Journal of Parenteral and Enteral Nutrition A New Graduated Dosing Regimen for Phosphorus Replacement in Patients Receiving Nutrition
Kaleb A. Brown, Roland N. Dickerson, Laurie M. Morgan, Kathryn H. Alexander, Gayle Minard and Rex O. Brown JPEN J Parenter Enteral Nutr 2006; 30; 209 The online version of this article can be found at: Additional services and information for
can be found at:
Journal of Parenteral and Enteral Nutrition
Citations (this article cites 31 articles hosted on the
SAGE Journals Online and HighWire Press platforms): JOURNAL OF PARENTERAL AND ENTERAL NUTRITION Copyright 2006 by the American Society for Parenteral and Enteral Nutrition A New Graduated Dosing Regimen for Phosphorus Replacement in
Patients Receiving Nutrition Support
Kaleb A. Brown, PharmD*†; Roland N. Dickerson, PharmD*; Laurie M. Morgan, RN‡; Kathryn H. Alexander, MS, RD§; Gayle Minard, MDʈ; and Rex O. Brown, PharmD* From the *Department of Pharmacy, University of Tennessee Health Science Center, Memphis, Tennessee; Department of Pharmacy, Methodist Healthcare–North Hospital, Memphis, Tennessee; Department of Pharmacy, Regional Medical Center at Memphis, Memphis, Tennessee; §Department of Food and Nutrition, Regional Medical Center at Memphis, Memphis, Tennessee; and the ʈDepartment of Surgery, University of Tennessee Health Science Center, Memphis, Tennessee ABSTRACT. Background: Hypophosphatemia is a common
Results: Of the 79 patients studied, 57 were male and 22 were metabolic complication in patients receiving specialized female with a mean age of 44.8 Ϯ 20.6 years. Mean Injury nutrition support. We changed our previously reported dos- Severity Scores and APACHE-II scores were 27.1 Ϯ 11.6 and ing algorithm because the low dose no longer appeared to be 15.2 Ϯ 6.8, respectively. There was no difference in baseline effective at increasing serum phosphorus concentrations. The characteristics among the 3 dosing groups. Of the 79 purpose of this study was to evaluate the safety and efficacy patients, 34 received the low dose, 30 received the moderate of a revised weight-based phosphorus-dosing algorithm in dose, and 15 received the high dose of phosphorous. Mean critically ill trauma patients receiving specialized nutrition serum phosphorous concentrations on day 2 were signifi- support. Methods: Seventy-nine adult trauma patients with cantly increased in the moderate-dosed group (0.64 Ϯ 0.06 to hypophosphatemia (serum phosphorus concentration Յ0.96 0.77 Ϯ 0.22 mmol/L, p Ͻ .05) and high-dosed group (0.38 Ϯ mmol/L) receiving nutrition support received an IV dose of 0.06 to 0.93 Ϯ 0.32 mmol/L, p Ͻ .01), respectively, when phosphorus on day 1 according to the serum concentration compared with day 1. Mean serum phosphorus concentra- of phosphorus: 0.73– 0.96 mmol/L (0.32 mmol/kg, low dose), tions were normal in all 3 groups on day 3. Serum concen- 0.51– 0.72 mmol/L (0.64 mmol/kg, moderate dose), and Յ0.5mmol/L (1 mmol/kg, high dose). The IV phosphorus bolus trations of magnesium, sodium, and potassium, as well as dose was administered at 7.5 mmol/hour. Generally, pa- arterial pH, were stable across the study. Mean concentra- tients with a serum potassium concentration Ͻ4 mmol/L tions of ionized calcium were not significantly different in received potassium phosphate and patients with a serum any of the 3 dosing groups across the study period. Conclu- potassium concentration Ն4 mmol/L received sodium phos- sions: This weight-based phosphorus-dosing algorithm is safe phate. Patients who still had hypophosphatemia on day 2 for use in critically ill patients receiving nutrition support.
were dosed using the new dosing algorithm by the nutrition The moderate- and severe-dose regimens effectively increase support service according to that day’s serum concentra- serum phosphorus concentrations. ( Journal of Parenteral and tion of phosphorus, or empirically by the trauma service.
