Nylon-6 Capillary Channeled Fibers as a Stationary Phase for Ion-Exchange Chr...maramirezcnr
Nylon-6 Capillary Channeled Fibers as a Stationary Phase for Ion-Exchange Chromatography Separations of Proteins, by Michelle Permaul, Christine Straut, and R. Kenneth Marcus.
Nylon-6 Capillary Channeled Fibers as a Stationary Phase for Ion-Exchange Chr...maramirezcnr
Nylon-6 Capillary Channeled Fibers as a Stationary Phase for Ion-Exchange Chromatography Separations of Proteins, by Michelle Permaul, Christine Straut, and R. Kenneth Marcus.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
APPROACH TO AKI IN CHILDREN
ACUTE KIDNEY INJURY
It is defined as abrupt loss of kidney function leading to rapid decline in GFR , accumulation of waste products BUN and creatinine and dysregulation of extracellular volume and electrolyte homeostasis.
AKI can ranges from small increase in creatinine to complete anuric renal failure .
INCIDENCE
2-5 % of all hospitalization.
>25% in critically ill children .
CLASSIFICATION OF AKI
CAUSES
CLINICAL MANIFESTATION
DIAGNOSTIC TEST
HISTORY AND PHYSICAL
EXAMINATION
IDENTIFICATION OF PRECIPTATING CAUSE
COMPLICATION
MANAGEMENT
MANAGEMENT
There is no definitive therapy for AKI, supportive care is mainstay of management regardless of aetiology.
Goal of treatment is :
Minimize degree of insult.
Reduce extrarenal complication.
Restoration of AKI.
Optimize the systemic and renal hemodynamic(fluid resuscitation or use of vasopressor).
Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE inhibitor, ARB blocker, acyclovir) or adjust the dose .
Catheterize the patient in case of obstruction like PUV, UPJ obstruction
POST-RENAL AKI
Prompt relieve of urinary tract obstruction.
Relief of obstruction is usually followed by an appropriate diuresis and may require continue administration of iv fluids and electrolyte.
RENAL REPLACEMENT THERAPY
The purpose of RRT is to prevent morbidity.
It may be necessary for days or upto 12 weeks.
Mostly require dialysis support for 1-3 weeks.
Indication Of RRT :
A= ACIDOSIS, ANURIA
E= ELECTROLYTE DISTURBANCE (hypokalemia)
I= INTOXICATION
O= OVERLOAD(hypertension, pulmonary edema)
U= UREMIA
PROGNOSIS
Pre-renal and post-renal have better prognosis.
In case of post-infectious glomerulonephritis is 1%
In case of multi organ failure >50%.
Kidney may recover even after dialysis .
10% cases requiring dialysis develop CKD.
CARRY HOME MESSAGE
Diagnose early- biomarkers have great potential.
Look for aetiology.
Prevent rather than treat.
No role of low dose dopamine prevention and treatment .
Initiate RRT when indicated.
As this herbicide poisoning is frequent with poor outcomes so its management needs to be discussed and awareness should be raised among farmers about its use and pre-hospital treatments.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
APPROACH TO AKI IN CHILDREN
ACUTE KIDNEY INJURY
It is defined as abrupt loss of kidney function leading to rapid decline in GFR , accumulation of waste products BUN and creatinine and dysregulation of extracellular volume and electrolyte homeostasis.
AKI can ranges from small increase in creatinine to complete anuric renal failure .
INCIDENCE
2-5 % of all hospitalization.
>25% in critically ill children .
CLASSIFICATION OF AKI
CAUSES
CLINICAL MANIFESTATION
DIAGNOSTIC TEST
HISTORY AND PHYSICAL
EXAMINATION
IDENTIFICATION OF PRECIPTATING CAUSE
COMPLICATION
MANAGEMENT
MANAGEMENT
There is no definitive therapy for AKI, supportive care is mainstay of management regardless of aetiology.
Goal of treatment is :
Minimize degree of insult.
Reduce extrarenal complication.
Restoration of AKI.
Optimize the systemic and renal hemodynamic(fluid resuscitation or use of vasopressor).
Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE inhibitor, ARB blocker, acyclovir) or adjust the dose .
Catheterize the patient in case of obstruction like PUV, UPJ obstruction
POST-RENAL AKI
Prompt relieve of urinary tract obstruction.
Relief of obstruction is usually followed by an appropriate diuresis and may require continue administration of iv fluids and electrolyte.
