DOCSLIB.ORG

Hypercalcemic Crisis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hypercalcemic Crisis J Am Soc Nephrol 12: S3–S9, 2001 Hypercalcemic Crisis REINHARD ZIEGLER Medizinische Universitätsklinik und Poliklinik, Heidelberg, Germany. Abstract. Hypercalcemia may decompensate from a more or program has to be followed either to prove or to exclude less chronic status into a critical and life-threatening condition, primary hyperparathyroidism. In the first case, surgical neck hypercalcemic crisis. In the majority of cases, primary hyper- exploration is the only way to avoid fatal outcome. The diag- parathyroidism is the cause; humoral hypercalcemia of malig- nostic program should be performed within hours; during this nancy or rarer conditions of hypercalcemia will decompensate time, serum calcium should be lowered. Treatment of choice is less often. The leading symptoms that characterize the crisis hemodialysis against a calcium-free dialysate. Bisphospho- are oliguria and anuria as well as somnolence and coma. After nates could be useful as adjuvant drugs. a hypercalcemic crisis is recognized, an emergency diagnostic Hypercalcemic crisis is a condition involving the decompen- patient received (in addition to intravenously administered sation of hypercalcemia, which could have existed for longer saline solution and furosemide) 300 mg of clodronate admin- periods or could be acute at the first instance of this electrolyte istered intravenously, 100 mg of prednisolone administered disturbance. Compensated hypercalcemia is caused by malig- intravenously, and 100 units of calcitonin administered subcu- nancies in 70% of cases, by primary hyperparathyroidism taneously. Because diuresis did not begin within 6 h, hemodi- (pHPT) in 20% of cases, and by other (rarer) conditions in the alysis was performed, using a calcium-free dialysate. After remaining 10% (1); the majority of cases of hypercalcemic 12 h, arteriovenous hemofiltration was performed for further crisis are caused by pHPT (2). The disease is then parathyro- lowering of the serum calcium concentrations, and then hemo- toxic crisis. The following case history should illustrate this dialysis was repeated. Clodronate (300 mg) administration was situation (3). repeated after 12 h, and calcitonin (100 U) was administered A 42-yr-old woman had experienced episodes of nausea and subcutaneously every 4 h. stomach pain for approximately 1 yr. Three months before Meanwhile, the diagnostic procedure led to the diagnosis of admission, she felt weak and lost initiative; these symptoms parathyroid toxicosis. There was no evidence for tumoral hy- were related to professional and familial stress. An outpatient percalcemia, and parathyroid hormone (PTH) levels, measured examination revealed increased alkaline phosphatase levels. in a fast assay, were 2.5-fold elevated. Neck surgery was Because other liver function test results were normal, the performed. The patient was asystolic for seconds when anes- alkaline phosphatase was thought to be of skeletal origin. thesia was initiated, but the operation could be performed. A Skeletal scintigraphy demonstrated only nonspecific spots near parathyroid adenoma of 8.3 g was found and removed. Post- the ankles. Further examinations were refused. The patient operatively, the patient again became asystolic. Despite all developed tiredness, vomiting, weight loss, and dehydration, efforts at resuscitation, the patient could not be revived. An and she needed to be admitted to the hospital. Clinical chem- autopsy revealed nephrocalcinosis and severe myocardial istry assays revealed extreme hypercalcemia of 5.9 mM, mild calcinosis. hypokalemia of 3.1 mM, and borderline creatinine and urea Approximately 20 yr ago, there were more reports of hyper- concentrations. Fluid supply for rehydration decreased the cal- calcemic crisis (2). It is evident that the current use of earlier cium concentration only to 5.4 mM; the patient was oliguric. fluid supply for critically ill patients and optimized strategies Three days later, she was transferred to our hospital, presenting for intensive care medicine have made hypercalcemic crisis a with hypercalcemic crisis. Renal insufficiency and somnolence rare event. However, the life-threatening condition requires were the primary symptoms. From the history of the patient, rapid action, to avoid a lethal course such as in this case. previous goiter resection must be noted. A diagnostic program to exclude causes other than pHPT was initiated. To decrease the calcium concentrations, the