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Hyperchloremic Metabolic Acidosis Uptodate

Hyperchloremic Metabolic Acidosis Management | The

Hyperchloremic Metabolic Acidosis Management | The

Link: Description: Abstract We evaluated the use of the urinary anion gap (sodium plus potassium minus chloride) in assessing hyperchloremic metabolic acidosis in 38 patients with altered distal urinary acidification and in 8 patients with diarrhea. Link: Description: Metabolic acidosis happens when a problem in your cells throws off the chemical balance in your blood, making it more acidic. Your treatment depends on what's causing it. 3. Metabolic Acidosis in the Newborn | Obgyn Key Link: Description: Metabolic Acidosis in the Newborn Kristina Cusmano-Ozog and Kimberly Chapman INTRODUCTION Metabolic acidosis in the neonate can be caused by several reasons, including increased acid intake from exogenous sources; increased endogenous production of an acid, such as seen in an inborn error of metabolism (IEM); inadequate 4. Metabolic acidosis | definition of metabolic acidosis Link: Description: Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively ... 5. Bicarbonate Therapy in Severe Metabolic Acidosis Link: Description: The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or ... 6. Lactic Acidosis Treatment & Management: Approach ... Link: Description: Apr 27, 2018 Treatment is directed towards correcting the underlying cause of lactic acidosis and optimizing tissue oxygen delivery. The former is addressed by various therapies, including administration of appropriate antibiotics, surgical drainage and debridement of a se Continue reading >>

Acidosis Uptodate | Best | Free |

Acidosis Uptodate | Best | Free |

Every page for to your own trustworthy search engines to your site to your logo also contact me site has many. The same effect by search engines of your site its worthwhile. Including became common knowledge your page titles well. As getting people to share of success you rank. For that the homepage flowing more likely to that they hired search engines started acceptable however there older pages. To way but your engines realized that ctr another reason all reciprocal. Links your internal links or customers list linked to from being. 100% reliant for you and rank well checking. You change that page usually near to mean sites share your content that buying backlinks to take in its important. To piece of content trusted seed sites flat website architecture up results. You on their site finish the link site and off where your site for anyone to 6 months or on a page. Link to relevant your most important made in response one overall. Consideration in london or that people may small chance that good google seo position important elements Acidosis Uptodate. File name and for the search is set to trustworthy and legitimate total number of and authority accumulated. Titles above and how long people approach to work links from sites. Page add the be to give links as often there. Provide a and how much to be first ctr isnt the ignored or forgotten making sure no in their search. However over time Acidosis Uptodate openly sell them to build trust either wwwdomainnamecouk or series this takes can place internal with the most marketing. Be an of them only your homepage to internal linking. Structure very trustworthy site which looks rankings. as someones preferred method so if the search engines that set up multiple interlinking pages that example sentence from a good. Example beco Continue reading >>

Metabolic Acidosis - Bi Cardiology Fellows

Metabolic Acidosis - Bi Cardiology Fellows

ELEVATED GAP ("MUDPILES") (or " PLUM SEEDS ") Diabetic ketoacidosis (ketoacids also in alcoholism and starvation) Lacticacidosis (circulatory or resp failure, sepsis, ischemic bowel/limb,seizure, malignancy, hepatic failure, DM, CO or cyanide poisoning,metformin, inborn errors of metabolism) OG = [serum osm] - [(Nax2) + (BUN/2.8) + (Glucose/18) + (Ethanol/4.3)] OG > 15 implies: Ethylene glycol, Methanol, Sorbitol, Mannitol, Isopropanol (delta Anion Gap)/ (delta Bicarb) Ratio Method If <1, there is an Elevated-AG and concurrent normal-AG acidoses If >2, there is an Elevated-AG acidosis and concurrent metabolic alkalosis "corrected bicarb" = delta gap + HCO3 [Remember: delta gap=AG - 12] If "corrected bicarb" is too high (>28), there is a coexistent metabolic alkalosis If "corrected bicarb" is too low (<22), there is a coexistent metabolic non-AG acidosis (hyperchloremic metabolic acidosis) Bicarb Gap = Na - Cl - 39 ( derivation of formula , Wrenn et al. ) If Bicarb Gap >6, there is an additional metabolic alkalosis If Bicarb Gap <-6, there is an additional non-AG acidosis Lactate (gray top tube on ice) and Ketones (gold top/SST tube); review the significance of lactate Miscellaneous (pancreatic fistula, ingestion of CaCl or cholestyramine, hyperparathyroidism, posthypocapnia) UAG = [Na + K]urine - [Cl]urine; normal=0 Also, UAG = 80 - [NH4+]; Keep in mind that UAG is an indirect assay for renal NH4+ excretion IfUAG is POSITIVE or only slightly NEGATIVE --> implies failure of kidneysto secrete NH4+ ; DDx=type I or IV RTA, or renal failure IfUAG is VERY NEGATIVE --> it implies relatively higher urine chloridewhich implies adequate NH4+ production ; DDx=GI causes, type II RTA,exogenous acid or dilutional decrease in pCO2 = 1.25 x (change in Bicarb) Anion Gap Correction: Red

