’t even meeting the current RDA
levels. According to data obtained from the USDA’s
1987-88 Nationwide Food Consumption Survey, the mean
per capita daily consumption of calcium for the U.S.
population was 737 mg. The data for women as a group was
even worse: after age 11, no age group of females achieved
even 75% of the RDA for calcium. And between the ages of
12 to 29, when calcium requirements reach their peak because
of rapid skeletal growth, women consumed <60% of the RDA
for calcium. Therefore, the challenge for the health-care
professional is to educate patients on the importance of lifetime
maintenance of adequate calcium intake.

VITAMIN D


Vitamin D plays an essential role in maintaining a
healthy mineralized skeleton. The main physiologic function
of vitamin D is to maintain serum calcium and phosphorus
concentrations within the normal range to maintain essential
cellular functions and to promote mineralization of the
skeleton. Vitamin D acts primarily to increase serum
calcium by stimulating intestinal absorption of calcium.
Vitamin D insufficiency results in reduced calcium absorption,
a rise in circulating parathyroid hormone, and increased bone
resorption. The elderly often have a low level of vitamin D
deficiency owing to less efficient skin synthesis of vitamin D,
less efficient intestinal absorption, and reduced sun exposure
and vitamin D intake.

Vitamin D deficiency can result in secondary
hyperparathyroidism, a condition that accelerates bone
resorption and thus exacerbates osteoporosis. Vitamin D
deficiency is associated with increased risk of hip fracture,
and several studies have demonstrated that an increase in
calcium intake of 800-1000 mg/day with supplementation of
400-800 units of vitamin D daily will decrease the risk of
vertebral and nonvertebral fractures and increase bone
mineral density.

MAGNESIUM

Although decreased bone mass is the hallmark of
osteoporosis, qualitative changes in bone matrix are also
present, which could result in fragile or brittle bones that are
more susceptible to fracture. There is growing evidence that
magnesium may be an important factor in the qualitative
changes of the bone matrix that determine bone fragility.
Magnesium influences both matrix and mineral metabolism in
bone by a combination of effects on hormones and other
factors that regulate skeletal and mineral metabolism, and by
direct effects on bone itself. Magnesium depletion affects all
stages of skeletal metabolism adversely, causing cessation of
bone growth, decreased osteoblastic and osteoclastic activity,
osteopenia, and bone fragility.

SUPPLEMENTATIONS

Microcrystalline hydroxyapatite concentrate (MCHC) is

an excellent source of bioavailable calcium.27,53-56 MCHC is
derived from whole bone and is complete with the minerals
and organic matrix found in raw bone. In addition to calcium
and the organic components (mostly collagen protein and
mucopolysaccharides), MCHC contains phosphorus,
magnesium, fluoride, zinc, silicon, manganese, and other
trace minerals in the same physiological proportions found in
healthy bone.

Talk to your endocrinologist or primary health care provider
if you are osteoporotic and they may need to prescribe medications
as well to increase the density of your bones to prevent fractures,
improve bone healing potential, and allow for more active and
healthy lifestyles to be preserved.

Smoking is a major problem:


More than 1 billion people worldwide smoke and annually, 5.4 million deaths or 1 death every 6 seconds, is due to tobacco smoking. The prevalence of cigarette smoking in England is at a record low with 21% adult smokers in 2008. Nevertheless, smoking is attributable to 80,000 deaths per year in England and an estimated 8.5 million people still smoke in the United Kingdom.

It is now well known that cigarette smoking has adverse effects on the human body, notably its association with lung cancer.

Anecdotal experiences associating wound healing complications with smoking are well documented in the literature. Despite this, there are only a few large clinical trials attempting to elucidate the relationship between tobacco smoking and wound healing. This has resounding implications not only on the surgical patient, the surgeon but the economics of the NHS as well. The repercussions of abnormal wound healing are perhaps best felt in plastic surgery and in podiatry, where aesthetic value is as important as functional value.

A good portion of patients that we perform surgery on are undergoing elective procedures for reduction in pain, ease of fitting in shoes, and to a lesser degree small digit cosmesis to realign a toe or toes. This is imperitive to understand that as the vessels branch from the popliteal fossa to medium and small named vessels, they become even smaller passed the midtarsal joint into the toes. This directly is impacted by the mechanism which nicotine and other chemicals that are found in cigarrette smoke directly and indirectly lead to vasoconstriction which pinches closed the supply to the tissues which have been traumatized by surgery. This leads to delayed wound healing time and thickened scars, and may lead to gangrene and amputation in select cases.

Effects of smoking at a cellular level


There are more than 4,000 chemicals present in a cigarette. Amongst these chemicals, nicotine and carbon monoxide are important contributors to the detrimental effects smoking has on wound healing.

Carbon monoxide has a 200 times greater affinity to haemoglobin than oxygen. This results in tissue hypoxia as the oxygen-haemoglobin saturation curve shifts to the left. Consequently, the wound healing process is impaired due to the hypoxic state in tissues.

Nicotine acts on the dermal-subcutaneous vascular plexus to cause vasoconstriction. This has serious consequences as many random patterned flaps rely heavily on the plexus for survival. Besides inducing a hypoxic state and causing vasoconstriction, smoking also leads to increased platelet aggregation, creating microangiopathic thromboses which are tiny blood clots in the capillaries. This is particularly detrimental at the wound site as healing depends heavily on existing and new capillaries.

High levels of fibrinogen and haemoglobin are found in smokers and coupled with reduced fibrinolytic activity, local perfusion to the wound site is greatly attenuated, resulting in delayed wound healing.

This is supported by the work of Sarin et al who found that smoking one cigarette could reduce blood velocity by 42%.

In summary, if you smoke, you may be greatly compromising the chances your elective surgery will not be without complications.
 
Here is a published algorithm which may answer why you may be denied elective surgery if you smoke, because it is in your best interests: