Challenges in Management of Diabetic Ketoacidosis in Hemodialysis Patients, Case Presentation and Review of Literature

Total Page:16

File Type:pdf, Size:1020Kb

Challenges in Management of Diabetic Ketoacidosis in Hemodialysis Patients, Case Presentation and Review of Literature Diabetes & Metabolic Syndrome: Clinical Research & Reviews 13 (2019) 2481e2487 Contents lists available at ScienceDirect Diabetes & Metabolic Syndrome: Clinical Research & Reviews journal homepage: www.elsevier.com/locate/dsx Review Challenges in management of diabetic ketoacidosis in hemodialysis patients, case presentation and review of literature * Ayman Aly Seddik a, 1, Alaaeldin Bashier b, , 1, Amna Khalifa Alhadari a, Fakhryia AlAlawi a, Hind Hassan Alnour a, Azza Abdulaziz Bin Hussain b, Andrew Frankel c, Mohammed Jaffer Railey a a Nephrology Units, Dubai Hospital, Dubai Health Authority, United Arab Emirates b Endocrine Department, Dubai Hospital, Dubai Health Authority, United Arab Emirates c Imperial College Healthcare NHS Trust, UK article info abstract Article history: Chronic kidney disease is associated with accumulation of uremic toxins that increases insulin resistance Received 22 May 2019 which will lead to blunted ability to suppress hepatic gluconeogenesis and reduce peripheral utilization Accepted 27 June 2019 of insulin. CKD patients fail to increase insulin secretion in response to insulin resistance because of acidosis, 1,25 vitamin D deficiency, and secondary hyperparathyroidism. Hemodialysis causes further Keywords: fluctuations in glycemic control due to alterations in insulin secretion, clearance and resistance. DKA is Diabetes mellitus uncommon in hemodialysis patients because of the absence of glycosuria and osmotic diuresis which Diabetic ketoacidosis accounts for most of the fluid and electrolyte losses seen in DKA, anuric patients may be somewhat ESRD Hemodialysis protected from dehydration and shock, although still subject to hyperkalemia and metabolic acidosis. Hyperkalaemia However, substantial volume loss can still occur due to a prolonged decrease in oral intake or increased Hyperphosphatemia insensible water losses related to tachypnoea and fever. There is no current guidelines for the man- Hypomagnesemia agement of diabetic ketoacidosis in anuric hemodialysis patients considering their differences than Insulin therapy general population. In this review article we reviewed the literature and came with specific recom- mendations for management of Ketoacidosis in patients with CKD treated by hemodialysis. © 2019 Diabetes India. Published by Elsevier Ltd. All rights reserved. 1. Background to the metabolic complications of hyperglycaemia or ketoacidosis, but it is a consequence of the underlying precipitating illness [6,7]. Diabetes is leading cause of end-stage renal failure (ESRF) in Acute complications of diabetes such as Diabetic Ketoacidosis developed countries accounting for 40% of new ESRF cases in the (DKA) can be encountered in ESRF. DKA in ESRF presents a diag- USA and 25% of incident cases in the UK. The mortality rates for nostic and therapeutic challenge as illustrated by the five cases dialysis patients are high [1], with 10% first-year mortality rate for described in Supplement 1. The Japanese Society for Dialysis patients on maintenance hemodialysis (HD) reported in UK [2]. Therapy has also published a series of 14 case reports which These patients are at a particularly high-risk and the overall sur- describe the varying clinical presentation of DKA in ESRF [8] vival for patients with diabetes on maintenance HD is reported to (Table 1). The purpose of this paper is to provide recommendations be approximately halved compared to their non-diabetic peers (3.7 for the diagnosis and treatment of DKA in ESRF with particular vs. 7 years) [2]. In adult subjects with DKA (Diabetic Ketoacidosis), focus on areas where management differs from patients with the overall mortality is <1%; however, a mortality rate >5% has been preserved renal function. reported in the elderly and in patients with concomitant life- threatening illnesses [3e5]. In such situations, death is rarely due 2. Metabolic alterations In DKA, the effective insulin concentration is decreased while the concentration of counter-regulatory hormones (catechol- * Corresponding author. P.O. Box 94132, Dubai, United Arab Emirates. E-mail address: [email protected] (A. Bashier). amines, cortisol, glucagon and growth hormone) is increased 1 Joint first authors. resulting in hyperglycemia and ketosis. Hyperglycemia occurs due https://doi.org/10.1016/j.dsx.2019.06.022 1871-4021/© 2019 Diabetes India. Published by Elsevier Ltd. All rights reserved. 