Tham Acidosis

Tham - Fda Prescribing Information, Side Effects And Uses

For the Prevention and Correction of Severe Metabolic Acidosis Tham Solution (tromeThamine injection) is a sterile, non-pyrogenic 0.3 M solution of tromeThamine, adjusted to a pH of approximately 8.6 with glacial acetic acid. It is administered by intravenous injection, by addition to ACD blood for priming cardiac bypass equipment and by injection into the ventricular cavity during cardiac arrest. Each 100 mL contains tromeThamine 3.6 g (30 mEq) in water for injection. The solution is hypertonic 389 mOsmol/L (calc.). pH 8.6 (8.4-8.7). The solution contains no bacteriostat, antimicrobial agent or added buffer (except acetic acid for pH adjustment) and is intended only for use as a single-dose injection. When smaller doses are required the unused portion should be discarded. Tham solution is a parenteral systemic alkalizer and fluid replenisher. TromeThamine, USP (sometimes called tris or tris buffer) is chemically designated 2-amino-2-(hydroxymethyl)-1, 3-propanediol, a solid readily soluble in water, also classified as an organic amine buffer. It has the following structural formula: Water for Injection, USP is chemically designated H20. Amyotrophic Lateral Sclerosis (ALS): Evolving Science For a Fatal Disease When administered intravenously as a 0.3 M solution, tromeThamine act as a proton acceptor and prevents or corrects acidosis by actively binding hydrogen ions (H+). It binds not only cations of fixed or metabolic acids, but also hydrogen ions of carbonic acid, thus increasing bicarbonate anion (HCO3). TromeThamine also acts as an osmotic diuretic, increasing urine flow, urinary pH, and excretion of fixed acids, carbon dioxide and electrolytes. A significant fraction of tromeThamine (30% at pH 7.40) is not ionized and therefore is capable of reaching equilibrium i Continue reading >>

Tham (tromethamine) Dosing, Indications, Interactions, Adverse Effects, And More

IV dosage estimation: Tromethamine solution (mL of 0.3 M) required = Body Weight (kg) x Base Deficit (mEq/L) x 1.1 given by IV infusion 1 mL/kg for each drop in pH below 7.4; determine additiona doses through changes in pH, PaO2, and pCO2 Hypoglycemia (usu doses >500 mg/kg over <1hr) Hepatic necrosis (resulted during delivery via umbilical venous catheter) Neonates: chronic respiratory acidosis, salicylate intoxication Extravasation may cause inflammation & tissue necrosis Risk of overhydration, that may cause serum electrolyte dilution, pulm edema, CHF Risk of hypoglycemia with extremely large doses Lactation: not known if present in breast milk, use caution A:Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk. B:May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk. C:Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done. D:Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk. X:Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist. Continue reading >>

Your Patient In Extremis: Tham To The Rescue?

Your Patient In Extremis: THAM To The Rescue? By: Prathap Sooriyakumaran, MD and Curtis Geier, PharmD One of the final common denominators dictating the success or failure of any resuscitative effort, be it a trauma or medical code, is the patients acid-base status. In the presence of acidosis, many of the tools at your disposal, including vasopressors, become impotent and the patients ability to strike a balance between bleeding and clotting or mounting an appropriate inflammatory response become deranged.16 So what are the options to tilt the acid-base status in our favor? One thing is clear, sodium bicarbonate is not the hero we have been searching for. Unfortunately, the buffer we all know and want to love is ineffective in producing any significant change that will alter outcomes in the setting of the acutely acidemic patient.7,8 Why? Well to understand this, well have to do a brief dive (a wade) into the relevant human biochemistry. So if you give sodium bicarbonate in an attempt to scavenge your troublemaking protons, youll get carbonic acid which dissociates into carbon dioxide and water, which can freely diffuse across the cell membrane creating an intracellular acidosis.9 If you can get rid of carbon dioxide (blow it off), you will force the equation to the right and get rid of your protons. However, patients in extremis may not be able to compensate for the increased carbon dioxide with increased respiratory drive further exacerbating intracellular acidemia. THAM (trometanol; tris-hydroxymethyl aminomethane) is an inert amino alcohol which is theoretically amore effective buffer than bicarbonate in the physiological range of blood pH because it has a pKa of 7.8 at normal body temperatures (compared to a pKa of 6.1 for sodium bicarbonate). Why may it be more Continue reading >>

The Use Of Tris-hydroxymethyl Aminomethane In The Emergency Department

The use of tris-hydroxymethyl aminomethane in the emergency department Lu, Leibner, and Wright: The use of tris-hydroxymethyl aminomethane in the emergency department Christina Lu , Evan Leibner , Brian Wright Department of Emergency Medicine, Stony Brook University, Stony Brook, NY, USA Correspondence to: Brian Wright Department of Emergency Medicine, Stony Brook University, Hsc, Level 4, Room 080, Stony Brook, NY 11794, USA Received: July 20, 2016 Revised: August 22, 2016 Accepted: August 22, 2016 Copyright 2016 The Korean Society of Emergency Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ). Bicarbonate therapy is often not effective for alkalinizing the blood pH in critically ill patients because it requires patients to augment their already maxed respiratory drive. Tris-hydroxymethyl aminomethane is a little known amine buffer that works in a closed system independent of pulmonary function and may be an effective alternative to sodium bicarbonate. Treatment of critically ill patients is a multi-faceted problem. Often the physician is faced with multiple complex tasks that range from correctly diagnosing the underlying disease process to appropriately managing the hemodynamics and homeostasis. Critically ill patients commonly have acid-base abnormalities, especially acidosis. Critical care dogma teaches that treatment of the primary condition will lead to a correction of the acidosis. That acidosis, however, can be so severe that it needs to be addressed before the underlying medical condition can be reversed. This review will discuss tris-hydroxymethyl aminomethane (THAM). THAM is a rarely used buffer approved by the Food and Drug Administration for treatment of metabolic acidosis as Continue reading >>

Nicu Medication Manual

used for the treatment of severe metabolic acidosis, primarily in infants with hypercarbia or hypernatremia NOT indicated for the management of metabolic acidosis associated with bicarbonate deficiency (renal tubular acidosis) THAM is a highly alkaline, sodium-free organic amine alkalizing agent THAM binds with hydrogen ions to form bicarbonate and a cationic buffer which is excreted in the urine 1 mM of THAM can buffer no more than 1 mM of CO2 PCO2 may decrease slightly after treatment THAM is rapidly eliminated by glomerular filtration respiratory depression may occur (maintain assisted ventilation) urine flow and electrolyte content of urine may increase because of the osmotic diuretic action of THAM tissue necrosis from infiltration and extravasation phlebitis and thrombosis at injection site hyperkalemia and hypoglycemia have been reported avoid infusion through low umbilical vein catheters (UVC) (increases risk of hepatic necrosis) May be given through a UVC when the line tip is certain to be in the UVC or right atrium. do not use in patients who are anuric, uremic or who have chronic respiratory acidosis monitor IV site closely for signs of extravasation monitor urine output, serum glucose, potassium and calcium infuse into as large a vein as possible - a central vein is preferred the appropriate dose of tromethamine is arbitrary based on minimizing the osmotic challenge while maximizing the buffering capacity Standard IV dose of 0.3 M undiluted solution: administer undiluted by slow IV infusion through a large vein Continue reading >>

Tham As An Alternative Buffer Circuit Surfers

Tham Solution (tromeThamine injection) is a sterile, non-pyrogenic 0.3 M solution of tromeThamine, adjusted to a pH of approximately 8.6 with glacial acetic acid. It is administered by intravenous injection, by addition to ACD blood for priming cardiac bypass equipment and by injection into the ventricular cavity during cardiac arrest. Each 100 mL contains tromeThamine 3.6 g (30 mEq) in water for injection. The solution is hypertonic 389 mOsmol/L (calc.). pH 8.6 (8.4-8.7). The solution contains no bacteriostat, antimicrobial agent or added buffer (except acetic acid for pH adjustment) and is intended only for use as a single-dose injection. When smaller doses are required the unused portion should be discarded. Tham solution is a parenteral systemic alkalizer and fluid replenisher. TromeThamine, USP (sometimes called tris or tris buffer) is chemically designated 2-amino-2-(hydroxymethyl)-1, 3-propanediol, a solid readily soluble in water, also classified as an organic amine buffer. It has the following structural formula: Water for Injection, USP is chemically designated H20. When administered intravenously as a 0.3 M solution, tromeThamine act as a proton acceptor and prevents or corrects acidosis by actively binding hydrogen ions (H+). It binds not only cations of fixed or metabolic acids, but also hydrogen ions of carbonic acid, thus increasing bicarbonate anion (HCO3). TromeThamine also acts as an osmotic diuretic, increasing urine flow, urinary pH, and excretion of fixed acids, carbon dioxide and electrolytes. A significant fraction of tromeThamine (30% at pH 7.40) is not ionized and therefore is capable of reaching equilibrium in total body water. This portion may penetrate cells and may neutralize acidic ions of the intracellular fluid. The drug is rapidly elimi Continue reading >>

Benefits of Camel Milk: Low Allergen Alternative to Dairy

Tham-tromethamine: Mechanism, Indication, Contraindications, Dosing, Adverse Effect, Interaction | Pediatric Oncall

It is a sodium free organic buffer used to treat metabolic acidosis, primarily in patients who have received maximum sodium bicarbonate therapy or who have hypercarbia or hypernatremia. Tromethamine is used to treat metabolic acidosis (an electrolyte imbalance). Metabolic acidosis can have many causes. It often occurs after heart bypass surgery or cardiac arrest. allergic to any drugs, or if you have asthma, kidney disease, or congestive heart failure.uremia Wt (Kg) x 1.1 x base deficit (Meq/L) as loading dose. Continuous infusion=3ml/kg/hour. Do not give for more than 24 hours hyperosmolality, hepatotoxicity, hyperkalemia, hypoglycemia, hypocalcemia, respiratory depression, apnea, and tissue necrosis on extravasation. aspirin ? tromethamineApplies to:acetaminophen/aspirin and Tham (tromethamine)Using tromethamine together with aspirin may decrease the effects of aspirin. Contact your doctor if your condition changes.tromethamine ? pseudoephedrineApplies to:Tham (tromethamine) and Allermed (pseudoephedrine)Using pseudoephedrine together with tromethamine may increase the effects of pseudoephedrine. Contact your doctor if you experience tremor, anxiety, insomnia, irritability, or nervousness. Continue reading >>

Sodium Bicarbonate Versus Tham In Icu Patients With Mild Metabolic Acidosis.

Sodium bicarbonate versus THAM in ICU patients with mild metabolic acidosis. Intensive Care Unit, Ghent University Hospital, Gent, Belgium. [email protected] Sodium bicarbonate is despite its side effects, considered the standard alkali therapy in metabolic acidosis. THAM is an alternative alkalizing agent; however, there are limited data on the use of THAM in metabolic acidosis. The aim of this study was to compare the efficacy and adverse effects of a single dose of sodium bicarbonate and THAM in intensive care unit (ICU) patients with mild metabolic acidosis. 18 adult ICU patients with mild metabolic acidosis (serum bicarbonate < 20 mmol/L) were randomized to a single dose of either sodium bicarbonate or THAM, administered over a 1-hour period, and titrated to buffer the excess of acid load. Sodium bicarbonate and THAM had equivalent alkalinizing effect during the infusion period. This was still present 4 hours after start of infusion of sodium bicarbonate, and until 3 hours after start of infusion of THAM. Serum potassium levels decreased after sodium bicarbonate infusion, and remained unchanged after THAM. After sodium bicarbonate, sodium increased, and after THAM, serum sodium decreased. Sodium bicarbonate and THAM had a similar alkalinizing effect in patients with mild metabolic acidosis; however, the effect of sodium bicarbonate was longer lasting. Sodium bicarbonate did decrease serum potassium, and THAM did not; THAM is therefore not recommended in patient with hyperkalemia. As sodium bicarbonate leads to an increase of serum sodium and THAM to a decrease, THAM may be the alkalinizing agent of choice in patients with hypernatremia. Similarly, because sodium bicarbonate increases PaCO2 and THAM may even decrease PaCO2, sodium bicarbonate is contraindicated a Continue reading >>