RENAL REPLACEMENT THERAPY
The purpose of RRT is to prevent morbidity.
It may be necessary for days or upto 12 weeks.
Mostly require dialysis support for 1-3 weeks.
Indication Of RRT :
A= ACIDOSIS, ANURIA
E= ELECTROLYTE DISTURBANCE (hypokalemia)
I= INTOXICATION
O= OVERLOAD(hypertension, pulmonary edema)
U= UREMIA
PROGNOSIS
Pre-renal and post-renal have better prognosis.
In case of post-infectious glomerulonephritis is 1%
In case of multi organ failure >50%.
Kidney may recover even after dialysis .
10% cases requiring dialysis develop CKD.
CARRY HOME MESSAGE
Diagnose early- biomarkers have great potential.
Look for aetiology.
Prevent rather than treat.
No role of low dose dopamine prevention and treatment .
Initiate RRT when indicated.
As this herbicide poisoning is frequent with poor outcomes so its management needs to be discussed and awareness should be raised among farmers about its use and pre-hospital treatments.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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46 Electrolyte Replacement
1. Calcium, Phosphate and Magnesium Replacement
I. Calcium (25 mEq = 500 mg elemental calcium).
A. Parenteral Calcium Salts
Calcium chloride 1 gram 13.6mEq (272mg) of elemental Calcium
Calcium gluconate 1 gram 4.65mEq (90mg) of elemental Calcium
B. Parenteral Calcium Therapy
Indication Dose Rate of Infusion
Symptomatic 4.65 to 18.6 mEq of 1 gram (Calcium gluconate
Hypocalcemia elemental Calcium (1-4 or chloride) over 10
(tetany) grams of Calcium minutes, then 1-2
gluconate) gram(s)/hour. Calcium
infusion should be
continued until Calcium
level reaches 8-9 mg/dl.
For calcium replacement, the rate of infusion should be about 1-2 gram(s)/hour.
Calcium chloride should be given via a central line due to a higher incidence of
thrombophlebitis.
Calcium chloride is compatible in most common IV infusion solutions, i.e. 0.9%
NaCl, 5% dextrose.
II. Phosphorus
A. Parenteral Phosphate Salts
Potassium Phosphate: 4.4 mEq of K+/ml and 3 mM of phosphate/ml
Sodium Phosphate: 4 mEq of Na+/ml and 3 mM of phosphate/ml
B. Parenteral Phosphate Therapy
Serum PO Action
Serum phosphorus 1-2 mg/dl Give 0.2 mmol/kg over 4-6 hours
Serum phosphorus < 1 mg/dl Give 0.3 mmol/kg over 4-6 hours
Parenteral phosphate should be diluted and mixed in as large a volume of fluid (i.e.
250 ml) as possible. When ordering parenteral phosphate, always order the amount
of phosphate in mmol units.
C. Oral: Neutra-Phos Powder (1 packet) 250 mg (8 mmol)/packet
2. III. Magnesium
A. Magnesium Salts: Magnesium (elemental) 1 gram = 83.3 mEq
Magnesium sulfate 1 gram = 8.1 mEq
B. Oral Preparation: Mg Chloride 535 mg = 64 mg (5.33mEq) Mg/tablet
Mg gluconate 500 mg = 27 mg (2.25 mEq) Mg/tablet
Mg oxide 400 mg = 241.3 mg (20.1 mEq) Mg/tablet
Magnesium Citrate 1.745 gram/30 ml
C. Parenteral Magnesium Therapy
In patients with normal renal function, up to 50 mEq (6 grams) of magnesium may
be given IV over 4 to 6 hours (usually infuse 1 gram/hour), mixed in 50 to 100 ml of
0.9% NaCl or 5% dextrose.
Magnesium sulfate is incompatible with soluble phosphates and with alkali
carbonates and bicarbonates (except in dilute solutions).
3. DISCLAIMER: These guidelines were prepared by the Department of Surgical Education, Orlando Regional Medical Center in
conjunction with the Pharmacy Department. They are intended to serve as a general statement regarding appropriate patient care
practices based upon the available medical literature at the time of development. They should not be considered to be accepted
protocol or policy, nor are intended to replace clinical judgment or dictate care of individual patients.
