DOCSLIB.ORG

Assessment and Management of Patients with Abnormal Calcium

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Assessment and Management of Patients with Abnormal Calcium Assessment and management of patients with abnormal calcium Charlotte Eielson Ariyan, MD, PhD; Julie Ann Sosa, MA, MD Calcium is essential for homeostasis, and normocalcemia should calcitonin. Some of these patients may require an urgent para- be maintained strictly during the perioperative period. The biochem- thyroidectomy for calcium control. istry of calcium equilibrium results from the calcium-sensing recep- Hypocalcemia needs to be verified, as many cases of hypocalce- tors on the parathyroid glands, which detect changes in calcium mia are the artifact of hypoalbuminemia. Severe hypocalcemia oc- concentrations and initiate the proper response. curs after subtotal or total parathyroidectomy with auto transplan- Asymptomatic hypercalcemia is a common metabolic de- tation as well as after massive resuscitation or blood transfusion. rangement that is often discovered on routine serum screening. Strategies aimed at correcting calcium concentrations depend on the The most common etiologies are primary hyperparathyroidism severity of symptomatology. If symptoms are mild, oral calcium sup- and cancer. Increasingly, parathyroidectomy is the preferred ther- plementation can be given; otherwise, intravenous calcium should be apy for primary hyperparathyroidism. Severe hypercalcemia (“hy- administered. (Crit Care Med 2004; 32[Suppl.]:S146–S154) percalcemic crisis”) should be managed aggressively with a KEY WORDS: calcium; hypercalcemia; hypocalcemia; parathy- combination of intravenous fluids, steroids, bisphosphonates, and roid; sestamibi alcium is a highly regulated, concentration also affects platelet aggre- tients with metabolic alkalosis often are ubiquitous cation that has gation and function (9). hypocalcemic (13). multiple roles in the body. Normal Calcium Concentrations and Control of Calcium Concentrations. Since the development of life Distribution. Calcium exists in the extra- Concentrations of calcium are highly Con earth, calcium has bound with organic cellular plasma in a free ionized state as modulated through a delicate interplay ligands. Theoretically, calcium evolved well as bound to other molecules. “Nor- between parathyroid hormone (PTH), into this role because its traits facilitate mal” plasma concentrations of total cal- calcitonin, and vitamin D acting on tar- ligand interactions: It is large, positively cium vary between laboratories, but the get organs such as bone, kidney, and the charged, and spherical in shape (1). With range of (bound and unbound) calcium is gastrointestinal tract (Fig. 1). Chief cells evolution, calcium localized to specific usually between 8.5 and 10.2 mg/dL (2.2– in the parathyroid glands secrete PTH, an areas. For example, the extracellular 2.5 mmol/L). The biologically inert 84-amino acid protein, whenever calcium space is abundant with calcium, whereas bound fraction (55% of the total) binds to concentrations decrease. This, in turn, the intracellular concentration remains proteins. Changes in albumin alter total stimulates osteoclasts to increase bone low, except in specialized compartments resorption, the kidney to increase cal- such as the mitochondria and the endo- calcium concentrations significantly, since the majority of protein-bound cal- cium resorption and renal production of plasmic, sarcoplasmic, and nuclear retic- 1,25-dihydroxyvitamin D [1,25(OH) D], ula (2). Gradients in calcium concentra- cium associates with albumin (80%). A 2 small percentage of calcium is associated and the intestine to increase absorption tion are achieved through channels that of calcium and phosphate. Together, with other proteins, such as ␤-globulins, regulate ion flow. The principal calcium these processes raise the calcium