Effects Of Tham And Sodium Bicarbonate On Metabolic Acidosis And Mineral Metabolism

EFFECTS OF THAM AND SODIUM BICARBONATE ON METABOLIC ACIDOSIS AND MINERAL METABOLISM Pediatric Research volume 10, page 557 (1976) We caused in rabbits an acidosis by infusion of NH4Cl solution. Following we infused NaHCO3 solution, THAM solution pH 10.2 or THAM acetic acid solution pH 8.6. In correcting the metabolic acidosis the buffers had an equal efficacy. The correction of pH and base excess in erythrocytes was more alowly by use of NaHCO3 than by use of THAM solutions, Hematocrit, plasma K, Cl and phosphate decreased by infusion of buffer solutions. Na increased by use of NaHCO3, it-decreased by use of THAM solutions. Ca was not influenced. After the infusion of THAM followed by infusion of glucose solution in newborns we could see a fall of plasma electrolytes. Therefore we think that it is not sufficient to add minerals after 24 hours or later. but it is necessary to applicate minerals earlier. From the view of Na metabolism it is our opinion that we should not use NaHCO3 for the therapy of an acid osis in newborns. Paediatric Hospitals of Universities, Halle and Rostock, GDR. Continue reading >>

Tris - Wikipedia

This article is about the chemical widely used as a biochemical buffer. For other uses, see Tris (disambiguation) . Tris, or tris(hydroxymethyl)aminomethane, or known during medical use as tromethamine or THAM, is an organic compound with the formula (HOCH2)3CNH2. It is extensively used in biochemistry and molecular biology as a component of buffer solutions [1] such as in TAE and TBE buffers , especially for solutions of nucleic acids . It contains a primary amine and thus undergoes the reactions associated with typical amines, e.g. condensations with aldehydes . In medicine, tromethamine is occasionally used as a drug, given in intensive care for its properties as a buffer for the treatment of severe metabolic acidosis in specific circumstances. [2] [3] Some medications are formulated as the "tromethamine salt" including hemabate ( carboprost as trometamol salt), and " ketorolac trometamol". [4] TRIS, Tris, Tris base, Tris buffer, Trizma, Trisamine, THAM, Tromethamine, Trometamol, Tromethane, Trisaminol Except where otherwise noted, data are given for materials in their standard state (at 25C [77F], 100kPa). The conjugate acid of tris has a pKa of 8.07 at 25C, which implies that the buffer has an effective pH range between 7.5 and 9.0. The pKa declines approximately 0.03 units per degree Celsius rise in temperature. [5] [6] Silver -containing single-junction pH electrodes (e.g., silver chloride electrodes ) are incompatible with tris since an Ag-tris precipitate forms which clogs the junction. Double-junction electrodes are resistant to this problem, and non-silver containing electrodes are immune. Tris inhibits a number of enzymes, [7] [8] and therefore should be used with care when studying proteins. Tris is prepared industrially by the exhaustive condensation of n Continue reading >>

Payperview: Effects Of A Continuous Infusion Of Tris(hydroxymethyl)aminomethane On Acidosis, Oxygen Affinity, And Serum Osmolality - Karger Publishers

