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A 3,480 g male neonate showed tachypnea symptom with a serum ionized calcium level of 0.66 mmol/L by routine clinical analysis. He was injected calcium gluconate intravenously through femoral vein catheter to treat the hypocalcemia. On second day after the injection, he started to show erythema in the flank area. The lesion became firm and changed into whitish crust consist of small crystals. Abdominal X-ray and ultrasonography showed the accumulation of calcium deposit in the subcutaneous layer of the lesion. Surgical debridement was performed to remove the crust with calcium deposit and acellular fish skin graft rich in omega-3 (Kerecis) was applied to the defect site for secondary intention of the defect wound. After 2 months, the skin and soft tissue defect were fully covered with healthy normal skin without depression or contracture. This report is a first case of iatrogenic calcinosis cutis without extravasation symptom.

Iatrogenic calcinosis cutis occurs when insoluble calcium salts deposit in cutaneous and subcutaneous tissue. Iatrogenic calcinosis cutis is a rare complication from a variety of medical interventions, most commonly due to extravasated intravenous calcium-containing solutions. We present a severe case of iatrogenic calcinosis cutis in a patient with end-stage renal disease and an elevated serum calcium-phosphate product. Iatrogenic calcinosis cutis has a wide range of clinical presentations. Either subclinical or clinically noticeable extravasations may cause mild to severe calcinosis cutis. Patients with increased serum calcium and phosphate may be at increased risk of iatrogenic calcinosis cutis. Treatment options include conservative, pharmacologic, or surgical management.

Calcinosis cutis is a term used to describe a group of disorders in which calcium salt deposits form in the skin and subcutaneous tissue. We report a 6-year-old boy with hypoparathyroidism after thyroidectomy who was admitted to the hospital for severe hypocalcemia being treated with calcium gluconate intravenous infusion through peripheral veins. Within a few days we made a diagnosis of iatrogenic calcinosis cutis and treatment with 10% topical sodium thiosulfate was prescribed; complete resolution of lesions was achieved after 6 months, with no local or systemic adverse effects. Because of the lack of noninvasive alternatives and the good tolerance of the treatment, especially in childhood, we suggest the topical use of this drug as an option for this condition.