Pathophysiologic Features and Clinical Findings Calcium homeostasis has been a very stable system from early periods of evolution. Our extracellular fluid, including Correspondence to Dr. Reinhard Ziegler, Medizinische Universitätsklinik und the circulation, conserves the calcium content of the primordial Poliklinik, Bergheimer Strasse 58, D-69115 Heidelberg, Germany. Phone: ocean. When life left that ocean to live on land, systems for the 6221-568601; Fax: 6221-56522; E-mail: sekretariat_ziegler@med. uni-heidelberg.de maintenance of optimal calcium concentrations in body fluids 1046-6673/1202-0003 were developed. Calcium was no longer the content of the Journal of the American Society of Nephrology surrounding water; it needed to be taken in and conserved from Copyright © 2001 by the American Society of Nephrology food. The skeleton had the double tasks of taking up calcium S4 Journal of the American Society of Nephrology J Am Soc Nephrol 12: S3–S9, 2001 for stability and acting as a depot for times of poor calcium decreased and contributes to this hypercalcemia. This condi- supply. tion is a disturbance but not a disease. PTH is one of the principal factors in the prevention of Hypercalcemia induces functional disturbances in a group of hypocalcemia. By decreasing calcium excretion, increasing organs, which are considered together as the “hypercalcemic calcium absorption (via calcitriol), and resorbing depot cal- syndrome” (2). Single components are often nonspecific and cium from the skeleton in cases of emergency, it is a major are also observed in many other diseases. If several compo- contributor to normocalcemia. If PTH is autonomously se- nents of the syndrome are present, hypercalcemia is suggested creted in excess, e.g., in pHPT, hypercalcemia develops. (Table 1). Because serum calcium concentration determina- Renal PTH effects are threefold. In addition to the increase tions are not very expensive, they should be performed in cases in calcium reabsorption, PTH stimulates phosphaturia. Phos- with single symptoms and in all cases of the syndrome. phate loss favors an increase in blood calcium levels via the Renal symptoms are polyuria and polydipsia. Diabetes hy- constancy of the calcium ϫ phosphorus ion product. Being a percalcemicus must be investigated in any case of polyuria, glandotrophic hormone, PTH activates renal 1-␣-hydroxylase especially when diabetes mellitus, diabetes insipidus, and tu- and increases the formation of calcitriol. Normal concentra- bulopathies have been excluded. Diuresis attributable to hy- tions of PTH stimulate bone turnover without bone loss, percalcemia is accompanied by potassium loss; hypercalcemia whereas PTH excess induces bone resorption to an extent that generally leads to hypokalemia. cannot be compensated for by new bone formation. In this Intestinal symptoms are nausea, vomiting, and constipation situation, the released calcium is needed for the prevention of more than diarrhea. The secretion of gastric acid and pancreatic hypocalcemia and is not recycled into the newly formed bone. enzymes is increased. The kidneys act as one of the regulatory elements of calcium Central nervous system symptoms are less characteristic, homeostasis by increasing or decreasing calciuria. If calciuria including tiredness, headache, components of an endocrine is abruptly stopped because of renal insufficiency, stored cal- psychologic syndrome (e.g., loss of initiative), and depression. cium may induce a phase of hypercalcemia until the other Cardiac symptoms also are nonspecific. The QT interval is regulatory links have adapted and counter-regulated levels. shortened, and tachycardias may be observed. The increased Intestinal calcium absorption is increased if higher levels of sensitivity to digitalis is relevant. The mechanism of hyperten- calcitriol are present. Whether increased calcitriol concentra- sion accompanying chronic hypercalcemia attributable to tions result from hyperparathyroidism or diseases with in- pHPT is unclear. Chondrocalcinosis (pseudogout) is occasion- creased calcitriol formation (sarcoidosis and other diseases) ally observed. does not make a difference. With the complexity of malignant When hypercalcemia reaches a critical level (Ͼ4mM),two diseases, several mechanisms may lead to hypercalcemia, in- organs are at risk for decompensation. Polyuria may develop cluding the paraneoplastic production and secretion of calcit- into oliguria and finally anuria, especially in case of exsiccosis. riol, the production of PTH-related peptide (PTHrP), and the Untreated hypercalcemic renal insufficiency is lethal. The production of hypercalcemic cytokines such as interleukin-1, other organ at risk is the brain. Psychologic disturbances may interleukin-6, tumor necrosis factor-␣, and prostaglandins (4). develop into somnolence and finally coma. For all patients In addition to these endogenous causes of hypercalcemia, with comas of questionable cause, a calcium-related coma exogenous factors may play causative roles. One factor con- must be excluded. sists of medications that induce hypercalcemia