2482 A.A. Seddik et al. / Diabetes & Metabolic Syndrome: Clinical Research & Reviews 13 (2019) 2481e2487 Table 1 Case Reports published by The Japanese Soceity for Dialysis Therapy (Adapted from Ref. [8]). þ No. Age (yrs) Gender Type of DM Blood Glucose level (mg/dl) Arterial Blood pH Serum K level (mEq/L) 1 46 M 1 1467 7.09 6.6 2 63 F 1 1270 6.97 e 3 32 F 1 1912 6.76 7.2 465F e 609 7.15 e 536F ee e e 665M ee e e 7 71 F 2 1645 e 8.6 8 40s M 1 1365 7.10 8.5 9 35 M 1 1686 6.54 e 10 46 M 1 1520 7.10 7.5 11 58 M 1 1363 6.84 9.6 12 45 M 1 1360 ee 13 62 M 2 838 7.09 8.3 14 58 M e 1001 6.81 e Mean 52 1336 6.54 8.0 SD 13 369 0.20 1.0 SD e Standard Deviation, M e Male, F e Female, DM e Diabetes Mellitus. to increased gluconeogenesis, accelerated glycogenolysis, and [where Na is the serum sodium concentration, the multiple 2 ac- impaired glucose utilization by peripheral tissues [9e12]. This is counts for the osmotic contribution of the anions accompanying accompanied by transient insulin resistance. Insulin deficiency sodium (primarily chloride and bicarbonate), and 18 and 28 are combined with elevated counterregulatory hormones in DKA leads conversion factors from units of mg/dL into mmol/L respectively to the release of free fatty acids into the circulation from adipose [16e18]]. tissue (lipolysis) resulting in unrestrained hepatic fatty acid Interestingly, reports of DH and DKA are more frequently seen oxidation in the liver to ketone bodies (b-hydroxybutyrate and with patients on hemodialysis (HD) as compared to peritoneal acetoacetate) [13], leading to ketonemia and metabolic acidosis. dialysis (PD) [19e21]. No difference in serum sodium concentration In a state of preserved renal function, hyperglycemia-induced or tonicity was found between the two dialysis modalities for a osmotic diuresis can result in clinically significant extracellular comparable degree of hyperglycemia. volume deficits, dehydration and sodium depletion. The estimated The solute and fluid disturbances seen in patients with DH is fluid loss is nearly 6e10L with raised serum osmolality of different from the changes caused by hyperglycemia in patients 320e340mOsmol/L [14]. Hyperglycemia leads to a hypertonic state with preserved renal function as it is not complicated by osmotic in patients with preserved renal function as well as in patients on diuresis. The presence of hyperglycemia should lead to the devel- dialysis. In dialysis patients, diuresis is absent or minimal. However, opment of a hypertonic state in patients on dialysis and in those the accumulation of glucose in the extracellular space (EC) during with preserved renal function. However, DH results in extracellular development of hyperglycemia causes both hypertonicity and shifts volume expansion while severe hyperglycemia in preserved renal of intracellular fluid into the EC resulting in what is called dialysis function causes a clinically significant extracellular volume deficit. associated hyperglycemia (DH). In Dialysis associated hyperglyce- In DH baseline extracellular volume is theoretically an important mia (DH) and DKA or Hyperosmolar Hyperglycemic State (HHS) determinant of the degree of hypertonicity and extracellular vol- there is extracellular volume expansion resulting in edematous ume expansion in edematous patients is expected to result in patients having greater hypertonicity and extracellular hyper- greater hypertonicity and greater extracellular hypervolemia volemia than euvolemic or hypovolemic subjects with the same compared to euvolemic or hypovolemic subjects with the same degree of hyperglycemia [15,16]. degree of hyperglycemia. It is important to distinguish between tonicity and osmolality to understand the hyperglycemic changes in body fluids and solutes. 3. Diagnosis Osmolality and tonicity are related but not synonymous. Serum osmolality is the sum of all solutes in the serum (intracellular and Recommendation 1: DKA in patients with ESRD on HD is a rare extracellular), while tonicity (or effective osmolality) is the part of clinical presentation and difficult to diagnose. Since ESRD is a state total osmolality contributed by extracellular solutes having diffi- of persistent chronic metabolic acidosis, DKA should be suspected culty crossing cell membranes, therefore resulting in steady-state in patients with diabetes (specially type 1) who are unwell with an fluid shifts between extracellular compartment and intracellular acidosis that is greater than would normally be (persistent). In such compartment [15,16]. A high urea concentration is usually case measurement of Serum b-hydroxybutyrate is a useful tool in encountered in these situations, but it does not contribute to establishing diagnosis of DKA in patients with ESRD on HD. tonicity. Diagnostic criteria for DKA include presence of blood glucose The parameter of interest in DH patients and its management is >250 mg/dl, arterial pH of 7.30, bicarbonate level of 18 mEq/L, tonicity because it is the source of changes in cell volume and can and adjusted for albumin anion gap of >10e12 [22]. There is also an cause neurological manifestations in hyperglycemia [17]. Tonicity increase in the blood
Recommended publications
  • 1 Fluid and Elect. Disorders of Serum Sodium Concentration
    DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol.