ADULT ELECTROLYTE REPLACEMENT PROTOCOLS
SUMMARY
Standing electrolyte replacement protocols are available for use in adult patients admitted to Orlando
Regional Healthcare hospitals. These are instituted upon direct physician order entry into Sunrise XA.
The protocols are listed below.
SPECIFIC REQUIREMENTS:
• Intravenous piggyback infusions of electrolytes must be administered with free-flow protected infusion
devices (i.e. infusion pump).
• Patients must meet the following criteria prior to initiation of the Potassium, Magnesium, or
Phosphorus protocols:
o SCr < 2 mg/dL
o Weight > 40 kg
• The electrolyte replacement protocols, Calcium chloride (Level I areas only) or Calcium gluconate (all
levels of care), Magnesium sulfate, Potassium chloride, or Potassium Phosphate, may be ordered
individually or in combination.
POTASSIUM REPLACEMENT PROTOCOL – INTRAVENOUS
• Recommended rate of infusion is 10 mEq/h
• Maximum rate of intravenous replacement is 20 mEq/h with continuous ECG monitoring (the
maximum rate may be increased to 40 mEq/h in emergency situations – see Policy #5080)
• Standard Concentrations: 10 mEq/50 mL, 10 mEq/100mL, 20 mEq/50 mL and 20 mEq/100 mL
o Maximum Concentration for Central IV administration = 20 mEq/50 mL
o Maximum Concentration for Peripheral IV administration = 10 mEq/50 mL
Current Serum Central IV Peripheral IV Administration Monitoring
Potassium Level Administration
3.6 – 3.9 mEq/L 20 mEq IV over 2 HR x 1 10 mEq IV over 1 HR x 2 No additional action
20 mEq IV over 2 HR x 1
3.4 – 3.5 mEq/L AND 10 mEq IV over 1 HR x 3 No additional action
10 mEq IV over 1 HR x 1
Recheck serum potassium
3.1 – 3.3 mEq/L 20 mEq IV over 2 HR x 2 10 mEq IV over 1 HR x 4 level 2 hours after infusion
complete
20 mEq IV over 2 HR x 2 Recheck serum potassium
2.6 – 3 mEq/L AND 10 mEq IV over 1 HR x 5 level 2 hours after infusion
10 mEq IV over 1 HR x 1 complete
Recheck serum potassium
2.3 – 2.5 mEq/L 20 mEq IV over 2 HR x 3 10 mEq IV over 1 HR x 6 level 2 hours after infusion
complete
Recheck serum potassium
Call Physician AND Call Physician AND
< 2.3 mEq/L level 2 hours after infusion
20 mEq IV over 2 HR x 3 10 mEq IV over 1 HR x 6
complete
• If both potassium and phosphorus replacement required, subtract the mEq of potassium given as potassium phosphate from
+
total amount of potassium required. (Conversion: 3 mmols KPO4 = 4.4 mEq K )
• Call pharmacy for assistance if needed.
1 Approved 05/29/01
Revised 01/14/08
4. POTASSIUM REPLACEMENT PROTOCOL – ORAL or ENTERAL (PT)
• Standard dosage forms: KCl 20mEQ tablet or KCl 10% solution (20 mEq/15 mL)
Current Serum
Total Potassium Replacement Monitoring
Potassium Level
3.7 – 3.9 mEq/L 20 mEq KCl PO/Per feeding tube x 1 dose No additional action
3.5 – 3.6 mEq/L 20 mEq KCl PO/Per feeding tube Q2H x 2 doses No additional action
3.3 – 3.4 mEq/L 20 mEq KCl PO/Per feeding tube Q2H x 3 doses Recheck serum potassium level 4 hours
after last oral dose
3.1 – 3.2 mEq/L 20 mEq KCl PO/Per feeding tube Q2H x 4 doses Recheck serum potassium level 4 hours
after last oral dose
Call Physician AND Recheck serum potassium level 4 hours
< 3.1 mEq/L
20 mEq KCl PO/Per feeding tube Q2H x 4 doses after last oral dose
MAGNESIUM REPLACEMENT PROTOCOL
• Infusions should be no faster than 1gm of magnesium sulfate every 30 minutes.