Enteral Nutrition 30:209 –214, 2006)
Hypophosphatemia is a common occurrence in criti- alcohol consumption.5 In nondepleted patients, risk cally ill patients that can result in serious complica- factors for the development of hypophosphatemia can tions, given the important role phosphorus plays in include glucose infusion with or without aggressive normal physiology. Hypophosphatemia is encountered refeeding,3,6–8 medications,9,10 trauma,11 severe head in hospitalized medical and surgical patients but may injury,12 thermal injury,13,14 and sepsis.3 In recent be even more prevalent in patients receiving nutrition years, several studies have been published that detail support.1–4 This metabolic complication can occur as the negative effects of hypophosphatemia and empha- the result of phosphorus depletion or due to a shifting size the importance of maintaining normal serum of phosphorus to the intracellular compartment. Deple- phosphorus concentrations. Depending on the degree tion of total body phosphorus can be encountered in of hypophosphatemia, manifestations can include leu- nutritionally wasted patients, such as those with can- kocyte dysfunction,6 rhabdomyolysis,15 glucose intoler- cer cachexia, HIV infection, and patients with chronic arrythmias,18 reduced cardiac output,4,19,20 and evendeath.21 Received for publication July 26, 2005.
We previously reported a weight-based phosphorus- Accepted for publication December 29, 2005.
Correspondence: Rex O. Brown, PharmD, 847 Monroe Street, Suite repletion regimen for hypophosphatemic patients 208, University of Tennessee Health Science Center, Memphis, TN receiving nutrition support.22 Recently, we reevalu- 38163. Electronic mail may be sent to [email protected]
ated this algorithm internally as we had noticed an There was no financial support for this study.
ineffectiveness of the low dose (0.16 mmol/kg) used in This study was presented as a scientific abstract at Nutrition Weekin Orlando, Florida, on January 31, 2005.
our previous study. This necessitated the development of a more aggressive dosing regimen. The purpose of received sodium phosphorus. Due to the amount of this study was to assess the safety and efficacy of this phosphorus required in select subjects, especially in revised algorithm in critically ill trauma patients the severe group, a combination of the 2 salt forms of phosphorus was occasionally used (eg, mild hypokale-mia with severe hypophosphatemia). Doses of phospho-rus were diluted in 100 mL (mild and moderate groups) or 250 mL (severe group) of normal saline (NS) or 5% dextrose in water, and given intravenously at a rate approved by the University of Tennessee Health Sci- not to exceed 7.5 mmol phosphorus/hour. Phosphorus ence Center institutional review board, and the need infusions were given in the morning after calculation for informed consent was waived. Adult trauma and preparation of the respective phosphorus dose.
patients Ͼ18 years old who were hospitalized at the The phosphorus infusions were given in addition to Regional Medical Center at Memphis were included in the phosphorus provided in patients’ nutrition support the study. Study patients resided in the Trauma Inten- formulation. The only enteral formulas used in the sive Care Unit (Trauma ICU), General ICU, Neuro- study were Isosource VHN (26 mmol phosphorus/L), trauma ICU, or the Trauma Stepdown Unit and were Impact Glutamine (39 mmol phosphorous/L), and followed by the Nutrition Support Service (NSS) dur- Resource Diabetic (34 mmol phosphorous/L; all formu- ing data collection. Any subject receiving nutrition sup- las by Novartis Medical Nutrition, Minneapolis, MN).
port via enteral or parenteral routes who also had a Most patients enrolled were receiving either enteral serum phosphorus concentration Յ0.96 mmol/L was formulas without additional phosphorus or parenteral nutrition (PN) containing only standard amounts of Patients with acute renal failure, chronic kidney dis- ease (calculated creatinine clearance Ͻ30 mL/min23, Data for the 2 days after the phosphorus infusion hypercalcemia [serum ionized calcium Ͼ1.32 mmol/L], were collected. Patients who required phosphorus Ͻ1.12 replacement on the subsequent day were dosed by the mmol/L]) were excluded. Other patient exclusions NSS according to the algorithm or by the primary included a history of parathyroid hormone disease, trauma team. On day 2, patients generally had the metabolic bone disease, or class III obesity (body mass increased if they still had hypophosphatemia. This Patients admitted to the above units had daily blood could be accomplished by increasing the phosphorus in drawn at 3 AM, which was sent for a basic metabolic the parenteral formulation or by adding injectable panel with magnesium, ionized calcium, and phospho- potassium phosphate or sodium phosphate (Fleet rus, and a complete blood count with differential.