    [Show full text]
  • Evaluation and Treatment of Alkalosis in Children
    Review Article 51 Evaluation and Treatment of Alkalosis in Children Matjaž Kopač1 1 Division of Pediatrics, Department of Nephrology, University Address for correspondence Matjaž Kopač, MD, DSc, Division of Medical Centre Ljubljana, Ljubljana, Slovenia Pediatrics, Department of Nephrology, University Medical Centre Ljubljana, Bohoričeva 20, 1000 Ljubljana, Slovenia J Pediatr Intensive Care 2019;8:51–56. (e-mail: [email protected]). Abstract Alkalosisisadisorderofacid–base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Keywords Respiratory alkalosis is a consequence of dysfunction of respiratory system’s control ► alkalosis center. There are no pathognomonic symptoms. History is important in the evaluation ► children of alkalosis and usually reveals the cause. It is important to evaluate volemia during ► chloride physical examination. Treatment must be causal and prognosis depends on a cause. Introduction hydrogen ion concentration and an alkalosis is a pathologic Alkalosis is a disorder of acid–base balance defined by process that causes a decrease in the hydrogen ion concentra- elevated pH of the arterial blood. According to the origin, it tion. Therefore, acidemia and alkalemia indicate the pH can be metabolic or respiratory. Metabolic alkalosis is char- abnormality while acidosis and alkalosis indicate the patho- acterized by primary elevation of the serum bicarbonate that logic process that is taking place.3 can result from several mechanisms. It is the most common Regulation of hydrogen ion balance is basically similar to form of acid–base balance disorders.
    [Show full text]
  • Managing Hyponatremia in Patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion
    REVIEW Managing Hyponatremia in Patients With Syndrome of Inappropriate Antidiuretic Hormone Secretion Joseph G. Verbalis, MD Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University Medical Center, Washington DC. J.G. Verbalis received an honorarium funded by an unrestricted educational grant from Otsuka America Pharmaceuticals, Inc., for time and expertise spent in the composition of this article. No editorial assistance was provided. No other conflicts exist. This review will address the management of hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in hospitalized patients. To do so requires an understanding of the pathogenesis and diagnosis of SIADH, as well as currently available treatment options. The review will be structured as responses to a series of questions, followed by a presentation of an algorithm for determining the most appropriate treatments for individual patients with SIADH based on their presenting symptoms. Journal of Hospital Medicine 2010;5:S18–S26. VC 2010 Society of Hospital Medicine. Why is SIADH Important to Hospitalists? What Causes Hyponatremia in Patients with SIADH? Disorders of body fluids, and particularly hyponatremia, are Hyponatremia can be caused by 1 of 2 potential disruptions among the most commonly encountered problems in clinical in fluid balance: dilution from retained water, or depletion medicine, affecting up to 30% of hospitalized patients. In a from electrolyte losses in excess of water. Dilutional hypo- study of 303,577 laboratory samples collected from 120,137 natremias are associated with either a normal (euvolemic) patients, the prevalence of hyponatremia (serum [Naþ] <135 or an increased (hypervolemic) extracellular fluid (ECF) vol- mmol/L) on initial presentation to a healthcare provider was ume, whereas depletional hyponatremias generally are asso- 28.2% among those treated in an acute hospital care setting, ciated with a decreased ECF volume (hypovolemic).