• Standard Concentrations: 1 gm/100 mL and 2 gm/50 mL
Current Serum Magnesium Level Total Magnesium Replacement Monitoring
1.5 – 2 mEq/L 2 grams Magnesium Sulfate IV over 1 HR No additional action
2 grams Magnesium Sulfate IV over 1 HR x
0.9 – 1.4 mEq/L Recheck serum magnesium level 2 hours
2 doses after infusion complete
Call Physician AND Recheck serum magnesium level 2 hours
< 0.9 mEq/L 2 grams Magnesium Sulfate IV over 1 HR x
after infusion complete
2 doses
2 Approved 05/29/01
Revised 01/14/08
5. PHOSPHORUS REPLACEMENT PROTOCOL
• Replacement must be ordered in mmol of phosphorus.
• Recommended rate = 3mmol/hr (= 4.4 mEq/h of K)
• Maximum rate = 10 mmol/hr (= 15 mEq/h of K)
• Use SODIUM phosphate for patients with serum potassium > 4.5 mEq/L and serum sodium < 145
mEq/L
• Standard Concentrations:
o Potassium Phosphate: 15 mmol/250 mL and 21 mmol/250 mL
o Sodium Phosphate: 15 mmol/250 mL, 21 mmol/250 mL, and 30 mmol/250 mL
Current Serum
Total Phosphorus Replacement Monitoring
Phosphorus Level
2 – 2.5 mg/dL 15 mmol Potassium Phosphate IV over 4 HR No additional action
Recheck serum phosphorus level 2 hours
1 – 1.9 mg/dL 21 mmol Potassium Phosphate IV over 4 HR
after infusion complete
Call Physician AND
30 mmol Potassium Phosphate IV over 4 HR Recheck serum phosphorus level 2 hours
< 1 mg/dL
(Administered as: 15 mmol Potassium after infusion complete
Phosphate IV Q2H x 2 doses)
• If both potassium and phosphorus replacement required, subtract the mEq of potassium given as potassium phosphate from
+
total amount of potassium required. (Conversion: 3 mmols KPO4 = 4.4 mEq K )
• Call pharmacy for assistance if needed.
CALCIUM REPLACEMENT PROTOCOL
• You must specify the salt form (gluconate or chloride)
• Calcium chloride:
o Reserved for Level I areas only
o Must be administered via a central line
o Maximum rate = 1 gm IV over 10 minutes
• Calcium gluconate:
o May be used in all levels of care
o Administration via a central line is preferred; however, it may be given peripherally with
adequate IV access.
o Maximum rate = 3 gm IV over 10 minutes
• Standard concentrations:
o Calcium chloride: 1 gm/50 mL, 2 gm/100 mL, 3 gm/150 mL
o Calcium gluconate: 1 gm/50 mL, 2 gm/100 mL
Total Calcium CHLORIDE
Current Ionized Total Calcium GLUCONATE
Replacement Monitoring
Calcium Level Replacement
(Level I areas only)
1 – 1.1 mmol/L 1 gram IV over 1 HR 1 gram IV over 1 HR No additional action
0.85 – 0.99 mmol/L 2 grams IV over 1 HR 2 grams IV over 1 HR Recheck serum ionized calcium
2 hours after infusion complete
< 0.85 mmol/L Call Physician AND Call Physician AND Recheck serum ionized calcium
2 grams IV over 1 HR 3 grams IV over 1 HR 2 hours after infusion complete
3 Approved 05/29/01
Revised 01/14/08
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School of
Medicine
Citation: B. J. Phillips : Electrolyte Replacement: A Review . The Internet Journal of
Internal Medicine. 2004 Volume 5 Number 1
Table of Contents
Introduction
Electrolytes
I. CALCIUM
II. MAGNESIUM
A. ORAL
MAGNESIUM
7. REPLACEMENT
B. INTRAVENOUS
MAGNESIUM
REPLACE...
III. PHOSPHOROUS
A. ORAL
PHOSPHORUS
REPLACEMENT
B. INTRAVENOUS
PHOSPHOROUS
REPLA...
IV. POTASSIUM
INTRAVENOUS
POTASSIUM
ADMINISTRA...
Clinical
information
Warnings /
Precautions
Potassium Chloride
General State...
ORAL POTASSIUM
ADMINISTRATION
GU...
Abstract
In accordance with a best practice model for the delivery of care to
ICU Patients, a process of developing protocols for the standard
replacement of fluid & electrolytes should exist in most units. This is
an important step in an evolution towards a systems-based approach
in the ICU. As a baseline for these changes, we must alter the way in
which we monitor lab values.