concen- or nonprotein molecules such as phos- channels are voltage-gated, ligand-gated, tration. The recently cloned (14) calci- phate and citrate. Mathematical formulas and second messenger-operated, and this um-sensing receptors in the parathyroid correcting for disparate albumin concen- allows cells to use calcium as the most glands detect changes in calcium concen- trations (e.g., corrected calcium ϭ de- common second messenger (3). There- trations, which results in a negative feed- fore, changes in intracellular calcium crease of 0.8 mg/dL for every 1.0 mg back loop that decreases PTH production. concentration affect a myriad of cell func- ϩ decrease in albumin, or [total calcium Calcitonin is a 32-amino acid protein tions, including cell death or apoptosis ϫ Ϫ 0.025] [40 albumin]) can be notori- secreted by the parafollicular cells of the (4); the duration and strength of cardiac ously inaccurate, and an ionized calcium thyroid gland in response to high calcium muscle contraction (5); and smooth mus- concentration should be measured (10). concentrations. Its actions oppose those cle contraction in blood vessels (6), air- Forty-five percent of the total calcium is of PTH. Calcitonin rapidly inhibits bone ways (7), and the uterus (8). Calcium biologically active and exists in the ion- resorption, leading to a transient de- ized form, with a normal concentration crease in serum calcium concentrations. of 4.5–5.0 mg/dL (11). Ionized calcium Vitamin D is ingested or synthesized concentrations are inversely affected by From Yale University School of Medicine, Depart- in precursor form, which then under- ment of Surgery, New Haven, CT. the pH of blood; an increase in pH will goes two hydroxylation steps before Copyright © 2004 by Lippincott Williams & Wilkins decrease the ionized calcium concentra- becoming a molecule that influences DOI: 10.1097/01.CCM.0000117172.51403.AF tion by 0.36 mmol/L (12), such that pa- calcium concentrations. The first hy- S146 Crit Care Med 2004 Vol. 32, No. 4 (Suppl.) Figure 1. Calcium homeostasis and parathyroid hormone (PTH). droxylation step at carbon 25 occurs in paradoxically worsens hypercalcemia cause of hypercalcemia. The biochemical the liver, and the second hydroxylation (16). diagnosis is established by elevated serum step at carbon 1 occurs in the kidney in Hypercalcemia also affects the electric calcium and intact parathyroid hormone response to increased PTH concentra- conduction pathways of the heart. Pa- (iPTH) concentrations with an inappro- tions. The 1,25(OH)2D increases cal- tients with elevated calcium concentra- priately normal or increased 24-hr urine cium and phosphate resorption from tions have electrocardiographic changes calcium concentration, all in the setting the gastrointestinal tract and stimu- marked by shortened QTc intervals (17) of normal renal function. lates bone resorption, thereby raising (Fig. 2). Patients with hyperparathyroid- The most common cause of primary calcium concentrations. ism will demonstrate these electrocardio- hyperparathyroidism is a parathyroid ad- Preoperative Assessment: Hypercalce- graphic findings, which normalize with enoma (85%). Adenomas are benign and mia. Hypercalcemia is defined as an in- successful parathyroidectomy. However, typically affect only one gland, but in 5% crease in serum calcium Ͼ1 mg/mL cardiac arrhythmias or conduction prob- of cases, two glands are affected. Parathy- above the normal range (15). It affects lems generally are not associated with roid hyperplasia affects all glands and is multiple organ systems and leads to a this phenomenon (18). In addition, se- the underlying cause of primary hyper- myriad of clinical symptoms and signs. vere hypercalcemia can cause the Os- parathyroidism in 10% of cases. It can be Gastrointestinal symptoms result from born, or J wave, seen at the tail end of the associated with the multiple endocrine smooth