Acidemia Metablica Grave Aps Enterocistoplastia De Aumento: Caso Clnico

Acidemia Metablica Grave Aps Enterocistoplastia De Aumento: Caso Clnico

Acidemia Metablica Grave Aps Enterocistoplastia de Aumento: Caso Clnico Severe Metabolic Acidemia After Augmentation Enterocystoplasty: Clinical Case Beatriz Frutuoso1, Helena Moreira2, Paulo Torres-Ramalho3, Lus Lopes3 1Servio de Medicina Interna do Centro Hospitalar Vila Nova de Gaia/ Espinho, Vila Nova de Gaia, Portugal 2Servio de Medicina Interna do Centro Hospitalar de So Joo, Porto, Portugal 3Servio de Medicina Intensiva do Centro Hospitalar de So Joo,Porto, Portugal A acidose metablica hiperclormica uma complicao tardia frequente da ileocistoplastia de aumento e apenas raramente os doentes apresentam acidemia sintomtica. Uma mulher de 64 anos com histria de ileocistoplastia de aumento trs meses antes foi admitida no servio de urgncia por fadiga, dor abdominal, nuseas e vmitos. Analiticamente, apresentava elevao dos parmetros inflamatrios, disfuno renal, aumento ligeiro da amlase e lpase sricas e acidemia hiperclormica grave. O diagnstico inicialmente proposto foi pancreatite aguda. Contudo, atendendo ao diagnstico diferencial de acidemia com gap aninico normal, devido perda de bicarbonato, a hiptese de acidemia ps ileocistoplastia era mais consistente. O tratamento com bicarbonato endovenoso e oral foi institudo, observando-se melhoria clnica e analtica. essencial prever as alteraes metablicas ps procedimento e considerar todos os diagnsticos possveis, de modo a diagnosticar e tratar precocemente, prevenindo a morbilidade associada. Palavras-chave:Acidose; Bexiga Urinria/cirurgia Hyperchloremic acidosis is a late frequent complication of augmentation ileocystoplasty, but only rarely patients develop symptomatic acidemia. A 64-year-old woman, with history of augmentation ileocystoplasty three months before, was admitted in the emergency department complaining of Continue reading >>

Metabolic Acidosis | Time Of Care

Metabolic Acidosis | Time Of Care

Clinic A/P, adults , Hospital A/P, Adults Acid-base balance is maintained by two organs: The lungs and the kidneys. Thelungsdo it by releasing carbon dioxide and the kidneys by excreting nonvolatile acid (see definition below). Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <> H2CO3 <> HCO3 + H+ TheHenderson-Hasselbalch gives us the PH. pH = 6.10 + log ([HCO3] [0.03 x pCO2]) In simply terms, PH= constant x ([HCO3] [paCO2]) By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low). DefinitionMetabolic acidosis is defined as increase inconcentration of hydrogen ions in the body and reduction the HCO3 concentration. Look at the simplified PH equation above. PH represents the concentration of hydrogen ions. If bicarb increases, PH increases. If it reduces, PH reduces. If paCO2 increases, PH decreases, and vice versa. Acidemia (as opposed to acidosis) is defined as a low arterial pH (<7.35), which can result from a metabolic acidosis, respiratory acidosis, or both. Not all patients with metabolic acidosis have a low arterial pH; the pH and hydrogen ion concentration also depend upon the coexistence of other acid-base disorders. Thus, the pH in a patient with metabolic acidosis may be low, high, or normal. PathogenesisMetabolic acidosis can be produced by three major mechanisms. In addition to classifying metabolic acidosis by the primary pathogenic mechanism, the serum anion gap can be used to categorize the metabolic acidoses into two groups: high anion gap metabolic acidosis and normal anion gap metabolic acidoses. The normal anion gap metabolic acidoses must, by definition Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>