Introduction
8. We recommend checking “routine labs” on a 4am-4pm cycle (every 12
hours) on ALL stable ICU patients. Other phlebotomy draws should
only be performed when clinically indicated; we must become more
efficient with our use and interpretation of laboratory values.
Depending on the underlying abnormality, aggressive replacement will
be expected. During the pre-rounds at 6am, house-staff begin
addressing any underlying fluid or electrolyte deficiencies. We then
review the “morning labs” as a team during the 7am rounds and
decide further treatment. Urine electrolytes should also be followed as
deemed necessary by clinical judgment.
Our goals should be:
K > 4.0
Mg > 2.0
Phos > 3.5
Ion. Ca > 4.0
Alb > 2.5
Hct > 30.
Also, it is important to ensure that ALL of our patients are receiving
their daily requirements of the electrolytes. Oral Potassium (at least 2
mEq/kg/day) should be the routine and can either be given in divided
oral doses or added to the tube feedings (continuous replacement via
tube feedings is an efficacious method of electrolyte replacement. and
we are reviewing our current policies in this regard). If a patient is on
diuretics, then we will need to increase the oral replacement. Oral
daily Mg replacement should also become standard (either with Mg-
sulfate or Mg-oxide and should range from 400mg – 1 g/day, based on
the weight of the patient). If the oral form is not well tolerated, then
we will need to shift towards IV replacement.
Our medical and surgical approaches have proven to significantly lower
9. both morbidity and mortality over the past thirty years; they are
aggressive and have set new standards for our field. Similarly, our
routine approaches should strive for the same level of care. By
successfully implementing such a system in your ICU, you can establish
a far more efficient approach in regards to fluid and electrolyte
management. We certainly do not wish to remove clinical judgment
from the system nor create a “robotic-like” atmosphere, however we
must recognize the fact that wide variations in care do exist and at
times, lead to unacceptable clinical states. By establishing these
guidelines, we hope to create a consistent baseline in order to
improve patient safety and the overall efficiency of intensive care
units.
Electrolytes
I. CALCIUM
TREATMENT OF HYPOCALCEMIA
SYMPTOMS: Tetany, muscle spasms, lethargy, seizures
NORMAL LEVELS: Total Calcium: 8.4-10.2 mg/dl (2.1-2.6 mmol/L)
Ionized Calcium: 3.8-5.3 mg/dl (0.95-1.35 mmol/L)
CORRECTION FOR LOW ALBUMIN
For every 1mg/dl of albumin below 4 mg/dl, add 0.8 mg/dl to total
calcium
= [(4 - alb) x 0.8] + calcium
1. Determine Ca x PO4 product in mg/dl before administering calcium.
If product is greater than 60 mg/dl, there is an increased risk of
10. calcium phosphate precipitation in the cornea, lung, kidney, cardiac
conduction system, and blood vessels.
2. Determine potassium, phosphorus and magnesium levels. If the
magnesium concentration is low, it should be corrected, otherwise it
will be difficult to normalize potassium and calcium.
3. Hyperkalemia and hypomagnesemia potentiate the cardiac
neuromuscular irritability produced by hypocalcemia. Hypokalemia and
hypermagnesemia protect against the effects of hypocalcemia.
4. For each 5 units of packed RBCs transfused, administer 1-2 gms (1-
2 amps) of calcium gluconate.
5. As a guideline, the total calcium will increase by 0.5 mg/dl for every
gram of calcium gluconate given intravenously.
6. Patients who develop acute hypocalcemia after parathyroidectomy,
may require up to 10 gms of calcium gluconate intravenously in 1000
ml fluid at a rate of 1 gm/hr (100 ml/hr)
A. ORAL CALCIUM REPLACEMENT
*Absorption is variable and depends on PTH, Vitamin D, and gastric
pH.
TRADE ELEMENTAL
FORMULARY AGENTS NAME CALCIUM
Calcium Carbonate 500 mg chewable tabs Tums® 200 mg
Calcium Carbonate 650 mg tablets 260 mg
Calcium Carbonate 1250 mg tablets OsCal 500® 500 mg
Calcium Carb 250 mg + Vit D 125 IU/tablet OsCal 250 +D® 100 mg
Calcium Glubionate syrup 1.8 gm/5ml NeoCalglucon® 115 mg/5ml
11. Calcium acetate (Phos Lo®) is available for phosphate binding and not
calcium replacement in patients with renal insufficiency since its
calcium absorption is poor.