Load more

Recommended publications
  • Early Manifestation of Calcinosis Cutis in Pseudohypoparathyroidism Type
    European Journal of Endocrinology (2005) 152 515–519 ISSN 0804-4643 CASE REPORT Early manifestation of calcinosis cutis in pseudohypoparathyroidism type Ia associated with a novel mutation in the GNAS gene Felix G Riepe, Wiebke Ahrens1, Nils Krone, Regina Fo¨lster-Holst2, Jochen Brasch2, Wolfgang G Sippell, Olaf Hiort1 and Carl-Joachim Partsch3 Department of Pediatrics, Division of Pediatric Endocrinology, Universita¨tsklinikum Schleswig-Holstein, Campus Kiel, Christian-Albrechts-Universita¨t, 24105 Kiel, Germany, 1Department of Pediatrics, Division of Pediatric Endocrinology and Diabetes, Universita¨tsklinikum Schleswig-Holstein, Campus Lu¨beck, Universita¨t zu Lu¨beck, 23538 Lu¨beck, Germany, 2Department of Dermatology, Universita¨tsklinikum Schleswig-Holstein, Campus Kiel, Christian-Albrechts-Universita¨t, 24105 Kiel, Germany and 3Children’s Hospital, Sta¨dtische Kliniken Esslingen, 73730 Esslingen a.N., Germany (Correspondence should be addressed to W G Sippell; Email: [email protected]) Abstract Objective: To clarify the molecular defect for the clinical finding of congenital hypothyroidism com- bined with the manifestation of calcinosis cutis in infancy. Case report: The male patient presented with moderately elevated blood thyrotropin levels at neonatal screening combined with slightly decreased plasma thyroxine and tri-iodothyronine concentrations, necessitating thyroid hormone substitution 2 weeks after birth. At the age of 7 months calcinosis cutis was seen and the patient underwent further investigation. Typical features of Albright’s heredi- tary osteodystrophy (AHO), including round face, obesity and delayed psychomotor development, were found. Methods and results: Laboratory investigation revealed a resistance to parathyroid hormone (PTH) with highly elevated PTH levels and a reduction in adenylyl cyclase-stimulating protein (Gsa) activity leading to the diagnosis of pseudohypoparathyroidism type Ia (PHP Ia).
    [Show full text]
  • Tumoral Calcinosis and Calciphylaxis Treated with Subtotal Parathyroidectomy and Sodium Thiosulphate
    CASE REPORT eISSN 2384-0293 Yeungnam Univ J Med 2016;33(1):68-71 http://dx.doi.org/10.12701/yujm.2016.33.1.68 Tumoral calcinosis and calciphylaxis treated with subtotal parathyroidectomy and sodium thiosulphate Hyunjeong Cho1, Yongjin Yi1, Eunjeong Kang1, Seokwoo Park1, Eun Jin Cho2, Sung Tae Cho3, Rho Won Chun3, Kyu Eun Lee4, Kook-Hwan Oh1 1Department of Internal Medicine, Seoul National University College of Medicine, Seoul; 2Department of Internal Medicine, Hongseong Medical Center, Hongseong; 3Dr. Chun & Cho`s Medical Clinic & Dialysis Center; 4Department of Surgery, Seoul National University College of Medicine, Seoul, Korea Tumoral calcinosis (TC) is a condition resulting from extensive calcium phosphate precipitation, primarily in the periarticular tissues around major joints. Calciphylaxis is a fatal ischemic vasculopathy mainly affecting dermal blood vessels and subcutaneous fat. This syndrome is rare and predominantly occurs in patients with end-stage renal disease. Here, we report on a rare case involving a patient with TC complicated with calciphylaxis. Our patient was a 31-year-old man undergoing hemodialysis who presented with masses on both shoulders and necrotic cutaneous ulcers, which were associated with secondary hyperparathyroidism, on his lower legs. He underwent subtotal parathyroidectomy, and sodium thiosulfate (STS) was administered for 27 weeks. Twenty months after beginning the STS treatment course, he experienced dramatic relief of his TC and calciphylaxis. Keywords: Tumoral calcinosis; Calciphylaxis; Parathyroidectomy; Sodium thiosulphate INTRODUCTION reported to range from 0.5-3% [2]. The pathomechanisms of these two disorders are poorly understood, but believed to Calcinosis cutis is characterized by the deposition of in- be related to disturbances in mineral metabolism.