Calcinosis cutis is a condition in which calcium salts are deposited in the skin and subcutaneous tissue due to various causes. These deposits are classified as dystrophic, metastatic, idiopathic, and iatrogenic calcifications [1]. Dystrophic calcification is characterized by damaged or abnormal local tissues without elevated serum calcium and phosphate levels. Metastatic calcification is caused by abnormal calcium and/or phosphate metabolism. Idiopathic calcification occurs even in the absence of tissue damage or metabolic disorders. Moreover, calcification may also occur as a result of tissue damage or impaired mineral metabolism after medical interventions [2]. We experienced a case of an 18-year-old man who had been diagnosed with acute lymphoblastic leukemia (ALL) as a child and developed iatrogenic calcinosis cutis due to the extravasation of intravenous anticancer drugs. Here, we report our case with a review of the literature. In January 2015, a patient initially diagnosed with ALL in June 2001 visited us for the further evaluation and treatment of a mass. Until September 2004, the patient had been treated with methotrexate, vincristine, and cyclophosphamide at the outpatient clinic of the Department of Pediatrics. In 2002, the patient exhibited extravasation of intravenous anticancer drugs on the dorsum of the right hand. At that time, the patient presented with pain, swelling, redness, and tender inflammation. Over two weeks, the redness and inflammation had improved, but the lesion exhibited a gradual tendency towards firmness. A routine laboratory test showed calcium levels of 9.9 mg/dL and inorganic phosphate levels of 5.4 mg/dL. In February 2007, the patient experienced a relapse of ALL. Until August 2010, the patient received secondary chemotherapy using the same drugs. During this period, in 2008, the patient experienced extravasation of intravenous anticancer drugs on the elbow of the right arm. As in 2002, the patient developed a larger mass two weeks later. A routine laboratory test showed calcium levels of 9.5 mg/dL and inorganic phosphate levels of 5.3 mg/dL. Both masses persisted without changes in their size (Fig. 1). Fig. 1 Preoperative view of the patient. (A) The mass on the dorsum of the right hand. (B) The mass on the elbow of the right arm. On radiography, the patient had a radiopaque lesion at the site of each mass. On sonography, the patient had calcified lesions in the subcutaneous fat layer; the lesion on the dorsum of the right hand measured 3.0×1.1×0.5 cm, and the lesion on the elbow of the right arm measured 4.0×2.6×1.3 cm. These findings were interpreted as a heterotopic ossification. On January 21, 2015, the patient underwent resection of the mass under general anesthesia. Intraoperatively, two subcutaneous encapsulated masses were found: one was found on the dorsum of the right hand and measured 2.4×1.5×0.5 cm, and the other was found on the elbow of the right arm and measured 5.2×2.8×1.4 cm (Fig. 2). Postoperatively, the patient underwent tissue biopsy and was diagnosed with calcinosis cutis (Fig. 3). Thereafter, the patient underwent follow-up at our outpatient clinic, but showed no episodes of recurrence. Fig. 2 Intraoperative view of the patient. (A) The mass on the dorsum of the right hand. (B) The mass on the elbow of the right arm. Fig. 3 Pathologic image showing calcium salts, which can be recognized as either fine granules or small deposits in the dermis (H&E, ×100). Calcinosis cutis may be misdiagnosed as cellulitis, osteomyelitis, arthritis, abscess, periostitis, myositis ossificans, and thrombophlebitis. It is frequently encountered in a clinical setting. When a preoperative X-ray or sonography shows heterotopic ossification, differential diagnoses should include osteoma cutis and calcinosis cutis. Osteoma cutis is a condition in which bone tissue is formed on the skin, with the emergence of a focus of calcification arising from the inflammatory scar or from a granuloma of bony tissue. In contrast, calcinosis cutis is characterized by the deposition of calcium salt in the skin and soft tissue, with the involvement of bony tissue. The pathogenesis of calcinosis cutis has not been fully elucidated. However, many factors causing this disease have been established, and different clinical scenarios, involving various forms of calcinosis cutis, arise from different causes. Tumoral calcinosis is characterized by calcium deposition around joints, and appears in healthy adolescents. It is a type of metastatic calcification that accompanies hyperphosphatemia, and develops after swelling without pain at the major joints such as the shoulder, hips, and elbows. Leukemia cutis occurs with paraneoplastic hypercalcemia due to bony metastases or the production of an abnormal hormone that directly affects calcium and bone metabolism. According to Lestringant et al. [3], this disease is widespread and mainly affects the blood vessels, kidneys, lungs, and gastric mucosa, as well as the skin or subcutaneous tissue. Furthermore, diffuse osteoporosis or spontaneous fractures of small bones may appear. In our case, it was possible to distinguish the clinical course of tumoral calcinosis from leukemia cutis. When the mass first developed, the patient's serum calcium levels were within the normal range and phosphate was slightly elevated, but within the normal range considering that the patient was a child at the time. Therefore, we were able to exclude metastatic calcification with hyperphosphatemia and hypercalcemia. Unlike the general pattern of occurrence observed in diffuse leukemia cutis, the mass arose at the venipuncture site after intravenous injections, subsequent to pain, swelling, and redness. Some case reports have described iatrogenic calcinosis cutis as a complication of the intravenous use of calcium chloride or calcium gluconate [4]. These authors have also noted that iatrogenic calcinosis cutis occurs between two hours and 24 days after extravasation, with an average delay of 13 days [5]. The case of our patient corresponded to this pattern, with calcinosis cutis caused by the extravasation of calcium solutions. The patient developed a mass two weeks after the extravasation of anticancer drugs, which is consistent with the clinical manifestation of calcinosis cutis arising from the extravasation of calcium chloride. According to Goldminz et al. [5], the pathophysiology of calcinosis cutis is based on tissue damage arising from the extravasation of a solution followed by the deposition of crystalline or insoluble calcium phosphate minerals. However, we did not use intravenous calcium therapy. We assume that this case was solely caused by the extravasation of anticancer drugs. The tissue damage caused by the extravasation of anticancer drugs may be assumed to have played an important role in the onset of calcinosis cutis. This is the first case report of calcinosis cutis caused by the extravasation of intravenous anticancer drugs. We believe that our rare case may help elucidate the pathogenesis of calcinosis cutis.