Phosphasoda, C.B. Fleet Company, Lynchburg, VA) to According to initial serum phosphorus concentrations, patients were placed into one of 3 categories. The nor- All interval data are reported as means Ϯ SD. Data mal range for serum phosphorus concentrations at our analysis was conducted using SPSS for Windows, ver- institution is 0.8 –1.44 mmol/L (2.5– 4.5 mg/dL). Those sion 12 (SPSS, Inc, Chicago, IL) or SigmaStat for Win- who had a serum phosphorus concentration of 0.73– dows, version 3.1 (Systat Software, Inc, Point Rich- 0.96 mmol/L (2.3–3 mg/dL) were empirically desig- mond, CA). Continuous or interval data were analyzed nated as having mild hypophosphatemia; those with a by 1-way analysis of variance with post hoc pairwise serum concentration of 0.51– 0.72 mmol/L (1.6 –2.2 mg/dL) were assigned to the moderate hypophos- Tukey’s honestly significant difference test. For data phatemic group; and those with a value of Ͻ0.5 mmol/L expressing the same variable measured on multiple (Յ1.5 mg/dL) were placed in the severe hypophos- occasions over time, repeated-measures analysis of phatemic group, as previously described.22 Phosphorus variance (RMANOVA) was performed to detect differ- laboratory tests were determined by a colorimetric ences in these measurements between the 2 popula- phosphorus molybdate reaction in the presence of sul- tions. The populations were tested for sphericity, and furic acid. The patients were then assigned to an IV then the univariate RMANOVA was conducted if the phosphorus bolus according to their assigned group as assumption was correct. If the sphericity assumption follows: mild hypophosphatemia (0.32 mmol/kg, low was rejected, then the multivariate RMANOVA was dose), moderate hypophosphatemia (0.64 mmol/kg, performed. The significance testing and reported p val- moderate dose), and severe hypophosphatemia (1 ues were 2 sided for all variables. A p value Ͻ0.05 was mmol/kg, high dose). For ease of preparation, phospho- considered statistically significant.
rus doses were rounded to the nearest 7.5 mmol. Doseswere calculated according to actual body weight for subjects weighing Ͻ130% of their ideal body weight(IBW). In subjects who exceeded 130% of IBW and had We identified 79 patients during a 5-month period a body mass index Ͻ40 kg/m2, an adjusted body weight who met entrance criteria. Of these 79 patients, there was used with the following equation [IBW ϩ were 34 in the mild group, 30 in the moderate group, 0.25(actual body weight Ϫ IBW)]. Patients with a and 15 in the severe group. Demographic data includ- serum potassium concentration Ͻ4 mmol/L on study ing age, gender, height, weight, admission diagnosis, day 1 received potassium phosphate, whereas subjects Injury Severity Score (ISS), Modified Trauma Score, with a serum potassium concentration Ն4 mmol/L and APACHE II score are presented in Table I. There GRADUATED DOSING REGIMEN FOR PHOSPHORUS REPLACEMENT Demographics of the 79 patients included in the study* *The data are presented as mean Ϯ SD.
was no statistical difference in any baseline character-istic between the 3 hypophosphatemic groups. Admit-ting diagnoses included motor vehicle crash (61%),gunshot wound (11.4%), falls (10.1%), miscellaneoustrauma (6.3%), pedestrian struck (6%), knife stabwound patients received only enteral nutrition, 2 received PN FIGURE 1. Mean change in serum phosphorus concentration (mmol/L) only, and 3 patients received both parenteral and from day 1 to day 2 by dosing group. *The change in serum phos-phorus concentration in the group receiving 1 mmol/kg was statisti- enteral nutrition during the study. The majority of cally greater than the changes with either of the other 2 doses.
patients were studied early in their hospital stay, mostwithin the first week after admission.