I have read the Karger Terms and Conditions and agree. The effects of a continuous infusion of tris(hydroxymethyl)-aminomethane (THAM) on pH, base excess, p50, serum osmolality, and plasma drug concentration during respiratory acidosis were studied in newborn piglets. Measurements were made during three experimental periods: (1) control period with normal blood gases; (2) hypercapnia period, and (3) hypercapnia plus THAM period (THAM infusion: 1.65 mmol/kg/h). pH decreased and paCO2 increased between control period (7.40 0.05 and 45 3 mm Hg) and hypercapnia period (7.24 0.06 and 59 2 mm Hg; p < 0.001; mean SD). pH returned to baseline (7.37 0.04) during the hypercapnia plus THAM period, while paCO2remained elevated (63 4 mm Hg). p50 increased from 30.7 5.9 to 38.3 4.7 (p < 0.05) during hypercapnia and decreased with hypercapnia plus THAM. THAM concentration and base excess increased with time and were linearly related. Serum osmolality was unchanged during the THAM infusion. We conclude that continuous infusion of THAM is effective in normalizing pH during respiratory acidosis in the piglet. Continue reading >>

Buffer Therapies: Sodium Bicarbonate, Carbicarb And Tham - Deranged Physiology

Buffer Therapies: Sodium Bicarbonate, Carbicarb and THAM This has only come up once in the exam. Question 27 from the first paper of 2009 asked the candidates to compare and contrast the pharmacology of carbicarb, sodium bicarbonate and THAM. The unusual feature was of course the fact that carbicarb is not available in Australia, and THAM is so rarely used that our local supply consists of imported ampoules with labels exclusively in German. The answer to Question 27 works best as a table; it is reproduced below to simplify revision. As far as literature references go, the majority are from the 1980s and 90s (back when buffer therapy was still considered a viable option in cardiac arrest, for example). One potentially relevant article is a 1998 paper by Bar-Joseph et al , which compared THAM, Carbicarb and sodium bicarbonate in a canine cardiac arrest model. An 8.4% (1mol/L) solution of NaHCO3which offers 1000mmol/L of HCO3-and Na+ions. An equimolar (300mmol/L) solution of Na2CO3and NaHCO3which offers 666mmol/L of HCO3-ions, and 1000mmol/L of Na+ions An organic amine buffer, otherwise known as tris-hydroxymethyl-aminomethane, or tromethamine. Eliminated renally, as well as being converted to CO2and exhaled (in process of buffering reactions). These two substances differ mainly in the amount of bicarbonate anion they add. Rapidly eliminated by the kidney; 75% is excreted in the urine after 8 hours. Sodium bicarbonate contributes HCO3-which is a natural buffer, thus replenishing the buffer systems of the body in a state of acidosis. The sodium carbonate component is supposed to act as a bicarbonae precursor, regenerating HCO3-buffers without increasing the PaCO2. THAM is a "third buffer" to complement the buffering capacity of endogenous HCO3-and body protein. At pH of 7 Continue reading >>

The Treatment Of Acidosis In Acute Lung Injury With Tris-hydroxymethyl Aminomethane (tham)

American Journal of Respiratory and Critical Care Medicine Mechanical hyperventilation of acidemic patients with acute lung injury (ALI) requires the use of high volumes and pressures that may worsen lung injury. However, permissive hypercapnia in the presence of shock, metabolic acidosis, and multi-organ system dysfunction may compromise normal cellular function. Tris-hydroxymethyl aminomethane (THAM) may be an effective method to control acidosis in this circumstance. Protonated THAM is excreted by the kidneys, so that carbon dioxide production is not raised. In an uncontrolled study, we administered THAM to 10 patients with acidosis (mean pH = 7.14) and ALI (mean lung injury score = 3.28) in whom adequate control of arterial pH could not be maintained during either eucapnic ventilation or permissive hypercapnia ventilation. THAM was given at a mean dose of 0.55 mmol/kg/h. Administration of THAM was associated with significant improvements in arterial pH and base deficit, and a decrease in arterial carbon dioxide tension that could not be fully accounted for by ventilation. Although further studies are needed to confirm these observations, THAM appears to be an effective alternative to sodium bicarbonate for treating acidosis during ALI. Permissive hypercapnia is recommended to treat patients with acute lung injury (ALI) ( 1 ). However, permissive hypercapnia requires patient tolerance of respiratory acidosis for hours or days until renal compensation can correct arterial pH. ALI that develops as a consequence of sepsis and trauma commonly occurs with severe metabolic acidosis, shock, and multi-organ system dysfunction. In this situation, induced respiratory acidosis may compromise normal cellular function. Using high minute ventilation (Ve), with or without sodium b Continue reading >>