    [Show full text]
  • Section XI Extraskeletal (Ectopic) Calcification and Ossification
    Section XI Extraskeletal (Ectopic) Calcification and Ossification Michael P. Whyte Division of Bone and Mineral Diseases, Washington University School of Medicine at Barnes-Jewish Hospital and Center for Metabolic Bone Disease and Molecular Research, Shriners Hospitals for Children, St. Louis, Missouri INTRODUCTION somewhat higher value because they have greater serum phos- phate concentrations compared with adults. However, this is A significant number and variety of disorders cause extraskel- not well established.(5) etal deposition of calcium and phosphate (Table 1). In some, The material that comprises metastatic calcification may be mineral is precipitated as amorphous calcium phosphate or as amorphous calcium phosphate initially, but hydroxyapatite is crystals of hydroxyapatite; in others, osseous tissue is formed. deposited soon after.(2) The anatomic pattern of deposition The pathogenesis of ectopic mineralization is generally attrib- varies somewhat between hypercalcemia and hyperphos- uted to one of three mechanisms (Table 1). First, a supranormal phatemia, but occurs irrespective of the specific underlying “calcium-phosphate solubility product” in extracellular fluid condition or mechanism for the disturbed mineral homeostasis. can cause metastatic calcification. Second, mineral may be Additionally, there is a predilection for certain tissues. deposited as dystrophic calcification into metabolically im- Hypercalcemia is typically associated with mineral deposits paired or dead tissue despite normal serum levels of calcium in the kidneys, lungs, and fundus of the stomach. In these and phosphate. Third, ectopic ossification (or true bone forma- “acid-secreting” organs, a local alkaline milieu may account tion) occurs in a few disorders for which the pathogenesis is for the calcium deposition. In addition, the media of large becoming increasingly understood.
    [Show full text]
  • Parenteral Nutrition Primer: Balance Acid-Base, Fluid and Electrolytes
    Parenteral Nutrition Primer: Balancing Acid-Base, Fluids and Electrolytes Phil Ayers, PharmD, BCNSP, FASHP Todd W. Canada, PharmD, BCNSP, FASHP, FTSHP Michael Kraft, PharmD, BCNSP Gordon S. Sacks, Pharm.D., BCNSP, FCCP Disclosure . The program chair and presenters for this continuing education activity have reported no relevant financial relationships, except: . Phil Ayers - ASPEN: Board Member/Advisory Panel; B Braun: Consultant; Baxter: Consultant; Fresenius Kabi: Consultant; Janssen: Consultant; Mallinckrodt: Consultant . Todd Canada - Fresenius Kabi: Board Member/Advisory Panel, Consultant, Speaker's Bureau • Michael Kraft - Rockwell Medical: Consultant; Fresenius Kabi: Advisory Board; B. Braun: Advisory Board; Takeda Pharmaceuticals: Speaker’s Bureau (spouse) . Gordon Sacks - Grant Support: Fresenius Kabi Sodium Disorders and Fluid Balance Gordon S. Sacks, Pharm.D., BCNSP Professor and Department Head Department of Pharmacy Practice Harrison School of Pharmacy Auburn University Learning Objectives Upon completion of this session, the learner will be able to: 1. Differentiate between hypovolemic, euvolemic, and hypervolemic hyponatremia 2. Recommend appropriate changes in nutrition support formulations when hyponatremia occurs 3. Identify drug-induced causes of hypo- and hypernatremia No sodium for you! Presentation Outline . Overview of sodium and water . Dehydration vs. Volume Depletion . Water requirements & Equations . Hyponatremia • Hypotonic o Hypovolemic o Euvolemic o Hypervolemic . Hypernatremia • Hypovolemic • Euvolemic • Hypervolemic Sodium and Fluid Balance . Helpful hint: total body sodium determines volume status, not sodium status . Examples of this concept • Hypervolemic – too much volume • Hypovolemic – too little volume • Euvolemic – normal volume Water Distribution . Total body water content varies from 50-70% of body weight • Dependent on lean body mass: fat ratio o Fat water content is ~10% compared to ~75% for muscle mass .