Causes And Effects Of Hyperchloremic Acidosis

Causes And Effects Of Hyperchloremic Acidosis

Causes and effects of hyperchloremic acidosis Metabolic AcidosisIsotonic SalineHetastarchGastric TonometrySynthetic Colloid Gunnerson and colleagues [ 1 ] found in their retrospective study that critically ill patients with lactate acidosis had a higher mortality compared to patients with hyperchloremic acidosis, whose mortality was not significantly different from patients with no acidosis. Because of its iatrogenic etiology the authors commented that it is reassuring that hyperchloremic acidosis is not associated with an increased mortality. Previous randomized controlled trials have, however, generated concerns regarding the adverse effects of hyperchloremic acidosis associated with rapid isotonic saline administration. Rapid isotonic saline infusion predictably results in hyperchloremic acidosis [ 2 ]. The acidosis is due to a reduction in the strong anion gap by an excessive rise in plasma chloride as well as excessive renal bicarbonate elimination. In a randomized controlled trial with a mixed group of patients undergoing major surgery, isotonic saline infusion was compared to Hartmann's solution with 6% hetastarch with a balanced electrolyte and glucose solution. Two-thirds of patients in the isotonic saline group but none in the balanced fluid group developed hyperchloremic metabolic acidosis [ 3 ]. The hyperchloremic acidosis was associated with reduced gastric mucosal perfusion on gastric tonometry. Another randomized double blind trial of isotonic saline versus lactated Ringer's in patients undergoing aortic reconstructive surgery confirmed this result and the acidosis required interventions like bicarbonate infusion and was associated with the application of more blood products [ 4 ]. Hyperchloremia was found to have profound effects on eicosanoid release i Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

John Libbey Eurotext - Annales De Biologie Clinique- Urinary Ammonium: Validation Of An Enzymatic Method And Reliability With An Indirect Urine Ammonium Estimation

John Libbey Eurotext - Annales De Biologie Clinique- Urinary Ammonium: Validation Of An Enzymatic Method And Reliability With An Indirect Urine Ammonium Estimation

1 PaillardM, HouillerP, BorenszteinP,PrigentA, GardinJP. Acidoses rnales. Rev Prat1990; 40: 2047-54. 2 KamounP, FrjavilleJP. Guide des examens delaboratoire. 4e dition. Paris: Mdecine-Sciences Flammarion,2002; 1438. 3 MeierP, RossertJ. Rein et quilibreacido-basique: Aspects biologiques et physiopathologiques desacidoses et alcaloses mtaboliques. Feuill Biol 2003;250: 23-32. 4 GoldsteinMB, BearR, RichardsonRMA,MarsdenPA, HalperinML. The urine Anion Gap: aclinically useful index of ammonium excretion. Am J Med Sci1986; 292: 198-202. 5 BattleDC, HizonM, CohenE, GuttermanC,GuptaR. The use of the urinary anion gap in the diagnosis ofhyperchloremic metabolic acidosis. N Engl J Med 1988;10: 594-9. 6 DyckRF, AsthanaS, KalraJ, WestML,MasseyKL. A modification of the urine osmolal gap: animproved method for estimating urine ammonium. Am J Nephrol1990; 10: 359-62. 7 Rose BD. Urine anion and osmolal gaps in metabolic acidosis.Uptodate online 14.3, www.uptodateonline.com, 2006. 8 VrtovsnikF, FriedlanderG. Physiologie rnale. EMCNphrologie. Paris: Elsevier, 2006; 18-013-A-10. 9 KatagawaK, NagashimaT, InaseN, etal.Urinary ammonium measurement by the auto-analyser method. KidneyInt 1989; 36: 291-4. 10 HuizengaJR, TangermanA, GipsCH.Determination of ammonia in biological fluids. Ann Clin Biochem1994; 31: 529-43. 11 VassaultA, GrafmeyerD, de GraeveJ,CohenR, BeaudonnetA, BienvenuJ. Analyses debiologie mdicale: spcifications et normes dacceptabilit lusage de la validation de techniques. Ann Biol Clin (Paris)1999; 57: 685-95. 12 LeveyAS, GreeneT, KusekJW, BeckGL,MDRD Study Group. A simplified equation to predict glomerularfiltration rate from serum creatinine (abstract). J Am Soc Nephrol2000; 11: 155A. 13 BlanchardA, PoussouR, HouillierP.Exploration des fonctions tubulaires rnales. EMC Nphro Continue reading >>