Management Of Acidosis: The Role Of Buffer Agents

Management of acidosis: the role of buffer agents Sodium BicarbonateLactic AcidosisDiabetic KetoacidosisTHAMBicarbonate Buffer For more than 50 years, continuing up to about 1980, sodium bicarbonate was used for the treatment of metabolic acidosis. The rationale was that administration of an alkaline fluid would correct an acidotic state. However, the potential value of sodium bicarbonate was called into question when more recent studies demonstrated that it induced venous hypercarbia, and decreases in tissue and cerebrospinal fluid pH, as well as provoking tissue hypoxia, circulatory congestion, hypernatremia, and hyperosmolality, with consequent brain damage [ 1 , 2 , 3 , 4 , 5 , 6 ]. Bicarbonate buffers may intensify rather than ameliorate cellular acidosis because sodium bicarbonate generates CO2 and thereby increases intracellular (hypercarbic) acidosis [ 7 ]. Sodium bicarbonate administered to patients with diabetic ketoacidosis failed to favorably alter the clinical course or outcome. More specifically, the survival rate was similar in patients who did not receive bicarbonate [ 8 ]. During hypoxic lactic acidosis, sodium bicarbonate produced a decline in both systemic arterial pressure and cardiac output without improvement in outcome [ 9 ]. The declines in arterial pressure and cardiac output were associated with the hypertonicity of buffer agents which produced arterial vasodilation [ 10 ]. Several other agents have been investigated for the treatment of lactic acidosis. The intent was to increase blood pH during hypoxic states, without reducing oxygen delivery or increasing blood and tissue CO2. Among the most promising are the organic buffers, including TRIS (THAM), and a mixture of equimolar concentrations of sodium carbonate and bicarbonate named Carbicarb Continue reading >>

Clinical And Metabolic Effects Of Tromethamine (tham)

CLINICAL AND METABOLIC EFFECTS OF TROMETHAMINE (THAM) Anesthesia & Analgesia: February 1998 - Volume 86 - Issue 2S - p 473S Abstracts of Posters Presented at the International Anesthesia Research Society; 72nd Clinical and Scientific Congress; Orlando, FL; March 7-11, 1998: Pharmacology Introduction: Tromethamine (THAM) is a buffer used in the treatment of metabolic acidosis. It acts by proton buffering without generating carbon dioxide (CO2) which may be a problem with bicarbonate therapy [1] . THAM is non-ionic and penetrates cell membranes reducing acidosis, unlike bicarbonate which may exacerbate intracellular acidosis [2] . THAM is sodium-free and does not cause hypernatremia. Published clinical data on THAM usage is somewhat limited, and we sought to define the time course of the metabolic effects resulting from the use of THAM. Methods: Following ethical committee approval, we studied 15 patients undergoing major surgical procedures with metabolic acidosis, defined as pH<7.2 or base excess (BE) <-5 mmol.l-1. All patients had indwelling arterial catheters for blood sampling. After developing metabolic acidosis, patients were given THAM via a central vein in a dose of 1.1 x BE x weight (kg) ml 0.3M solution [3] . Arterial blood gas samples were taken at 15, 30, 60 and 120 minutes thereafter. Variables measured included: pH, BE, PaCO2, [Na+] and [K+]. Paired Student's t-test was used to analyze results. Results: See Figure 1 . There were no apparent adverse effects of THAM. Significance values displayed in each Figure arebaseline values compared with values 15 minutes after THAM infusion (Students t-test). Conclusions: In this heterogeneous group of patients, THAM conects metabolic acidosis in a predictable fashion with a fall in PaCO2. Changes in pH, BE and PaCO2 Continue reading >>