Download Calciphylaxis Induced Ulcerations

Calciphylaxis Induced Ulcerations.
John M. Lavelle,1 DO; Paul Liguori MD 2
1. Boston University Medical Center, Rehabilitation
Department
2. Whittier Rehabilitation Hospital, Physical Medicine and
Rehabilitation
Case Diagnosis: Calciphylaxis Induced Ulcerations
Case Description:
We present a case of a 48-year-old male with
multiple full thickness skin ulcers secondary to
calciphylaxis (CPX).The patient had a history
significant for End Stage Renal Disease (ESRD) on
hemodialysis, right nephrectomy,
hyperphosphatemia, hypercalcemia, morbid
obesity, calciphylaxis (CPX) and intractable pain
secondary to multiple necrotic skin ulcerations. The
wounds were located on his right and left lower
abdomen, right medial thigh and the dorsum of his
left foot. These wounds were present for 15
months and nonhealing. The patient experienced
8/10 constant sharp, burning pain in these areas.
The wounds were previously treated with frequent
manual debridement, sulfadiazine and dry clean
dressings (DCD).
The patient was transferred to acute inpatient
rehabilitation for management of his wounds and
intensive rehabilitation therapies. His wounds upon
presentation were full thickness wounds with
eschar formation, slough tissue and moderate to
heavy drainage. Venous mapping and ankle
brachial index were not tolerated secondary to
patient discomfort. Treatment with topical medical
grade honey and DCD, changed daily, along with
non contact, low frequency ultrasound three days
per week was initiated. After 4 weeks of treatment,
the wounds had no further eschar or slough tissue,
decreased in size, and began developing
granulation tissue.
Abdominal wound (descending order): Day
1, Week 2, Week 4
Discussion:
Calciphylaxis is a syndrome of vascular calcification and
skin necrosis. The incidence of CPX is rare and
represents only approximately 1% of patients with
ESRD. Disorders that coincide with calciphylaxis include
chronic renal failure, obesity, diabetes mellitus,
hypercalcemia, hyperphosphatemia, an elevated
calcium-phosphate product, and secondary
hyperparathyroidism. The pathogenesis consistently
involves renal failure–induced abnormalities in calcium
homeostasis. The initial clinical presentation of CPX is
typically skin lesions which appear suddenly over the
abdomen, thighs and buttocks as painful, indurated
nodules. These can progress to necrotic, non-healing
ulcerations. Our patient’s wounds had previously been
treated with standard wound care procedures and
were not healing. The application of non contact, low
frequency ultrasound promoted wound healing and
development of granulation tissue by drawing blood
flow into the wound beds and it provides gentle
debridement. In addition, the use of topical medical
grade honey provides antimicrobial treatment further
promoting an environment conducive to healing and
aids in autolytic debridement.
Conclusions:
The overall mortality rate of patients with CPX is
approximately 60%. We propose that early
treatment to prevent ulcer exacerbation may
reduce the mortality and morbidity rate. Also,
with proper wound healing patients will be able to
improve function and quality of life.