    [Show full text]
  • Palliative Care in Advanced Liver Disease (Marsano 2018)
    Palliative Care in Advanced Liver Disease Luis Marsano, MD 2018 Mortality in Cirrhosis • Stable Cirrhosis: – Prognosis determined by MELD-Na score – Provides 90 day mortality. – http://www.mdcalc.com/meldna-meld-na-score-for-liver-cirrhosis/ • Acute on Chronic Liver Failure (ACLF) – Mortality Provided by CLIF-C ACLF Calculator – Provides mortality at 1, 3, 6 and 12 months. – http://www.clifresearch.com/ToolsCalculators.aspx • Acute Decompensation (without ACLF): – Mortality Provided by CLIF-C Acute decompensation Calculator – Provides mortality at 1, 3, 6 and 12 months. – http://www.clifresearch.com/ToolsCalculators.aspx • Survival of Ambulatory Patients with HCC (MESIAH) – Provides survival at 1, 3, 6, 12, 24 and 36 months. – https://www.mayoclinic.org/medical-professionals/model-end-stage-liver- disease/model-estimate-survival-ambulatory-hepatocellular-carcinoma-patients- mesiah Acute Decompensation Type and Mortality Organ Failure in Acute-on-Chronic Liver Failure Organ Failure Mortality Impact Frequency of Organ Failure 48% have >/= 2 Organ Failures The MESIAH Score Model of Estimated Survival In Ambulatory patients with HCC Complications of Cirrhosis Affecting Palliative Care • Ascites and Hepatic Hydrothorax. • Hyponatremia. • Hepatorenal syndrome. • Hepatic Encephalopathy. • Malnutrition/ Anorexia. • GI bleeding: Varices, Portal gastropathy & Gastric Antral Vascular Ectasia • Pruritus • Hepatopulmonary Syndrome. Difficult Decisions with Shifting Balance • Is patient a liver transplant candidate? • Effect of illness in: – patient’s survival – patient’s Quality of Life • patient’s relation to family • family’s Quality of Life • Effect of therapy in: – patient’s survival – patient’s Quality of Life • patient’s relation to family • family’s Quality of life Ascites and Palliation • PATHOGENESIS • CONSEQUENCES • Hepatic sinusoidal HTN • Abdominal distention with early stimulates hepatic satiety.
    [Show full text]
  • Real Facts About Fluid Overload
    Real Facts About Fluid Overload Venkat K. Iyer, MD, MBA Assistant Professor, Mayo School of Medicine Medical Director, Quality and Process Improvement, Mayo Clinic Dialysis System ©2017 MFMER | slide-1 Disclosure • None Objectives Discuss the meaning of fluid overload and its negative physiological effects on the body of a person who has kidney failure. Two major functions of dialysis Uremic solute removal Excess ECF volume removal Main Process Diffusion Ultrafiltration How is adequacy Clearance of surrogate BP control, Dry weight measured? solute - urea Quantification of spKt/V, Std Kt/V, URR No objective measure to quantify adequacy adequacy of fluid removal. Trial & Error method to achieve DW Debate Small versus middle What is the best method to molecular clearance quantify ECF volume removal. (diffusive versus Clinical versus Non-clinical Convective clearance) methods What is dry weight? • Lowest tolerated post-dialysis weight achieved via a gradual reduction in post dialysis weight at which there are minimal signs or symptoms of hypovolemia or hypervolemia Dry Weight ECF volume LBM Initiation of HD High Low Adequate Maintenance HD Euvolemic Improves Acute illness Increases Decreases Negative Effects of Fluid Overload (“Volutrauma”) Acute Fluid Overload Chronic Fluid Overload • Dyspnea • Hypertension • CHF • LVH • Hospitalization • CHF • Decreased vascular compliance • Increased cardiovascular mortality • Organ dysfunction • Gut edema: malabsorption • Tissue edema: poor wound healing • Renal edema: renal BF, reduced GFR • Pulmonary edema Cost of Hospitalization for Volume Overload % of Fluid Overload admission % of 41,699 episodes 25,291 pts of 176,790 100 86 14.3 80 60 40 85.7 20 9 5 0 Inpatient ED Observation FO admission Others care Average cost per episode $6,372 Total cost $266 million • Arneson et al.