    [Show full text]
  • Case Report Calcinosis Cutis Associated with Chronic Sclerodermoid Graft Versus Host Disease: a Case and Review of the Literature
    Hindawi Case Reports in Dermatological Medicine Volume 2020, Article ID 9250923, 4 pages https://doi.org/10.1155/2020/9250923 Case Report Calcinosis Cutis Associated with Chronic Sclerodermoid Graft versus Host Disease: A Case and Review of the Literature Jacqueline Deen , Lisa Byrom, and Ivan Robertson Department of Dermatology, Royal Brisbane and Women’s Hospital, Brisbane, Queensland, Australia Correspondence should be addressed to Jacqueline Deen; [email protected] Received 11 December 2019; Revised 23 January 2020; Accepted 5 February 2020; Published 28 February 2020 Academic Editor: Alireza Firooz Copyright © 2020 Jacqueline Deen et al. )is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We present a rare case of calcinosis cutis associated with chronic sclerodermoid graft versus host disease in a 59-year-old male, 13 years following allogenic bone marrow transplantation. )e etiology of calcification was thought to be dystrophic. Further research is needed to understand the link between calcinosis cutis and chronic sclerodermoid graft versus host disease to assist with selecting appropriate management for these patients. 1. Introduction occurs from the deposition of calcium salts in the skin secondary to medical interventions, typically intravenous Calcinosis cutis is a descriptive term for the deposition of calcium gluconate and calcium chloride. Idiopathic calci- insoluble calcium salts in the dermis and subcutaneous fication occurs in the absence of an underlying tissue injury tissue and is associated with a number of underlying or metabolic disorder. )e final subtype, calciphylaxis, is a disorders.
    [Show full text]
  • Calcinosis Cutis,Calcinosis Circumscripta,And “Mille Feuille
    Calcinosis Cutis, Calcinosis Circumscripta, and “Mille Feuille” Lesions James Yi-Chien Lin, DVM MS; Han-Ju Tsai, DVM MS; Kau-Shen Hsu, DVM; Fun-In Wang, DVM PhD Skin and subcutaneous lesions of 2 cases with natural occurring Cushing’s disease and 1 case with calcinosis circumscripta were compared. Case 1 was typical of osteoma cutis, containing somewhat regularly arranged discrete ossification foci in the mid and deep dermis. Case 2 had layers of “mille feuille”, yellowish to white gritty chalky substances diffusely scattered in the sub- cutis, seen histologically as disseminatedly scattered light purple crystalloid and blue granular mineral salts. Lesions stained orange red with Alizarin Red S indicated the presence of calcium ions. Discrete ossification foci in the deep dermis and early multifocal collagenolysis with mine- ralization were also noted. Case 3 was typical of calcinosis circumscripta, seen grossly as yel- lowish chalky substance in both dermis and subcutis, and histologically as lakes of well- circumscribed light purple crystals and granular deep blue mineral salts. Case 2 had features of calcinosis cutis such as ossification foci and early multifocal collagenolysis. Case 2 also had “mille feuille” that was histologically similar to those mineral salts in case 3, but was not circum- scribed, and was not exactly calcinosis universalis. The component in case 1 was most likely hydroxyapatite Ca10(PO4)6(OH)2; the “mille feuille” of case 2 was most likely “calcium soap” after panniculitis and fat necrosis; and that in case 3 was most likely calcium phosphate CaPO4. Lo- cal factors, such as fluid exudation reflecting how well the inflammation was controlled clinically, may influence the wound healing, and thus the outcome of lesions.
    [Show full text]
  • Role of Phosphate in Biomineralization
    Henry Ford Health System Henry Ford Health System Scholarly Commons Endocrinology Articles Endocrinology and Metabolism 7-25-2020 Role of Phosphate in Biomineralization Sanjay Kumar Bhadada Sudhaker D. Rao Henry Ford Health System, [email protected] Follow this and additional works at: https://scholarlycommons.henryford.com/endocrinology_articles Recommended Citation Bhadada SK, and Rao SD. Role of Phosphate in Biomineralization. Calcif Tissue Int 2020. This Article is brought to you for free and open access by the Endocrinology and Metabolism at Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Endocrinology Articles by an authorized administrator of Henry Ford Health System Scholarly Commons. Calcifed Tissue International https://doi.org/10.1007/s00223-020-00729-9 REVIEW Role of Phosphate in Biomineralization Sanjay Kumar Bhadada1 · Sudhaker D. Rao2,3 Received: 31 March 2020 / Accepted: 14 July 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020 Abstract Inorganic phosphate is a vital constituent of cells and cell membranes, body fuids, and hard tissues. It is a major intracel- lular divalent anion, participates in many genetic, energy and intermediary metabolic pathways, and is important for bone health. Although we usually think of phosphate mostly in terms of its level in the serum, it is needed for many biological and structural functions of the body. Availability of adequate calcium and inorganic phosphate in the right proportions at the right place is essential for proper acquisition, biomineralization, and maintenance of mass and strength of the skeleton. The three specialized mineralized tissues, bones, teeth, and ossicles, difer from all other tissues in the human body because of their unique ability to mineralize, and the degree and process of mineralization in these tissues also difer to suit the specifc functions: locomotion, chewing, and hearing, respectively.