USUAL DOSE: 500- 2000 mg elemental calcium a day, in divided doses
(bid-qid)
ADVERSE EFFECT: Constipation
B. INTRAVENOUS CALCIUM REPLACEMENT
Intravenous replacement should be used if severe symptomatic
hypocalcemia exists (corrected calcium is <7.7 mg/dl) or if there is a
high risk for complications secondary to hypocalcemia.
FORMULARY AGENTS Elemental Calcium__
Calcium chloride 10 % 1 gm/10 ml syringe 272 mg (13.6 mEq)
Calcium gluconate 10% 1 gm/10 ml ampule 90 mg (4.5 mEq)___
Repeat calcium levels can be drawn the next day or sooner, if
necessary.
MAXIMUM CONCENTRATIONS: Calcium gluconate: 1 gm in 50 ml D5W
or NS
Calcium chloride*: 1 gm in 100 ml D5W or NS
*Calcium chloride should not be given IM or SC because severe tissue
necrosis may occur
INFUSION RATE: Infuse over 30-60 minutes. Rapid administration may
cause bradycardia, hypotension and vasodilation. Infiltration of IV
calcium may cause severe tissue necrosis and sloughing.
12. II. MAGNESIUM
TREATMENT OF HYPOMAGNESEMIA
SYMPTOMS: Irritability, confusion, arrhythmias, weakness,
fasciculation's, nystagmus, seizures
NORMAL LEVELS: 1.7-2.7 mg/dl
A. ORAL MAGNESIUM REPLACEMENT
For Mg levels > 1.2 mg/dl AND asymptomatic, oral* therapy may be
used:
*Oral absorption is variable with 15-50 % of a dose being absorbed.
Elemental Magnesium Usual
FORMULARY AGENTS mg mEq_____ Dose_________
MgOxide 400 mg tablets 240 20 1-2 tablets daily
MgHydroxide (MOM®) 10 ml 360 30 1-2 times a day
MgHydroxide (Maalox®) 10 ml 180 15 1-2 times a day
ADVERSE EFFECTS: Diarrhea (may be reduced by dividing daily doses)
B. INTRAVENOUS MAGNESIUM REPLACEMENT
For Mg levels < 1.2 mg/L or symptomatic or patient unable to take oral
Magnesium sulfate equivalencies: 1 gm MgSO4 =100 mg Mg= 8 mEq
Mg
SYMPTOMATIC/ASYMPTOMATIC
13. WEIGHT OR Mg < 1.2 mg/dl AND Mg > 1.2 mg/dl
< 50 kg 2-3 gm Mg Sulfate 1-2 gm Mg Sulfate
>50 kg 3-4 gm Mg Sulfate 2-3 gm Mg Sulfate
Additional doses of 1-2 gms/day of Mg sulfate may be required for
several days if the patient has not previously been receiving
magnesium.
Renal insufficiency (CLcr < 20ml/min) may require lower doses of
magnesium. Caution should be used when replacing magnesium in any
patient with renal insufficiency.
MAXIMUM CONCENTRATION: 1 gm in 5 ml D5W or NS
MAXIMUM INFUSION RATE: 1 gm over 7 minutes
Magnesium sulfate may be given IM, however it can be very painful.
Doses greater than 1 gm must be given in different injection sites.
For symptomatic patients, bolus doses of IV magnesium are required.
For asymptomatic patients, adding magnesium to the patient's
maintenance IV fluids will allow for better retention of magnesium
Repeat magnesium levels can be drawn the next day or sooner, if
necessary.
III. PHOSPHOROUS
TREATMENT OF HYPOPHOSPHATEMIA
SYMPTOMS: Anorexia, bone pain, muscle weakness, respiratory failure,
CHF, hemolysis, rhabdomyolysis
NORMAL LEVELS: 2.4 - 4.5 mg/dl (0.8 - 1.5 mmol/L)
14. 1. Determine Ca x PO4 product before administering phosphorus;
If the product is greater than 60 mg/dl, there is a risk of calcium
phosphate precipitation in the cornea, lung, kidney, cardiac
conduction system, and blood vessels.