muscle relaxation and include QRS complex, which usually is associated neoplasia I and IIa syndromes. A thor- constipation, anorexia, nausea, and vom- with hypothermia (19). ough history and physical exam should be iting. Neurologically, patients with hy- Increased calcium concentrations also performed to exclude these autosomal percalcemia can be lethargic, hypotonic, have been shown to cause pancreatitis (20, dominant, multiple-organ syndromes. confused, or even comatose. Effects on 21) (see case study presented subsequently). Multiple endocrine neoplasia I includes the kidneys include polyuria, dehydra- hyperparathyroidism, pituitary adenoma, tion, and nephrolithiasis. Dehydration Causes of Hypercalcemia and pancreatic tumors (most commonly leads to proximal tubule resorption of insulinomas or gastrinomas). Multiple sodium and calcium in an effort to ex- Hyperparathyroidism. Primary hyper- endocrine neoplasia IIa includes hyper- pand the extracellular volume, but this parathyroidism is the most common parathyroidism, medullary carcinoma of Crit Care Med 2004 Vol. 32, No. 4 (Suppl.) S147 (29), and bone (30). However, inappropri- ate PTHrp secretion is the primary cause of the hypercalcemia of malignancy. It can lead to pathologic bone fractures and other symptoms of hypercalcemia that portend a poor prognosis (26). PTHrp- induced hypercalcemia is associated with squamous cell (e.g., lung) (31), breast, (32), prostate (33), and (rarely) colon cancer (34) as well as adult T-cell malig- nancies (35, 36) and multiple myeloma (37). Granulomatous Diseases. The associ- ation between hypercalcemia and granu- lomatous diseases such as sarcoidosis was first documented in 1939 (38). Hypercal- cemia occurs secondary to increased 1,25(OH)2D production that is indepen- dent from the normal negative feedback mechanisms (39). Macrophages in gran- ulomas produce 1,25(OH)2D (40). Other granulomatous disease such as tubercu- losis, leprosy,
Load more

Recommended publications
  • A Case of Calciphylaxis with an Unfavorable Outcome
    CASE LETTER 671 However, the present patient exhibited the peculiarity References of an intense inflammatory infiltrate in the dermis rarely seen previously. According to this case, an atypical intense 1. Sitaru C, Zillikens D. Mechanisms of blister induction by autoan- inflammation could be a distinct histopathological feature tibodies. Exp Dermatol. 2005;14:861---75. of trauma-induced pemphigus. Further research is neces- 2. Sagi L, Trau H. The Koebner phenomenon. Clin Dermatol. sary to ascertain if greater inflammation in dermis is more 2011;29:231---6. related to trauma-induced pemphigus as opposed to those 3. Jang HW, Chun SH, Lee JM, Jeon J, Hashimoto T, Kim IH. Radiotherapy-induced pemphigus vulgaris. J Dermatol. not related to trauma. 2014;41:851---2. In conclusion, this report describes a presumably new 4. Daneshpazhooh M, Fatehnejad M, Rahbar Z, Balighi K, case of trauma-induced pemphigus. To the author’s knowl- Ghandi N, Ghiasi M, et al. Trauma-induced pemphigus: a edge, there are no prior reports of pemphigus involving case series of 36 patients. J Dtsch Dermatol Ges. 2016;14: predominantly the breasts with such a peculiar dispo- 166---71. sition. It is proposed that a hypothetical continuous 5. Balighi K, Daneshpazhooh M, Azizpour A, Lajevardi V, trauma with the bra could explain this unique loca- Mohammadi F, Chams-Davatchi C. Koebner phenomenon tion. in pemphigus vulgaris patients. JAAD Case Rep. 2016;2: 419---21. Financial support Fernando Garcia-Souto None declared. Department of Dermatology, Valme University Hospital, Seville, Spain Author’s contributions E-mail: [email protected] Received 14 November 2019; accepted 5 March 2020 Fernando Garcia-Souto: Conception and planning of the manuscript; writing and critical revision of the manuscript; https://doi.org/10.1016/j.abd.2020.03.010 approval of the final version.