Calcinosis cutis is an uncommon condition characterized by the deposition of calcium salts in the subcutaneous tissues of the body. Calcifications can also occur in a variety of other clinical settings and can be subjected to fine-needle aspiration (FNA). Since cutaneous calcific deposits may clinically mimic a tumor, it is feasible to diagnose them by FNA cytology (FNAC). We reported a case of calcinosis cutis by FNA in a 36-year-old male who presented with a solitary subcutaneous nodule in cubital fossa. Smears showed amorphous granular material consistent with calcium and occasional histiocytes. The diagnosis was confirmed when cytosmears were subjected to a special stain such as the von Kossa stain.

Iatrogenic calcinosis cutis is a rare disorder that can be due to the intravenous administration of calcium or phosphate-containing infusions such as calcium gluconate or calcium chloride with extravasation. Fortunately, the course of calcinosis cutis is benign in immunocompetent children. The treatment remains supportive therapy. After about 6 months, there is no evidence of tissue calcification. We describe a 4-year-old girl with Acute Lymphoblastic Leukemia (ALL) who developed severe calcinosis cutis in the left humerus after extravasation of calcium gluconate during the treatment for the tumor-lysissyndrome-related hypocalcaemia. Surgical debridement and local wound care were not successful, and so a temporary suspension of chemotherapy was necessary to achieve complete healing of the lesion. Notwithstanding this complication, her ALL is in complete hematological remission after 8 months from the diagnosis. No functional or sensitive impairment due to the cutis has persisted.

Calcinosis cutis is characterized by the deposition of insoluble calcium salts in the skin and subcutaneous tissue. The syndrome is separated into five subtypes: dystrophic calcification, metastatic calcification, idiopathic calcification, iatrogenic calcification, and calciphylaxis. Dystrophic calcification appears as a result of local tissue damage with normal calcium and phosphate levels in serum. Metastatic calcification is characterized by an abnormal calcium and/or phosphate metabolism, leading to the precipitation of calcium in cutaneous and subcutaneous tissue. Idiopathic calcification occurs without any underlying tissue damage or metabolic disorder. Skin calcification in iatrogenic calcinosis cutis is a side effect of therapy. Calciphylaxis presents with small vessel calcification mainly affecting blood vessels of the dermis or subcutaneous fat. Disturbances in calcium and phosphate metabolism and hyperparathyroidism can be observed.

A dog with calcinosis cutis was treated by topical dimethyl sulfoxide (DMSO) administration, reaching a complete involution of symptoms. DMSO is well-known for its transdermal penetration and anti-inflammatory capacity. For this reason, DMSO is proposed as a topical treatment for the management of calcinosis cutis in dogs. The authors present the clinical case of a dog with seropositive leishmaniosis and secondary immune-mediated haemolytic anaemia who was affected by intense dermatopathia on the dorsal area, diagnosed by a biopsy as calcinosis cutis. Injuries were described as necrotising ulcerative dermatitis. Currently, there are no specific treatments for its cure. The topical application of DMSO every other day was used as a unique treatment, and the use of other treatments like antibiotics or anti-inflammatory therapy was not necessary. Treating calcinosis cutis via a topical wash with DMSO every other day was effective for the symptoms of calcinosis cutis.

Hypocalcemia most frequently occurs in premature neonates. It is usually treated by intravenous (iv) calcium supplementation. However, complications caused by extravasation of iv calcium gluconate include localized soft tissue calcification, necrosis, cellulitis, osteomyelitis, and even compartment syndrome. We present a rare case of iatrogenic calcinosis cutis complicated by compartment syndrome secondary to extravasation of iv calcium gluconate in a neonate. Emergent fasciotomy was performed twice for decompression of compartment syndrome. Histologic findings revealed necrosis and calcification. Appropriate antibiotics were administered to control secondary infection. To the best of our knowledge, there were no previous case reports of calcinosis cutis with compartment syndrome in infants. Although iatrogenic calcinosis cutis is generally a benign entity, the early recognition of the presentation of extravasation of calcium gluconate is important to avoid severe complications and possible medical malpractice disputes. This report aims to raise doctors' awareness of the presentation, course, and management of this relatively rare iatrogenic complication.