A. ORAL PHOSPHORUS REPLACEMENT
For Phosphorus > 1 mg/dl (>0.3 mmol/L), oral therapy may be used:
FORMULARY Phosphorus Sodium Potassium
AGENTS mmol /mEq
Neutra-Phos® 8 7 7 per capsule/powder packet*
Neutra-Phos K® 8 0 14 per capsule/powder packet*
Skim milk per 8 oz 4 3 5
USUAL DOSE: 1-2 powder packets* or capsules* (8-16 mmol) of
Neutra-Phos or Neutra-Phos K po/ng tid.
*Each Neutra-phos capsule/packet must be opened and diluted with
75 ml of water before administration.
8 oz skim milk (4 mmol of Phos) tid
ADVERSE EFFECT: Diarrhea (will decrease Mg absorption)
NOTE: Magnesium, calcium and aluminum containing antacids may
bind phosphorus and prevent its absorption, so should be avoided in
patients with low phosphate levels.
15. B. INTRAVENOUS PHOSPHOROUS REPLACEMENT
For Phosphorus < 1 mg/dl (< 0.3mmol/L), IV phosphorus should be
given.
FORMULARY AGENTS Phosphorus Sodium Potassium
Potassium phosphate 3 mmol/ml 0 4.4 mEq/ml
Sodium phosphate 3 mmol/ml 4 mEq/ml 0
USUAL DOSE: For acute decreases in PO4: 0.25 mmol/kg IBW*
For chronic depletion of PO4: 0.5 mmol/kg IBW*
Renal insufficiency (CLcr <20ml/min): reduce dose by 50%
As a guideline, the phosphorus level will increase by an average of 1.2
mg/dl with a dose of 0.25mmol/kg
*IBW: Men = 50 + 2.3 (inches over 5 feet)
Women = 46 + 2.3 (inches over 5 feet)
Recommended concentrations and rate of administration:
KPhos 6 mmol / 100 ml NS or D5W over 4 hours peripherally or
centrally not to exceed 15 mmol per minibag*
NaPhos 10 mmol / 100 ml NS or D5W over 4 hours peripherally or
centrally.
Maximum concentrations and rate of administration:
Use of these concentrations and rates requires continuous monitoring
and is restricted to those areas which can provide that level of care
except in emergent situations.
16. This method of administration is NOT recommended if:
total calcium is < 7.5 mg/dL or > 11 mg/dL (corrected for albumin**)
phosphorus is > 2 mg/dL OR
significant renal dysfunction (Clcr < 10 ml/min)
KPhos 15 mmol / 100 ml NS or D5W over 2 hours centrally.*
NaPhos 15 mmol / 100 ml NS or D5W over 2 hours centrally.
*Although 15mmol of KPhos provides 22 meq of potassium which
exceeds the recommended dose of potassium per minibag (20 meq),
the maximum infusion rate of 2 hours complies with current
potassium administration guidelines (i.e., 20meq/100ml NS or D5W
over minimum 1 hour centrally).
**Correction for low albumin: For every 1mg/dL of albumin below 4
mg/dL, add 0.8 mg/dL to total calcium:
Ca corrected = [(4- albumin) x 0.8] + Ca measured
Phosphorus levels should be drawn at the end of the infusion and
should always be drawn prior to any additional doses administered.
Note: Phosphorus has historically been administered over 4 to 6 hours
due to the potential risk associated with high doses and rapid
administration (i.e., hypocalcemia, hypotension, metastatic
calcification, renal failure). However, most of this data comes from
cases of hypercalcemia treated with large doses of intravenous
phosphates in which phosphorus levels were typically normal. More
aggressive electrolyte replacement is not considered as risky.
IV. POTASSIUM
17. INTRAVENOUS POTASSIUM ADMINISTRATION
Clinical information
A. Normal serum potassium value is 4.0 - 5.0 mmol/L
B. Magnesium levels should be monitored and replacement given if
necessary since potassium repletion is ineffective in the presence of
hypomagnesemia.
Warnings / Precautions
A. Rapid infusion of KCl may cause cardiac arrest.
B. Avoid extravasation. Thrombophlebitis may result and is related to
the rate, concentration and size of vein.
C. Signs and symptoms of hypokalemia (K+ < 3.5 mmol/L)
muscle weakness 5. hypotension anorexia 6. weak pulse vomiting 7.