    [Show full text]
  • Extensive Skin Necrosis Ulcers and Systemic Vascular Insufficiency Syndrome with Calciphylaxis: a Case Report
    Urology & Nephrology Open Access Journal Case Report Open Access Extensive skin necrosis ulcers and systemic vascular insufficiency syndrome with calciphylaxis: a case report Abstract Volume 5 Issue 4 - 2017 Calciphylaxis is a part of systemic vascular calcification that is commonly seen in patients 1 2,3 with end stage renal disease. It presents as skin ischemia and necrosis due to calcification Alexander M Swan, Nancy J Fried, 2,3 2 of dermal arterioles. There is no consensus on optimal treatment and the condition is Charisma Lee, Thein Aung, Zaw Nyein associated with a high mortality rate. Here we report a patient on peritoneal dialysis with Aye,2 Deepthi Gunasekaran2 a high calcium-phosphorus product and extensive calciphylaxis involving the extremities, 1Wilkes University, USA back and scalp. We used a multi-interventional approach to treat this patient with a good 2Nephrology Hypertension Renal transplant and Renal Therapy, outcome. The underlying pathology of systemic vascular calcification and insufficiency USA 3 may involve other vascular beds such as the coronary and cerebral vasculature. Early Rutgers New Jersey Medical School, USA detection of these conditions may improve outcomes in these patents. Correspondence: Alexander M Swan, AA Prof of Medicine, Keywords: necrotic ulcer of skin, calciphylaxis, calcium-phosphorus product, vascular Rutgers New Jersey Medical School, 185 S Orange Ave, Newark, calcification, systemic vascular insufficiency NJ 07103, President, Garden State Kidney Center, 345 Main Street, Woodbridge, NJ 07095, USA, Tel 732-750-5555, Fax 732- 750-5550, Email Received: November 10, 2017 | Published: October 26, 2017 Abbreviations: ESRD, end-stage renal disease; CUA, calcific secondary to hypertension and peritoneal dialys is was initiated 5years uremic arterilopathy; LMWH, low molecular weight heparin ago after multiple access problems with hemodialysis.
    [Show full text]
  • AACE Annual Meeting 2021 Abstracts Editorial Board
    June 2021 Volume 27, Number 6S AACE Annual Meeting 2021 Abstracts Editorial board Editor-in-Chief Pauline M. Camacho, MD, FACE Suleiman Mustafa-Kutana, BSC, MB, CHB, MSC Maywood, Illinois, United States Boston, Massachusetts, United States Vin Tangpricha, MD, PhD, FACE Atlanta, Georgia, United States Andrea Coviello, MD, MSE, MMCi Karel Pacak, MD, PhD, DSc Durham, North Carolina, United States Bethesda, Maryland, United States Associate Editors Natalie E. Cusano, MD, MS Amanda Powell, MD Maria Papaleontiou, MD New York, New York, United States Boston, Massachusetts, United States Ann Arbor, Michigan, United States Tobias Else, MD Gregory Randolph, MD Melissa Putman, MD Ann Arbor, Michigan, United States Boston, Massachusetts, United States Boston, Massachusetts, United States Vahab Fatourechi, MD Daniel J. Rubin, MD, MSc Harold Rosen, MD Rochester, Minnesota, United States Philadelphia, Pennsylvania, United States Boston, Massachusetts, United States Ruth Freeman, MD Joshua D. Safer, MD Nicholas Tritos, MD, DS, FACP, FACE New York, New York, United States New York, New York, United States Boston, Massachusetts, United States Rajesh K. Garg, MD Pankaj Shah, MD Boston, Massachusetts, United States Staff Rochester, Minnesota, United States Eliza B. Geer, MD Joseph L. Shaker, MD Paul A. Markowski New York, New York, United States Milwaukee, Wisconsin, United States CEO Roma Gianchandani, MD Lance Sloan, MD, MS Elizabeth Lepkowski Ann Arbor, Michigan, United States Lufkin, Texas, United States Chief Learning Officer Martin M. Grajower, MD, FACP, FACE Takara L. Stanley, MD Lori Clawges The Bronx, New York, United States Boston, Massachusetts, United States Senior Managing Editor Allen S. Ho, MD Devin Steenkamp, MD Corrie Williams Los Angeles, California, United States Boston, Massachusetts, United States Peer Review Manager Michael F.