The mean serum phosphorus concentration for all group were also treated by increasing the phosphorus patients increased significantly at study days 2 and 3.
content of their nutrition support formulation on day 2.
Mean phosphorus values for all patients were 0.67 Ϯ In the mild group, 59% of patients had serum phospho- 0.19 mmol/L, 0.83 Ϯ 0.26 mmol/L, and 0.93 Ϯ 0.32 rus concentrations within the normal range on day 2, mmol/L for days 1, 2, and 3, respectively. When sepa- and 59% were normal on day 3. Fifty percent of the rated by dosing groups, the mild group experienced a moderate group had serum phosphorus concentrations slight increase in serum phosphorus concentrations within the normal range on day 2, which increased to from day 1 to 2, but the increase was not statistically 70% by day 3. Fifty-three percent of patients in the significant (Table II). In contrast, the graduated dosing severe group were within the normal range on day 2, algorithm produced a statistically significant increase and it increased to 60% on day 3. Phosphorus doses in serum phosphorus concentration from day 1 to 2 in were given as potassium phosphate in 42/79 (53%) both the moderate and severe hypophosphatemic patients, as sodium phosphate in 18/79 (23%) patients, groups (Table II). Serum phosphorus concentrations on and as a combination of the 2 salts in 19/79 (24%) day 3 were available in 77/79 patients. Both the mild patients. Mean doses of phosphorus on day 1 for the and moderate groups continued to increase from day 2 mild, moderate, and severe groups were 27.4 Ϯ 5.2 to 3, whereas the severe group decreased slightly. On mmol, 49.1 Ϯ 9.7 mmol, and 75 Ϯ 12 mmol, respec- day 3, serum phosphorus concentrations in the moder- ate and severe groups remained statistically increased Changes in serum concentrations of other electro- compared with day 1. All 3 groups had mean serum lytes between days 1 and day 2 are depicted in Table phosphorus concentrations within the normal range by III. Serum ionized calcium concentrations were avail- day 3. The change in serum phosphorus concentration able in 75 patients on day 1 and 76 patients on day 2.
from day 1 to day 2 in the respective dosing groups isdepicted in Figure 1. The change in the 1 mmol/kgdosing group was significantly greater than either of Mean (Ϯ SD) serum electrolyte concentrations for the mild, moderate, and severe hypophosphatemic groups for days 1 and 2* The number of patients who required an additional bolus on day 2 was 24 (71%), 24 (80%), and 11 (73%) for the mild, moderate, and severe groups, respectively.
Seventeen patients in the mild group, 12 patients in the moderate group, and 11 patients in the severe Mean serum phosphorus concentrations (mmol/L) by dosing group Creatinine 1 (micrommol/L) 70.7 Ϯ 17.7 70.7 Ϯ 17.7 79.6 Ϯ 17.7 *Divide serum magnesium, creatinine, and urea nitrogen concentra- *p Ͻ .05 compared to day 1; †p Ͻ .001 compared to day 1.
tions by 0.41, 88.4, and 0.36, respectively, to convert to mg/dL.
There was no statistically significant change in ionized phosphorus (as potassium phosphate) over 12 hours.25 calcium between days 1 and 2 in the study population All patients were Ͼ0.64 mmol/L by 48 hours; however, (p ϭ NS). Four of the 79 study patients (5%) became serum phosphorus concentrations were below the nor- hypocalcemic (ionized calcium Ͻ1.12 mmol/L), though mal range in 40% of patients. This study was the first none were symptomatic. These 4 patients all received to demonstrate the efficacy of a weight-based dosing the moderate dose of phosphorous for hypophos- regimen with a rapid rate of repletion.
phatemia. Serum potassium concentrations were clin- Two studies were later conducted to evaluate the ically unchanged in all 3 groups from day 1 to 2, as was effects of phosphorus doses as rapid infusions in criti- sodium, creatinine, and serum urea nitrogen. The cally ill patients.4,19 Both groups used doses of glucose- serum magnesium concentrations were clinically 1-phosphate over 30 or 60 minutes.4,19 These investi- unchanged in the mild- and moderate-dosed group. In gators documented a significant increase in myocardial the severe-hypophosphatemic group, the mean serum function and observed no adverse effects. It is impor- magnesium concentration increased from day 1 to 2, tant to note that the above 2 studies were not designed though the change was not statistically significant.
to show efficacy of replacement or safety, but rather the Patients with hypomagnesemia were treated with IV effects of phosphate repletion on myocardial function.