    [Show full text]
  • Understanding Calcinosis and Calciphylaxis
    PRACTICE DEVELOPMENT Understanding calcinosis and calciphylaxis KEY WORDS Calcinosis cutis is a rare cause of non-healing leg ulceration. There are many factors Calcinosis cutis that can delay the healing of venous leg ulceration and the deposition of calcium in Calciphylaxis the skin known as calcinosis cutis is one of these factors. There are five distinct forms: Warfarin-induced skin dystrophic calcification, metastatic calcification, idiopathic calcification, iatrogenic necrosis calcification and calciphylaxis. Warfarin skin necrosis has common clinical features with calciphylaxis and is therefore included in this article, which describes the types of calcinosis cutis, their clinical presentations and limited treatment options. The aim is to highlight these unusual causes and to assist healthcare professionals when faced with a non-healing ulcer. eg ulceration can be defined as a defect in neurotransmission and the blood coagulation the dermis located on the leg (Franks et al, pathway. At a cellular level, it is implicated in 2016). Leg ulceration is a significant clinical cell-to-cell communication (Walshe and Fairley, Lproblem with the majority attributing venous 1995). In the skin, it is specifically concerned with hypertension as the underlying disease process with keratinocyte proliferation, differentiation and venous leg ulceration affecting 1% of the population adhesion (Smith and Yamada, 2002). in the western world (Posnett et al, 2009). However, The level of serum calcium is closely there is a multitude of causative factors of leg ulcers, controlled by the parathyroid hormone. with the term leg ulcer purely signifying the clinical Regardless of this regulation, it is possible for manifestation and not the underlying aetiology.
    [Show full text]
  • Calciphylaxis
    Postgrad Med J 2001;77:557–561 557 Postgrad Med J: first published as 10.1136/pmj.77.911.557 on 1 September 2001. Downloaded from REVIEWS Calciphylaxis R V Mathur, J R Shortland, A M El Nahas Abstract phosphate diet act as sensitising agents result- The phenomenon of calciphylaxis is rare, ing in a high calcium-phosphate product (Ca × but potentially fatal. It has been recog- P; normal range 4.2–5.6 mmol2/l2) with result- nised for a long time in patients with ant precipitation of Ca-P crystals.14 This results chronic renal failure with secondary hy- in diVuse calcification of the media and perparathyroidism. Disturbed calcium internal elastic lamina of small to medium and phosphate metabolism can result in sized arteries and arterioles with intimal prolif- painful necrosis of skin, subcutaneous tis- eration and rarely arterial occlusion causing sue and acral gangrene. Appearance of the tissue necrosis. This entity was given the term lesions is distinctive but the pathogenesis calcinosis cutis to signify vascular calcification remains uncertain. The beneficial eVects with ischaemic epidermolysis as seen in of parathyroidectomy are controversial. patients with chronic renal failure on However, correction of hyperphosphatae- haemodialysis.15–17 Other triggering events in- mia or occasionally hypercalcaemia is clude intravenous iron dextran and albumin imperative. Fulminant sepsis as a conse- infusion, low serum albumin, corticosteroids, quence of secondary infection of necrotic immunosuppression, trauma, subcutaneous in- and gangrenous tissue is a frequent cause jections in obese patients, and protein C and S of patient morbidity and mortality. deficiencies causing hypercoagulability and 8 12 16 18–25 (Postgrad Med J 2001;77:557–561) subsequent thrombosis.