    [Show full text]
  • Outcome of Acute Kidney Injury: How to Make a Difference?
    Jamme et al. Ann. Intensive Care (2021) 11:60 https://doi.org/10.1186/s13613-021-00849-x REVIEW Open Access Outcome of acute kidney injury: how to make a diference? Matthieu Jamme1,2,3* , Matthieu Legrand4 and Guillaume Geri2,3,5 Abstract Background: Acute kidney injury (AKI) is one of the most frequent organ failure encountered among intensive care unit patients. In addition to the well-known immediate complications (hydroelectrolytic disorders, hypervolemia, drug overdose), the occurrence of long-term complications and/or chronic comorbidities related to AKI has long been underestimated. The aim of this manuscript is to briefy review the short- and long-term consequences of AKI and discuss strategies likely to improve outcome of AKI. Main body: We reviewed the literature, focusing on the consequences of AKI in all its aspects and the management of AKI. We addressed the importance of clinical management for improving outcomes AKI. Finally, we have also pro- posed candidate future strategies and management perspectives. Conclusion: AKI must be considered as a systemic disease. Due to its short- and long-term impact, measures to prevent AKI and limit the consequences of AKI are expected to improve global outcomes of patients sufering from critical illnesses. Keywords: Acute kidney injury, Long-term outcome, Chronic kidney disease, Intensive care Introduction Why physicians should worry about AKI? Acute kidney injury (AKI) is one of the most frequent Occurrence of AKI represents a sharp prognostic turn organ failure encountered in intensive care units (ICU). for patients by afecting both short- and long-term Since his frst defnition by Homer W.
    [Show full text]
  • 4 Edema in Childhood
    Kidney International, Vol. 51, Suppl. 59 (1997). pp. S-100-S-104 (1) Red Hypo Ne] Liv Edema in childhood Ma Pre Sev SATOSHI HISANO, SEUNGHOON HAHN, NANCY B. KUEMMERLE, JAMES CM. CHAN, (2) Incr. and NATALE G. DESANTO Cardi He: h Pediatric Nephrology Division, Virginia Commonwealth University's Medical College of Virginia, Richmond, Virginia, USA, and Divisione di Nefrologia Art dell' Adulto e del Bambino, Seconda Universita'degli Studi di Napoli, Naples, Italy Renal Act ACt Idiops Fan Edema in childhood. There are two types of edema: localized edema sympathetic nervous system (SNS) activity; and (3) antidiuretic Nor and generalized edema. The causes ofgeneralized edema in childhoodare hormone (ADH) release [4-6]. These forces and perhaps as yet diverse. Formation of generalizededema involves retention of sodium and Prej unidentified factors give rise to the consequential water and water in the kidney. The treatment of generalized edema depends on the (3) Incre primary etiology. Supportive nutritional and medicaltherapies are needed sodium retention, which promotes the development of edema, Allerg to prevent further edema. These and related features of edema in The sodium and water retention leads to further decreased Vascu childhood are discussed in this review. den plasma oncotic pressure, setting up a vicious cycle perpetuating dise the edema formation. The movement of water from intracellular space to interstitial space by itself also contributes to the devel­ opment of edema formation [1, 3]. Edema can be defined as the presence of excess fluid in the In contrast, the mechanism of "overfilling edema" is expanded interstitial space of the body. Edema is divided into two types, extracellular volume that results from primary renal sodium localized edema and generalized edema.