None of these patients were receiving nutrition sup- Over the 3 study days and 235 phosphorus values collected, only 8 serum phosphorus concentrations Our original study demonstrated safety and efficacy were above our normal range of 0.8 –1.44 mmol/L. Two using a graduated dosing algorithm of phosphorus patients in the severe group had serum phosphorus according to serum phosphorus concentrations and concentrations on day 2 of 1.57 and 1.63 mmol/L. The body weight in patients receiving specialized nutrition day 2 serum phosphorus concentrations had decreased support.22 Patients were enrolled into one of 3 groups: by day 3 to 0.74 and 0.96 mmol/L, respectively. These mild hypophosphatemia (0.73– 0.96 mmol/L), moderate data suggest that in patients requiring aggressive hypophosphatemia (0.51– 0.72 mmol/L), or severe treatment, mild hyperphosphatemia after this infusion hypophosphatemia (Յ0.5 mmol/L). Subjects were is not sustained. On day 3, 6 patients were above our dosed intravenously as follows: mild (0.16 mmol/kg), normal range. One patient had received only 1 dose moderate (0.32 mmol/kg), severe (0.64 mmol/kg).
(mild) on day 1 and continued to increase throughout Patients were followed for 2 days after the infusion and the study. Two of the other 5 patients had received rebolused as needed on day 2. Similar to the current aggressive doses on day 2 that were greater than the study, phosphorus was infused at a rate of 7.5 algorithm would have provided. The other 3 patients mmol/hour. After 24 hours, 81% of patients in the mild had received appropriate boluses of phosphorus on day group, 68% of the moderate group, and 21% of the 2. None of these patients were symptomatic or had any severe group had serum phosphorus concentrations complications as a result of their transient hyperphos- within the normal range. There were no significant changes in serum concentrations of total calcium, ureanitrogen, or creatinine. This study validated the use ofa graduated weight-based approach to phosphorus supplementation and documented the safety of using This is a follow-up to our previous study that dem- doses that were higher than those used in previous onstrated that phosphorus doses of 0.16, 0.32, and 0.64 mmol/kg resulted in increases in the serum phospho- Recently, a group of investigators studied the effects rus concentrations of 0.22, 0.26, and 0.32 mmol/L, of a more rapid repletion of phosphorus in 47 respectively.22 After we noticed a lack of effect with the medical/surgical ICU patients with moderate (Ͻ0.64 low dose (0.16 mmol/kg) from our original algorithm,22 mmol/L) to severe (Ͻ0.4 mmol/L) hypophosphatemia.26 this dose was abandoned. We then increased the doses Patients in the moderate group were randomized to 30 for phosphorus replacement given to each hypophos- mmol of IV phosphate over 2 or 4 hours, whereas phatemic group. The maximum dose of phosphorus of 1 patients in the severe group were randomized to 45 mmol/kg was decided upon according to earlier work mmol of phosphate over 3 or 6 hours (15 mmol/hour vs we published in thermally injured patients who had 7.5 mmol/hour). All patients received potassium phos- hypophosphatemia despite receiving approximately 1 phate. At the end of the infusion, 98% of the patients mmol/kg over a 24-hour period.14 Because our original had a phosphorus concentration Ͼ0.64 mmol/L. There dosing algorithm appeared in some book chapters and was, however, no statistical difference in end-of-infu- clinical guidelines, we felt obligated to study and report sion serum phosphorus concentrations between those the safety and efficacy of the new dosing regimen.