This case report describes a rare differential diagnosis of soft-tissue infection in a neonate. Fever, pain, inflammation, and acute tenderness in the limb of a neonate signify acute infection or osteomyelitis unless proved otherwise. Iatrogenic calcinosis cutis presents with similar symptoms and signs; its diagnosis may be easily confused with an infective condition by an unwary orthopaedic surgeon. This report aimed to raise doctors' awareness on the presentation, aetiopathogenesis, and course of the relatively rare iatrogenic calcinosis cutis.

Calcinosis cutis, the deposition of calcium in the dermis, can be dystrophic, metastatic, iatrogenic, or idiopathic. Here, we describe a case of iatrogenic calcinosis cutis secondary to extravasation of an intravenous calcium-containing solution in a child. We also review the literature regarding the pathogenic mechanisms involved in the development of calcinosis cutis after extravasation injuries. While iatrogenic calcinosis cutis is generally a benign entity, it is important to recognize its unique clinical and histopathologic presentation to avoid complications from misdiagnosis.

Accumulation of calcium in the skin is usually classified as a group of disorders referred to as calcinosis cutis. We report the case of a patient who developed iatrogenic calcinosis at the site of subcutaneous administration of low-molecular-weight heparins (LMWH) as nadroparin. This is usually used for the prevention of deep venous thrombosis, especially following renal transplantation. The role of calcium content in nadroparin is discussed.

Sodium thiosulfate has been successfully used to treat calcyphilaxis in adults and children, but its effect on iatrogenic calcinosis cutis secondary to extravasation of calcium solutions is less known. We describe a 5-year-old boy with acute lymphoblastic leukemia who developed severe calcinosis cutis in the right forearm and hand, and in the left leg and foot after extravasation of calcium gluconate during treatment for tumor-lysis-syndrome-related hypocalcaemia. Surgical debridement, local wound care, hyperbaric oxygen therapy, and sodium thiosulfate infusion achieved a complete healing of all lesions in an eight-month period with a short discontinuation of chemotherapy. No functional or sensitive impairment remained.

An adult male cat presented to the Ontario Veterinary College after having a seizure at the humane society. The cat was diagnosed with primary hypoparathyroidism and was treated with calcium and vitamin D3 supplementation. Calcium supplementation included subcutaneous (SC) administration of diluted calcium gluconate according to protocols described in recent literature. Seven days after SC calcium administration, firm SC masses developed in the intrascapular area where the injections were given and in the dependent axillary area. These areas became raised, formed crusts, necrosed, and left scars. Although not histopathologically confirmed, the author postulates that this was a direct reaction to SC calcium gluconate administration.

Calcification of soft tissues occur, secondary to trauma sustained in the course of neonatal intensive care. They can present with swelling and inflammatory signs, which mimic serious infections of bone, joints and soft tissues. The etiology of the presenting inflammatory response is often unknown and the clinical picture is variable. Hence babies get subjected to more invasive procedures and medications. Recognition is by awareness and radiography the key to diagnosis. Masterly inactivity and vigilance during followup is suggested.

A 27-year-old woman with hypoparathyroidism developed multiple firm white-yellow papules along the path of an infiltrated calcium chloride intravenous infusion. A biopsy specimen obtained ten days after the extravasation revealed an urticarial reaction. A subsequent biopsy specimen, obtained 25 days after the extravasation, showed diffuse dermal calcification, confirmed by roentgenographic analysis, with incipient transepidermal elimination. A biopsy specimen obtained 40 days after the extravasation was consistent with an elimination reaction. An increase in mast cells was not noted. Electron microscopy showed mineral deposits along collagen fibrils without significant collagenous degeneration. In this report we describe a complication of intravenous calcium chloride infusion.