    [Show full text]
  • Restrictive Fluid and Fluid Removal Approach in Diabetic Ketoacidosis with Septic AKI: a Case Report
    Case report Crit Care Shock (2021) 24:125-129 Restrictive fluid and fluid removal approach in diabetic ketoacidosis with septic AKI: A case report Elvia AS1, Mayang Indah Lestari2, Yohannes WH George3 Abstract to the intensive care unit. Aggressive fluid re- Diabetic ketoacidosis is a life-threatening com- suscitation carries potential adverse effects such plication that requires a rapid restoration of as hyperchloremic metabolic acidosis, intersti- intravascular volume usually with aggressive tial multi-organ edema, and increased incidence administration of intravenous fluid with 0.9% of acute kidney injury. The first day of ICU sodium chloride as recommended by the Ameri- treatment, positive cumulative fluid balance can Diabetes Association. We report a 50-year- occurred and fluid removal was indicated. Fluid old obese female patient with a history of diabe- removal using diuretic or ultrafiltration is a tes mellitus (DM) since 20 years ago and rou- part of the treatment of organ congestion and tinely using insulin. She experienced dyspnea fluid overload after the initial phase of shock and presumably was caused by diabetic ketoac- resuscitation to achieve negative fluid balance. idosis. The patient was given fluid resuscitation This case showed that restricted fluid and fluid with normal saline, but the dyspnea did not re- removal improve the patient outcome, especially solve and the work of breathing increased fur- in diabetic ketoacidosis and septic AKI patients. ther, so the patient was intubated and admitted . Key words: Diabetic ketoacidosis, septic AKI, restricted fluid, fluid removal, negative cumulative balance. Introduction (1) Recent guidelines from American Diabetes As- Diabetic ketoacidosis (DKA) is a life-threatening sociation (ADA) recommend fluid resuscitation complication that can occur in patients with diabe- using normal saline 15-20 ml/kg/hour (1-1.5 liter) tes mellitus.
    [Show full text]
  • Mechanisms and Management of Nephrotic Edema
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 45 (1994),pp.266—281 NEPHROLOGY FORUM Mechanisms and management of nephrotic edema Principal discussant: MICHAEL H. HUMPHREYS University of California San Francisco, San Francisco, California showed a normal heart size and regular rhythm; heart sounds were distant through a thickened chest wall, but no murmurs or gallops were Editors heard, The abdomen was nontender without evidence of hepatic or JORDAN J. COHEN splenic enlargement. The stool was guaiac positive. The extremities JOHN T. HARR1NGTON showed no clubbing, but massive anasarca was present, with pitting edema of all extremities as well as the abdominal and thoracic wall. The NICOLAOS B. MADIAS penis and scrotum were edematous, and paraphimosis was evident, Neurologic examination was normal except for a slowed relaxation Managing Editor phase of the deep-tendon reflexes. CHERYL J. ZUSMAN Laboratory values on admission were: hematocrit, 29.5; white blood cell count, 16,700/mm3 with a left shift; and a platelet count of 212 x 103/mm'. The serum sodium concentration was 145 mEq/liter; potas- sium, 4.3 mEq/liter; chloride, 121 mEq/liter; total CO2. 16 mmol/liter; State University of New York at Stony Brook BUN, 65 mg/dl; and serum creatinine, 5.5 mgldl. The serum albumin and concentration was 0.6 g/dl; calcium, 6.9 mg/dl; phosphorus, 5.4 mg/dl; and magnesium, 1.8 mg/dl. The erythrocyte sedimentation rate was 139 Tufts University School of Medicine mm/hr, and the serum cholesterol was 554 mg/dl.
    [Show full text]
  • Neurologic Complications of Electrolyte Disturbances and Acid–Base Balance
    Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved Chapter 23 Neurologic complications of electrolyte disturbances and acid–base balance ALBERTO J. ESPAY* James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, UC Neuroscience Institute, University of Cincinnati, Cincinnati, OH, USA INTRODUCTION hyperglycemia or mannitol intake, when plasma osmolal- ity is high (hypertonic) due to the presence of either of The complex interplay between respiratory and renal these osmotically active substances (Weisberg, 1989; function is at the center of the electrolytic and acid-based Lippi and Aloe, 2010). True or hypotonic hyponatremia environment in which the central and peripheral nervous is always due to a relative excess of water compared to systems function. Neurological manifestations are sodium, and can occur in the setting of hypovolemia, accompaniments of all electrolytic and acid–base distur- euvolemia, and hypervolemia (Table 23.2), invariably bances once certain thresholds are reached (Riggs, reflecting an abnormal relationship between water and 2002). This chapter reviews the major changes resulting sodium, whereby the former is retained at a rate faster alterations in the plasma concentration of sodium, from than the latter (Milionis et al., 2002). Homeostatic mech- potassium, calcium, magnesium, and phosphorus as well anisms protecting against changes in volume and sodium as from acidemia and alkalemia (Table 23.1). concentration include sympathetic activity, the renin– angiotensin–aldosterone system, which cause resorption HYPONATREMIA of sodium by the kidneys, and the hypothalamic arginine vasopressin, also known as antidiuretic hormone (ADH), History and terminology which prompts resorption of water (Eiskjaer et al., 1991).