who received slow infusions vs faster infusions. All The use of larger doses of phosphorus in critically ill groups had serum phosphorus concentrations above patients has steadily evolved. Vannatta et al24 were their baseline at 24 hours, though no statistical signif- one of the first groups of investigators to document icance was reported. When compared with the slower aggressive phosphorus repletion. They administered 9 infusion groups, more patients in the rapid infusion mmol of potassium phosphate over 12 hours to 10 groups experienced hyperkalemia. In addition, urinary fractional excretion of phosphorus was increased in mmol/L). In a follow-up study by this same group in 10 those patients who received phosphorus more rapidly.
patients with serum phosphorus concentrations Ͻ0.32 These data suggest that giving doses of phosphorus mmol/L, patients were administered 0.32 mmol/kg of rapidly (15 mmol/hour) may exceed the renal threshold GRADUATED DOSING REGIMEN FOR PHOSPHORUS REPLACEMENT for this mineral, resulting in a higher percentage of the patients who had hypomagnesemia did receive IV mag- dose being lost in the urine. These data also suggest that the use of potassium phosphate should be For reasons that are not entirely clear to us, the restricted for patients with hypokalemia or a low-nor- results of the current study differ from those of our mal serum concentration of potassium.
previous study. The changes in serum phosphorus con- Taylor and colleagues27 published the results of a centration produced from the common doses (0.32 and weight-based phosphorus-dosing protocol in surgical 0.64 mmol/kg) were greater in the original study than intensive care patients. This protocol used a single we observed in the current protocol. This occurred dose of phosphorus in an attempt to alleviate the need despite our elimination of the low dose and escalation for repeated dosing as had been documented in most of all doses for the respective serum phosphorus con- previously conducted studies. Patients were divided centrations. We anticipated success of the high dose (1 into 3 dosing categories according to serum phosphorus mmol/L), but the ineffectiveness of the low dose (0.32 concentrations (Ͻ0.32 mmol/L, 0.32– 0.55 mmol/L, and mmol/kg) was unexpected. It is likely that the patient 0.56 – 0.7 mmol/L) and prescribed doses based on these acuity level of our ICU population was higher than the concentrations and body weight (40 – 60 kg, 61– 80 kg, original population studied in 1995. All patients in the and 81–120kg). All doses, ranging from 10 to 50 mmol, current study were trauma patients hospitalized in the were given over 6 hours. Any patient who did not have ICU, whereas the patient population in the original a 18- to 24-hour postrepletion phosphorus concentra- study included some patients in step-down beds. We tion Ͼ0.74 mmol/L or who required additional phos- also report a large number of patients with closed head phorus supplementation at any point during their ICU injuries in this current study. This may have affected stay, regardless of postrepletion concentration, was the overall success of the dosing algorithm as patients deemed a treatment failure. In the 111 patients stud-ied in the prospective arm, the success rates of this with traumatic brain injury are at increased risk of protocol were 78% in moderate hypophosphatemia (defined as 0.51– 0.7 mmol/L) and 63% in severe The only patients we used in this study were those in hypophosphatemia (defined as Յ0.5 mmol/L). These whom clinicians used the current dosing algorithm. We success rates are higher than those of previously feel that these patients more closely represent the reported studies. It is not clear why these results were types of patients encountered by most NSS and help to obtained in this surgical intensive care population. The validate the use of these doses in patients who are number of patients in this study who received nutrition receiving extra phosphorus as part of their nutrition support was not reported. The dosing scheme used in formulation. It is important to note that the majority of this protocol contained 9 different dosing categories, these patients were studied early in their nutrition making it more cumbersome than other previously course (many on the day of NSS consult), and the reported protocols. It is also unclear why the investi- amount of phosphorus received from the nutrition for- gators used 3 categories of serum concentrations for mulation was likely quite low. Because the amount of dosing and then reported results in just 2 categories nutrition received was generally very low, we did not that were different from the dosing groups. In addition, record caloric intake or percent of goal received at the Taylor and colleagues27 did not address patients with time of phosphorus dosing. Most of the patients in this serum phosphorus concentrations Ͼ0.7 mmol/L, citing study were receiving exclusively enteral nutrition. We these patients as being within their institution’s nor- believe this to be an accurate reflection of our practice, given our aggressive use of early enteral nutrition, With respect to electrolytes other than phosphorus, our dosing algorithm had minimal adverse effects.