    [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]
  • 95F325afe6daa80601f51b046b3
    D.M. DEGREE EXAMINATIONEPHROLOGY-PAPER - I Basic Sciences And Applied Nephrology 30 m 1) Discuss renal acid handling and pathomechanism of renal tubular acidosis 2) Discuss the role of ‘Klotho – FGF 23 complex’ in health and chronic kidney disease 3) Enumerate causes for hypokalemia and describe in detail about potassium homeostasis 4) The ageing kidney 5) Discuss the role of complement in renal disease 6) Discuss in detail the pathogenesis of membranous glomerulonephritis and its management 7) Discuss the etiopathogenesis of the syndrome of inappropriate secretion of anti diuretic hormone. How can it be recognized and managed? 8) Describe Nephron dosing and its clinical relevance 9) Discuss the relevant physiological changes of pregnancy and pathogenesis of toxemia of Pregnancy 10) Discuss in brief Physiology of Vitamin D, vitamin D analogues and their role in nephrology practice 11) Discuss the pathogenesis, evaluation and management of disorders of micturition 12) Discuss in brief embryological development of the kidney and its clinical relevance 13) Discuss renal handling of sodium and diagnostic approach to hyponatremia 14) Discuss aetiology, pathogenesis, clinical features and management of hepato renal syndrome 15) Discuss the etiopathogenesis of the syndrome of inappropriate secretion of anti diuretic hormone. How can it be recognized and managed? 16) Describe the etiology, clinical manifestations, diagnosis & management of metabolic alkalosis 17) Describe the mechanism and types of proteinuria. What are the therapeutic interventions that may be used to reduce proteinuria 18) Describe the renin-angiotensin system and its physiologic role. Discuss its role in the pathophysiology of renal disease 19) Discuss pathophysiology of proteinuria, classify proteinuria, name diseases which produces different types of proteinuria.
    [Show full text]
  • A Fatal Complication Not Only in End-Stage Renal Disease Patients
    PRACA KAZUISTYCZNA Folia Cardiologica 2020 tom 15, nr 2, strony 164–168 DOI: 10.5603/FC.2020.0022 Copyright © 2020 Via Medica ISSN 2353–7752 Calciphylaxis — a fatal complication not only in end-stage renal disease patients Kalcyfilaksja — śmiertelne powikłanie nie tylko u pacjentów ze schyłkową niewydolnością nerek Ada Bielejewska1●iD, Arkadiusz Bociek1●iD, Andrzej Jaroszyński1, 2●iD 1Collegium Medicum, Jan Kochanowski University, Kielce, Poland 2Nephrology Clinic, Provincial Integrated Hospital in Kielce, Poland Abstract We present a fatal case of the end-stage renal disease complication that is calciphylaxis. Also known as calcific uremic arteriolopathy, it is characterised by vascular calcification, necrosis of the skin and adipose tissue, and constant severe pain of the affected areas. Key words: calciphylaxis, calcific uremic arteriolopathy, end-stage renal disease, complications Folia Cardiologica 2020; 15, 2: 164–168 Introduction some cancers (treated with chemotherapy), liver cirrhosis, and autoimmune diseases. Risk factors of calciphylaxis Calciphylaxis, also known as calcific uremic arteriolopathy include, among others, haemodialysis, female sex, obesi- (CUA), is a rare disease with an estimated annual incidence ty, diabetes mellitus, Caucasian ethnicity, hypercalcemia, ranging from 1 to 35 in every 10,000 haemodialysed pa- hyperphosphatemia, hyperparathyroidism (both primary tients worldwide [1]. Its pathogenesis in unclear. Calciphyla- and secondary), adynamic bone disease, elevated al- xis affects small vessels of the skin and fatty tissue, as cal- kaline phosphatase, autoimmune diseases, hypoalbu- cium deposits accumulate within their walls. This, together minemia, genetic polymorphisms, abnormalities within with thrombotic occlusion, leads to ischaemic necrosis of the coagulation system, recurring skin trauma (e.g. from the skin that causes severe pain within the affected areas subcutaneous injections) and medications (e.g.