    [Show full text]
  • Early Neonatal Death Caused by Severe Euglycemic Ketoacidosis in a Pregnant Woman with Type 1 Diabetes Mellitus
    SWISS SOCIETY OF NEONATOLOGY Early neonatal death caused by severe euglycemic ketoacidosis in a pregnant woman with type 1 diabetes mellitus July 2017 Seewald HC, Maletzki JA, Burkhard T, Schmid M, Clinic for Neonatology (SCH, MJA, SM), Clinic for Gynaecology and Obstetrics (BT), University Hospital Zürich, Switzerland Title figure: Pancreatic islet cells (source: www.cityofhope.org) © Swiss Society of Neonatology, Thomas M Berger, Webmaster 3 Diabetic ketoacidosis (DKA) is one of the most serious INTRODUCTION acute complications of diabetes mellitus and is cha- racterized by uncontrolled hyperglycemia, metabolic acidosis and ketosis. The reported incidence of dia- betes mellitus in pregnancy ranges from 6 to 7% with 90% occurring among women affected by gestatio- nal diabetes mellitus (GDM) (1). The overall incidence of DKA occurrence during pregnancy is difficult to ascertain but some articles have reported an incidence between 1 and 3% (2, 3). Although it is a rare con- dition, DKA in pregnancy is an urgent complication which can compromise both fetus and mother. DKA is the result of an absolute or relative deficiency of insulin which causes a state of starvation of cells accompanied by an increased secretion of the counter- regulatory hormones (cortisol, glucagon, epinephrine). The metabolic characteristics of DKA can trigger a chain of events that will self-perpetuate in a vicious cycle. Hyperglycemia gives rise to an osmotic gradient resulting in an excessive diuresis, which leads to severe dehydration and hypervolemia. This further aggravates the hyperglycemia and acidosis due to the activation of other stress hormones (growth hormone and corti- sol), and osmotic diuresis causes low sodium levels (4).
    [Show full text]
  • Fluid Overload and Acute Kidney Injury Vijaya P Patil1, Bindiya G Salunke2
    INVITED ARTICLE Fluid Overload and Acute Kidney Injury Vijaya P Patil1, Bindiya G Salunke2 ABSTRACT Commonest intervention in hospitalized patient is fluid therapy, and practically every critically ill patient receives fluid resuscitation. Commonest indication for fluid administration is to achieve hemodynamic stability and prevent or manage acute kidney injury (AKI). However, fluid administration is a two-edged sword, i.e., inadequate fluids give rise to hypoperfusion and organ injury and overzealous fluid therapy can give rise to fluid overload and related consequences. Though fluids are commonly given to prevent development of AKI, hypervolemia itself has the potential to cause AKI. Keywords: Acute kidney injury, Fluid movement, Fluid overload, Renal blood flow. Indian Journal of Critical Care Medicine (2020): 10.5005/jp-journals-10071-23401 INTRODUCTION 1,2Division of Clinical Anaesthesiology, Department of Anaesthesiology, Acute kidney injury (AKI) is commonly encountered in intensive care Critical Care and Pain, Tata Memorial Hospital, Homi Bhabha National unit (ICU) patients and is associated with increased morbidity and Institute, Parel, Mumbai, Maharashtra, India mortality. Incidence of AKI in critically ill patients is around 5.7% of Corresponding Author: Vijaya P Patil, Division of Clinical Anaesthesiology, 1 which almost 50% have sepsis and septic shock. Acute kidney injury Department of Anaesthesiology, Critical Care and Pain, Tata Memorial is a syndrome with multiple etiologies occurring at different clinical Hospital, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, settings. Therefore, it is of utmost importance to achieve early diagnosis India, Phone: +91 9819883535, e-mail: [email protected] of AKI; and once diagnosed, it should be promptly evaluated and How to cite this article: Patil VP, Salunke BG.
    [Show full text]