Large phosphorus doses have been documented todecrease calcium concentrations28; however, in our study, mean ionized calcium concentrations wereunchanged between days 1 to 2. Most previous studies The results of this study verify the safety and effi- have used total calcium concentrations to assess cacy of a weight-based phosphorus dosing algorithm in safety. It is well known that total calcium concentra- patients receiving specialized nutrition support. This tions are not accurate measures of calcium balance in algorithm is more aggressive than other published dos- critically ill patients, even when adjusted for a ing regimens and uses a higher dose of phosphorus depressed serum albumin concentration.29 Despite than previously documented, without compromising 77% of subjects receiving some or all potassium phos- safety. Serum phosphorus concentrations increased phate, mean serum potassium concentrations were significantly in the moderate and severe groups after 1 unchanged in the mild group, slightly decreased in the dose. All groups had a mean serum phosphorus con- moderate group, and slightly increased in the severe centration within our institution’s normal range by day group. None of these changes were statistically signif- 3. No adverse events were encountered, and other icant and point to the difficulty in regulating potas- serum electrolytes were not negatively affected.
sium balance in this type of patient. Serum magnesium Although this study included only trauma patients, concentrations were statistically unaffected; however, this nomogram is currently used by our NSS for the the increase in serum magnesium concentrations was treatment of hypophosphatemia in a variety of criti- greatest in the severe hypophosphatemia group. Those phatemia on diaphragmatic contractility in patients acute respi-ratory failure. N Engl J Med. 1985;313:420 – 424.
1. Sacks GS, Walker J, Dickerson RN, Kudsk KA, Brown RO.
18. Venditti FJ, Marotta C, Panezai FR, Oldewurtel HA, Regan Observations of hypophosphatemia and its management in TJ. Hypophosphatemia and cardiac arrhythmias. Miner Electro- nutrition support. Nutr Clin Pract. 1994;9:105–108.
lyte Metab. 1987;13:19 –25.
2. Weinser RL, Bacon J, Butterworth CE. Central venous alimen- 19. Bollaert PE, Levy B, Nace L, Laterre PF, Larcan A. Hemody- tation: a prospective study of the frequency of metabolic abnor-malities among medical and surgical patients. JPEN J Parenter namic and metabolic effects of rapid correction of hypophos- Enteral Nutr. 1982;6:421– 425.
phatemia in patients with septic shock. Chest. 1995;107:1698 – 3. Halevy J, Bulvik S. Severe hypophosphatemia in hospitalized patients. Arch Intern Med. 1988;148:153–155.
20. Darsee JR, Nutter DO. Reversible severe congestive cardiomy- 4. Zazzo JF, Troche G, Ruel P, Maintenant J. High incidence of opathy in three cases of hypophosphatemia. Ann Intern Med. hypophosphatemia in surgical intensive care patients: efficacy of phosphorus therapy on myocardial function. Intensive Care Med. 21. Weinser RL, Krumdieck CL. Death resulting from overzealous total parenteral nutrition: the refeeding syndrome revisited.
5. Knochel JP. Hypophosphatemia in the alcoholic. Arch Intern Am J Clin Nutr. 1980;34:393–399.
22. Clark CL, Sacks GS, Dickerson RN, Kudsk KA, Brown RO.
6. Berner YN, Shike M. Consequences of phosphate imbalance.
Treatment of hypophosphatemia in patients receiving special- Annu Rev Nutr. 1988;8:121–148.
ized nutrition support using a graduated dosing scheme: results 7. Betro MG, Pain RW. Hypophosphatemia and hyperphos- from a prospective clinical trial. Crit Care Med. 1995;23:1504 – phatemia in a hospital population. BMJ. 1972;1:273–276.
8. Solomon SM, Kirby DF. The refeeding syndrome: a review.
23. Cockroft DW, Gault MH. Prediction of creatinine clearance from JPEN J Parenter Enteral Nutr. 1990;14:90 –97.
serum creatinine. Nephron. 1976;16:31– 41.