    [Show full text]
  • CALCIUM DEPOSITS in the SKIN (Calcinosis)
    CALCIUM DEPOSITS IN THE SKIN (Calcinosis) What is this problem? Calcium deposits in the skin have a variety of causes, usually of minor significance in the young but indicating serious disease in some older animals. Calcinosis circumscripta is deposits of calcium at bony prominences or in the footpads and mouth. It is usually a disease of large dog breeds and occurs before two years of age. Calcinosis cutis is induced by local damage in susceptible animals. The cause may be either dystrophic (local factors only causing damage leading to calcification) or metastatic (too high a concentration of calcium in the blood leading to deposits of calcium in the locally damaged tissues). In the latter case, there may be multiple calcium deposits. What do we know about the cause? The reason why a particular pet may develop this, or any Image courtesy of Jan Hall, BVM&S, MS, MRCVS, DipACVD, cancer, is not straightforward. Cancer is often seemingly the Clinical Dermatology, culmination of a series of circumstances that come together for Ontario Veterinary College the unfortunate individual. The cause of calcinosis circumscripta is unknown but there is often a genetic component. The most probable immediate cause is an increase in the blood enzyme lipase leading to degeneration of the subcutaneous adipose tissue followed by calcification. Dystrophic causes of calcinosis cutis include idiosyncratic reactions to injections and other foreign materials. The most common cause of metastatic calcinosis cutis in dogs is overproduction of adrenal hormones (corticosteroids or “steroids”). This may be due to overgrowth or cancer of the adrenal glands, or of the pituitary, the gland that controls the adrenals.
    [Show full text]
  • Dermatology Grand Rounds 2019 Skin Signs of Internal Disease
    Dermatology Grand Rounds 2019 skin signs of internal disease John Strasswimmer, MD, PhD Affiliate Clinical Professor (Dermatology), FAU College of Medicine Research Professor of Biochemistry, FAU College of Science Associate Clinical Professor, U. Miami Miller School of Medicine Dermatologist and Internal Medicine “Normal” abnormal skin findings in internal disease • Thyroid • Renal insufficiency • Diabetes “Abnormal” skin findings as clue to internal disease • Markers of infectious disease • Markers of internal malignancy risk “Consultation Cases” • Very large dermatology finding • A very tiny dermatology finding Dermatologist and Internal Medicine The "Red and Scaly” patient “Big and Small” red rashes not to miss The "Red and Scaly” patient • 29 Year old man with two year pruritic eruption • PMHx: • seasonal allergies • childhood eczema • no medications Erythroderma Erythroderma • Also called “exfoliative dermatitis” • Not stevens-Johnson / toxic epidermal necrosis ( More sudden onset, associated with target lesions, mucosal) • Generalized erythema and scale >80-90% of body surface • May be associated with telogen effluvium It is not a diagnosis per se Erythroderma Erythroderma Work up 1) Exam for pertinent positives and negatives: • lymphadenopathy • primary skin lesions (i.e. nail pits of psoriasis) • mucosal involvement • Hepatosplenomagaly 2) laboratory • Chem 7, LFT, CBC • HIV • Multiple biopsies over time 3) review of medications 4) age-appropriate malignancy screening 5) evaluate hemodynamic stability Erythroderma Management 1)
    [Show full text]
  • Chapter 73 1009
    C h a p t e r 73 Fluid and Electrolyte Issues in Pediatric Critical Illness Robert Lynch, Ellen Glenn Wood, and Tara M. Neumayr intraoperative fluids influence acid-base and electrolyte status, PEARLS particularly of vulnerable patients.4 The choice of Na+ content • Hypotonic maintenance IV fluids are associated with mild to and balancing ions of IVF for postoperative or critical care moderate hyponatremia in postoperative patients. maintenance may be important for some patients thus justify- Anesthesia, stress, and inflammatory mediators probably ing additional expense. Clearly 0.18 and 0.225 mM saline is 5,6 contribute. Electrolyte monitoring in patients at risk is associated with a higher incidence of mild hyponatremia, essential for detection and management of the occasional although controlled trials do not show this effect for 0.46 mM 7,8 patient who develops severe hyponatremia. This critical saline. Severe hyponatremia has been associated with pul- effect of the syndrome of inappropriate antidiuretic hormone monary or CNS illness in pediatrics and is infrequent even may occur even in patients on isotonic IV fluids. within those categories, with the exception of children with • Medical patients with high levels of inflammatory mediators traumatic brain injury (TBI). Among patients with those and appear to be at increased risk of significant hyponatremia. other illnesses, the evolving study of the influence of inflam- Interleukin effects on antidiuretic hormone release may matory mediators directly on the hypothalamus and indirectly contribute. on vasopressin secretion may further clarify which patients are 9,10 • Albumin infusions have been generally safe but may at most risk of clinically significant hyponatremia.
    [Show full text]