    [Show full text]
  • A Case of Calciphylaxis and Chronic Myelomonocytic Leukemia
    A Case of Calciphylaxis and Chronic Myelomonocytic Leukemia Heather W. Goff, MD; Ronald E. Grimwood, MD A 70-year-old woman presented for evaluation of trauma as physiologic challengers in calciphylaxis in symmetric necrotic ulcers of the lower extremities. humans as well.5-7 Biopsy results revealed changes consistent with calciphylaxis. The predisposing factors in this Case Report patient included calcium supplementation, obe- A woman came to our hospital for a second opinion sity, female gender, viscous blood, renal failure, regarding symmetric necrotic ulcers with central and diabetes mellitus. To our knowledge, this is leathery eschar and surrounding violaceous erythema the first report of calciphylaxis occurring in the and bullae on the inferior and posterior aspects of setting of chronic myelomonocytic leukemia. We both lower extremities; these lesions had begun discuss the history, clinical presentation, diagno- developing 3 weeks earlier (Figure 1). According to sis, and treatment of calciphylaxis. the patient’s history, the lesions were initially Cutis. 2005;75:325-328. painful, hard, lumpy areas, which eventually pro- ceeded to break down into small individual viola- ceous papules with central ischemic ulceration; the alciphylaxis involves a pathologic calcifica- papules gradually eroded from about 1 cm to larger tion of nonosseous tissue for which neither than 10 cm in diameter. C hypercalcemia nor hyperphosphatemia is The patient also had risk factors for calciphy- necessary. The condition results in calcification of laxis, including calcium supplementation, obesity, subcutaneous arterioles and infarctions of subcuta- female gender, viscous blood, renal failure, and neous adipose tissue. Although the etiology of cal- diabetes mellitus. In addition, the patient had a ciphylaxis is unclear, many predisposing factors history of chronic myelomonocytic leukemia, hypo- have been identified.1-3 thyroidism, and recent colon cancer resection.
    [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]
  • 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]
  • Fast Facts Core Curriculum Renal
    ! Fast Facts Core Curriculum Renal #114 Myoclonus . 2-3 #133 Non-Oral Hydration in Palliative Care. 4-5 #134 Non-Oral Hydration Techniques in Palliative Care . .6-7 #161 Opioid Use in Renal Failure . 8-9 #163 Decision Making in Chronic Kidney Disease . 10-11 #191 Prognostication in Patients Receiving Dialysis . 12-14 #207 Withdrawal of Dialysis: Decision- Making . .15-16 #208 Clinical Care Following Withdrawal of Dialysis . 17-18 #220 Hypodermoclysis . 19-21 #287 Drug-Induced Acute Urinary Retention . 22-24 #313 Thirst in Palliative Care . 25-27 !1 #325 Uremic Calciphylaxis . .28-30 #337 Palliation of Bladder Spasms . 31-33 !2 ! FAST FACTS AND CONCEPTS #114 MYOCLONUS Nicholas DeMonaco and Robert Arnold MD Background Myoclonus is an abnormal movement described as a sudden, brief, shock-like, involuntary movement caused by active muscle contraction (positive myoclonus) or inhibition of ongoing muscle contraction (negative myoclonus). Myoclonus can have a distribution that is focal, multifocal, or generalized. This Fast Fact discusses its causes, evaluation, and therapy. Characteristics and Differential Diagnosis Hiccups are an example of normal, physiological positive myoclonus, while asterixis is an example of negative myoclonus seen with metabolic encephalopathy. In nocturnal myoclonus or periodic leg movement disorder, there is activity in the flexor muscles of the legs and feet during light sleep. It can be seen in the setting of chronic nervous system diseases or in elderly patients with no other abnormalities. The brief, shock-like movements of myoclonus may be difficult to distinguish from other involuntary movements such as cramps, spasms, fasciculations, and dystonia. Fasciculations are brief involuntary muscle twitches that, unlike myoclonus, often do not result in movement across a joint.