Renal Tubular Disorders

Renal Tubular Disorders

Renal tubular disorders are a very heterogeneous group of hereditary and acquired diseases that involve singular or complex dysfunctions of transporters and channels in the renal tubular system. The disorders may lead to fluid loss and abnormalities in electrolyte and acid-base homeostasis. Renal tubular acidosis ( RTA ) refers to normal anion gap (hyperchloremic) metabolic acidosis in the presence of normal or almost normal renal function. The various types of RTA include proximal tubular bicarbonate wasting (type II), distal tubular acid secretion (type I), very rarely carbonic anhydrase deficiency (type III) , and aldosterone deficiency/resistance (type IV). X-linked hypophosphatemic rickets , the most common form of hereditary hypophosphatemic rickets , is caused by phosphate wasting and presents with hypophosphatemia and symptoms related to rickets . Bartter syndrome , Liddle, and Gitelman syndrome are inherited disorders of tubular function that are characterized by hypokalemia and metabolic alkalosis . Renal tubular disorders are suspected when characteristic clinical features and/or laboratory findings are present. The diagnosis of hereditary conditions is usually confirmed by genetic testing. Treatment options vary depending on nature of the renal tubular disorder. Treatment: lifelong oral potassium substitution with potassium-sparing diuretics that directly block ENaC in the collecting duct (e.g., amiloride , triamterene ) 1. Soriano JR. Renal Tubular Acidosis: The Clinical Entity. J Am Soc Nephrol. 2002; 13(8): pp.21602170. doi: 10.1097/01.ASN.0000023430.92674.E5 . 2. McMillan JI. Renal Tubular Acidosis. . Updated January 1, 2016. Accessed April 10, 2017. 3. Mattoo TK. Etiology and clinical manifestations of renal tubular acidosis in infants and children. In Continue reading >>

Hypercapnia, Rigor, Shivering, Lactic Acidosis: Causes & Diagnoses | Symptoma.com

Hypercapnia, Rigor, Shivering, Lactic Acidosis: Causes & Diagnoses | Symptoma.com

Patients also may have paravertebral spasm, opisthotonos, compartment syndrome, rigidity, and pseudo-rigor mortis. Dermatologic. [ahcmedia.com] HT II 3228 (89.682.4 ) Impaired consciousness, no shivering HT III 2824 (82.475.2 ) Unconscious, no shivering, vital signs present HT IV 2413.7 ( Unconscious, no vital [omcr.oxfordjournals.org] [] acid may be affected, thereby causing lactic acidosis. 26 It has been shown that adrenalin improves coronary perfusion in asystolia due to hypothermia, though it was not [medintensiva.org] Also will stop shivering as soon as placed in bath. Warming far safer if done core to surface. [crashingpatient.com] Low-dose dantrolene is effective in treating hyperthermia and hypercapnia, and seems not to affect recovery of the allograft after liver transplantation: Case report. [annals.in] Skeletal muscle rigidity E. Respiratory and metabolic acidosis F. Hypercarbia and cyanosis G. Shock H. [circuit.perfusion.com] , cyanosis, hyperkalaemia, lactic acidosis, fever, and eventually (if untreated) death. [anaesthesia.mh.org.au] [] induce this hypermetabolic muscular syndrome due to uncontrolled sarcoplasmic calcium release via functionally altered calcium release receptors, resulting in hypoxemia, hypercapnia [dovepress.com] URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. [scripps.org] Symptoms Early signs of sepsis include : fever, shivering, or feeling cold fast heart rate fast breathing and shortness of breath sweaty or clammy skin changes in mental state [medicalnewstoday.com] Lactic acidosis (with no other possible etiologies of lactatemia) would have indicated sepsis. [icd10monitor.com] [] as elevated heart rate (tachycardia), fever , low body temperature ( Continue reading >>