ECG changes: flattened ST segment, T wave heart block,
dysrhythmias inversion and U wave elevation hypotension weak
pulseECG changes: flattened ST segment, T wave
D. Risk Factors for developing hypokalemia
diarrhea, vomiting amphotericin B diuretics metabolic alkalosis
insulin beta2 agonists (e.g., terbutaline)
E. Signs and symptoms of hyperkalemia (K+ > 5.0 mmol/L)
confusion 4. flaccid paralysis listlessness, irritability 5. bradycardia
paresthesias of extremities 6. peaked T-waves on ECG, dysrhythmias
flaccid paralysis bradycardia ECG changes peaked T-waves on ECG,
18. dysrhythmias
F. Risk Factors for developing hyperkalemia
renal impairmentuse of ACE Inhibitors (captopril, enalapril, lisinopril,
etc.)use of potassium sparing diuretics (spironolactone, amiloride,
etc.)use of high dose TMP/SMX for PCP in HIV infected patients
G. Patients on digoxin are more likely to develop digoxin toxicity if K+
is low.
H. If burning or stinging sensation occurs while KCl is being given via
peripheral line, the discomfort may be reduced by the following
methods:
decrease rate of infusionreduce the concentration of KCl
Potassium Chloride General Statements
I. Potassium chloride must never be administered by IV push or IM
injection.
II. All potassium chloride infusions will be supplied by the Pharmacy
Department. These infusions will be commercially prepared in
minibags, or compounded by the Pharmacy. Potassium Chloride vials
will not be stocked in any patient care areas. Any exceptions will need
to be petitioned to the P & T Committee. In pediatric or neonatal
patients, all infusions will be administered via an infusion pump and
burette, or by a syringe pump.
III. All IV maintenance infusions with KCl at a concentration greater
than 40 mEq/L must be administered via an infusion pump.
IV. Peripheral administration
19. A. In adults, the maximum concentration via peripheral line is 10
mEq/100 ml.
B. In adults, the maximum amount of KCl available in each IV minibag
is 20 mEq. In nenoates or pediatrics only two hours worth of fluid
volume will be added to the burette at anytime. Only one hour worth
of fluid should be in a syringe pump.
C. The maximum infusion rate via peripheral line is 10 mEq per hour.
In neonates and pediatrics, the maximum infusion rate via peripheral
line is 0.5 - 1 meq/kg/hour.
V. Central administration
A. In adults, the preferred concentration via central line is 20 mEq/100
ml. The maximum concentration for fluid restricted patients is 20
mEq/50 ml.
B. In adults, the maximum amount of KCl available in each IV minibag
is 20 mEq. In neonates or pediatrics only two hours worth of fluid
volume will be added to the burette at anytime. Only one hour worth
of fluid should be in a syringe pump.
C. The maximum infusion rate via central line is 20 mEq/hr. In
neonates and pediatrics, the maximum infusion rate via central line is
1 meq/kg/hour.
VI. In adults, potassium levels must be checked after a total of 60 mEq
has been administered. Potassium levels must be checked no sooner
than 60 minutes after a given IV dose. In neonates and pediatrics,
potassium levels must be checked after a total of 1 meq/kg has been
administered.
ORAL POTASSIUM ADMINISTRATION GUIDELINES
20. A. Oral potassium chloride replacement should be considered in
asymptomatic patients with serum potassium levels < 3.8 mEq/L.
B. Adult doses from 40-100 mEq/day may be required for potassium
repletion given in 2 - 4 divided doses per day. In the neonate and
pediatric patient, 1-3 meq/kg/day may be required for potassium
repletion given in 2 - 4 divided doses per day.
C. In adults, start with 20-40 mEq/day and titrate to desired level. A
40 mEq dose may be given every 2 hours for a maximum dose of 120
mEq within a 6 hour period. In the neonate, start with 0.5 - 1
meq/kg/day and titrate to desired level with the maximum dose of 3
meq/kg within a 6 hour period.
D. When oral potassium therapy is combined with parenteral
supplementation for adults, a maximum total dose (IV + PO) is 120
mEq within a 6 hour period. For the neonate, a maximum total dose
(IV + PO) is 3 meq/kg within a 6 hour period.
E. Do not use sustained release potassium products, (e.g., KDur™)
when an immediate response is desired. The potassium chloride
powder, dissolved in water, or potassium chloride solution, should be
used for a quicker response.
F. Potassium levels must be checked after each replacement dose. If
using immediate release preparations (KCl powder), a level should be
checked no sooner than 60 minutes. If using a sustained release
product, a level should be checked no sooner than 3 hours. Patients
receiving maintenance doses of oral potassium do not require levels
after each dose.
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