    [Show full text]
  • Calciphylaxis in Renal Substitution Therapy Calcifilaxis En Terapia De Sustitución Renal
    Rev. Colomb. Nefrol. 2019;6(1): 68-72, january – june 2019 http://www.revistanefrologia.org Rev. Colomb. Nefrol. 2019;6(1): 68-72Cas, eneroe - junireporto de 201 9 http://www.revistanefrologia.org doi: http://dx.doi.org/10.22265/acnef.6.1.327http:/ /dx.doi.org/10.22265/acnef.6.1.327 Calciphylaxis in renal substitution therapy Calcifilaxis en terapia de sustitución renal Diego Alexander Mendoza Panta, Jorge Washington Huertas Garzón, Washington Xavier Osorio Chuquitarco Servicio de Nefrología, Hospital de Especialidades FF. AA. No. 1. Quito, Ecuador Abstract Calciphylaxis is one of the less common complications of Chronic Advanced Kidney Disease, especially in renal replacement therapy, the exact pathophysiology of its appearance is unknown, but it is believed that it is due to an alteration in bone-mineral metabolism. We describe a clinical case of a patient with chronic kidney disease, who presented as a serious complication calciphylaxis, reaching this diagnosis thanks to the characteristic images of this pathology taken from the bank of the Hospital’s imaging service. In conclusion, calciphylaxis, despite being a pathology difficult to find nowadays due to better control of bone-mineral metabolism, should be considered especially in those patients with rapid progression of renal disease and presence of suppurative calcified lesions in extremities. Key words: chronic kidney disease, calciphylaxis, bone-mineral metabolism, renal replacement therapy. doi: http://dx.doi.org/10.22265/acnef.6.1.327 Resumen La calcifilaxis es una de las complicaciones menos comunes de la enfermedad renal crónica avanzada, sobre todo en terapia de sustitución renal, se desconoce la fisiopatología exacta de aparición, pero se cree, que es por una alteración en el metabolismo óseo- mineral.
    [Show full text]
  • Electrolytes in the ICU Syed Zaidi, Rahul Bollam and Kainat Saleem
    Chapter Electrolytes in the ICU Syed Zaidi, Rahul Bollam and Kainat Saleem Abstract Electrolyte disorders is an imbalance of certain ionized salts (sodium, potassium, calcium, bicarbonate, chloride) in the blood. Healthcare providers should be famil- iar with the principles of electrolyte physiology and pathophysiology. Disturbances in sodium homeostasis are primarily caused by volume abnormalities leading to primarily neurologic symptoms. Dyskalemias frequently present with cardiac man- ifestations therefore should be treated promptly before evaluating its cause. Ion deficiencies such as hypocalcemia, hypomagnesemia and hypophosphatemia should be corrected as they are associated with increased adverse events in critically ill patients. Keywords: Electrolytes, Sodium, Potassium, critically ill, ICU 1. Introduction Electrolytes are elements that naturally occur in the human body and help balance pH, facilitate passage of fluid through osmosis and regulate the function of neuromuscular, endocrine and excretory systems. Disturbances in these electrolytes are common clinical problems encountered in the intensive care unit with serious complications when they are depleted. Recent studies report that electrolyte imbal- ances are associated with increased morbidity and mortality. Possible mechanisms include damage to the kidney, activation of hormonal systems (such as RAAS) or the myriad of medication given in a critically ill patient. This chapter will focus on various electrolyte abnormalities seen in the critical care setting then touch on important ICU scenarios which could affect electrolytes. 2. Disorders of sodium homeostasis • Serum sodium reflects the plasma tonicity and is inversely related to total body water. Changes in sodium are generally due to changes in total body water, not serum sodium, which regulates plasma tonicity and effective arterial volume.
    [Show full text]