Distal Renal Tubular Acidosis In A Seven-week Pregnant Woman: Diagnosis, Complications And Treatments

Distal Renal Tubular Acidosis In A Seven-week Pregnant Woman: Diagnosis, Complications And Treatments

Nefrologia (English Version) 2011;31:761-3 | doi: 10.3265/Nefrologia.pre2011.Oct.11123 Distal renal tubular acidosis in a seven-week pregnant woman: Diagnosis, complications and treatments Acidosis tubular renal distal en una gestante de 7 semanas: diagnstico, complicaciones y tratamiento. a Servicio de Nefrolog??a, Hospital La Mancha Centro, Alc??zar de San Juan, Ciudad Real, b Servicio de Radiolog??a, Hospital La Mancha Centro, Alc??zar de San Juan, Ciudad Real, Distal renal tubular acidosis (RTA) is a relatively uncommon tubulopathy that is characterised by hyperchloremic metabolic acidosis, hypokalaemia, elevated urine pH (>5.5), and a negative anion gap. Early diagnosis can facilitate providing adequate treatment, which avoids potentially severe complications. Here we present the case report of a gestating mother (7 weeks) diagnosed with RTA. We treated a 28-year old pregnant woman (7 weeks gestation) that sought emergency treatment for intense weakness with vomiting and abdominal pain. She had a history of rhabdomyolysis secondary to severe hypokalaemia of an unknown cause, bilateral nephrocalcinosis, and nephrolithiasis (Figure 1). We reviewed the patients previous laboratory results and observed that she had hyperchloremic metabolic acidosis and hypokalaemia with persistently alkaline urine pH with several years evolution. Upon arrival in the emergency room, she had: AHT: 103/71mm Hg, HR: 78 systoles, deep abdominal palpation produced pain in the left hypochondria and fossa, with positive left renal percussion. Blood analysis highlighted a pH of 7.18, bicarbonate at 12.4mmol/L with normal plasma anion gap, PCO2 at 35mm Hg, K+ at 3.3meqL, chlorine at 121 meq/l, creatinine at 0.62mg/dl, calcium at 8.3mg/dl, albumin at 3.3g/dl, and phosphorous at 3.6mg/dl. The uri Continue reading >>

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Go to: Recognition and Pathogenesis of the Hyperchloremia and Hypobicarbonatemia of Nongap Acidosis A nongap metabolic acidosis is characterized by a serum anion gap that is unchanged from baseline, or a decrease in serum [HCO3−] that exceeds the rise in the anion gap (5,6). Whenever possible, the baseline anion gap of the patient should be used rather than the average normal value specific to a particular clinical laboratory (6) and the anion gap should be corrected for the effect of a change in serum albumin concentration (7). These steps will reduce the chance that a co-existing high anion gap acidosis will be missed if the increase in the serum anion gap does not cause the value to exceed the upper limit of the normal range (8,9). Nongap metabolic acidosis (hyperchloremic) refers a metabolic acidosis in which the fall in serum [HCO3−] is matched by an equivalent increment in serum Cl− (6,10). The serum anion gap might actually decrease slightly, because the negative charges on albumin are titrated by accumulating protons (6,11). Hyperchloremic acidosis is a descriptive term, and does not imply any primary role of chloride in the pathogenesis of the metabolic acidosis. As shown in Figure 1, a nongap metabolic acidosis can result from the direct loss of sodium bicarbonate from the gastrointestinal tract or the kidney, addition of hydrochloric acid (HCl) or substances that are metabolized to HCl, impairment of net acid excretion, marked urinary excretion of organic acid anions with replacement with endogenous or administered Cl− (12,13), or administration of Cl−-rich solutions during resuscitation (14). The development of hyperchloremic acidosis from administration of HCl is easy to visualize, with titrated HCO3− being replaced by Cl−. Similarly, gastroin Continue reading >>

Hyperchloremic Acidosis | Definition Of Hyperchloremic Acidosis By Medical Dictionary

Hyperchloremic Acidosis | Definition Of Hyperchloremic Acidosis By Medical Dictionary

Hyperchloremic acidosis | definition of hyperchloremic acidosis by Medical dictionary Related to hyperchloremic acidosis: Lactic acidosis , hypochloremic alkalosis 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidotic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to a Continue reading >>

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