9. Lotz M, Zisman E, Bartter FC. Evidence for a phosphorus deple- 24. Vannatta JB, Whang R, Papper S. Efficacy of intravenous phos- tion syndrome in man. N Engl J Med. 1968;278:409 – 415.
phorus therapy in the severely hypophosphatemic patient. Arch Intern Med. 1981;141:885– 887.
hypophosphatemia associated with sucralfate in the intensive 25. Vannatta JB, Andress DL, Whang R, Papper S. High-dose intra- care unit. Nutr Clin Pract. 1991;6:199 –201.
venous phosphorus therapy for severe complicated hypophos- 11. Daily WH, Tonnesen AS, Allen SJ. Hypophosphatemia-inci- phatemia. South Med J. 1983;76:1424 –1426.
dence, etiology, and prevention in the trauma patient. Crit Care 26. Charron T, Bernard F, Skrobik Y, Simoneau N, Gagnon N, Leblanc M. Intravenous phosphate in the intensive care unit: 12. Polderman KH, Bloemers FW, Peerdeman SM, Girbes AR. Hypo- more aggressive repletion regimens for moderate and severe magnesemia and hypophosphatemia at admission in patients hypophosphatemia. Intensive Care Med. 2003;29:1273–1278.
with severe head injury. Crit Care Med. 2000;28:2022–2025.
27. Taylor BE, Huey WY, Buchman TG, Boyle WA, Coopersmith 13. Loven L, Larsson L, Norstrom H, Lennquist S. Serum phosphate CM. Treatment of hypophosphatemia using a protocol based on and 2,3-diphosphoglycerate in severely burned patients withphosphate supplementation. J Trauma. 1986;26:348 –352.
patient weight and serum phosphorus level in a surgical inten- 14. Dickerson RN, Gervasio JM, Sherman JJ, Kudsk KA, Hickerson sive care unit. J Am Coll Surg. 2004;198:198 –204.
WL, Brown RO. A comparison of renal phosphorus regulation in 28. Winter RJ, Harris CJ, Phillips LS. Diabetic ketoacidosis: induc- thermally injured and multiple trauma patients receiving spe- tion of hypocalcemia and hypomagnesemia by phosphate ther- cialized nutrition support. JPEN J Parenter Enteral Nutr. 2001; apy. Am J Med. 1979;67:897–900.
29. Dickerson RN, Alexander KH, Minard G, Croce MA, Brown RO.
15. Singhal PC, Kumar A, DesRoches L, Gibbons N, Mattana J.
Accuracy of methods to estimate ionized and corrected serum Prevalence and predictors of rhabdomyolysis in patients with calcium concentrations in critically ill multiple trauma patients hypophosphatemia. Am J Med. 1992;92:458 – 464.
receiving specialized nutrition support. JPEN J Parenter 16. DeFronzo RA, Lanf R. Hypophosphatemia and glucose intoler- Enteral Nutr. 2004;28:133–141.
ance: evidence for tissue insensitivity to insulin. N Engl J Med. 30. Kudsk KA, Croce MA, Fabian TC, et al. Enteral versus paren- teral feeding: effects on septic morbidity after blunt and pene- 17. Aubier M, Murciano D, Lecocguic Y, et al. Effect of hypophos- trating abdominal trauma. Ann Surg. 1992;215:503–511.



SAMANTHI Screening and Characterization of Nitroglycerin Degrading MicroorganismsPadmavathy S., Ananthi V., Praveen Raja P. and Asha Devi N. K. 1. Department of Zoology and Microbiology, Thiagarajar College (Autonomous), Madurai - 625009, Tamilnadu, India. 2. Pharma Division, Aurolab, Madurai, India. Abstract Biodegradation process is a novel and economically feasible one for the degr

Erklärung zum Datenschutz und zur absoluten Vertraulichkeit Ihrer Angaben bei mündlichen oder schriftlichen Interviews Die ForschungsWerk GmbH – Mitglied im Arbeitskreis Falls die um Teilnahme gebetene Person noch nicht 18 Deutscher Markt- und Sozialforschungsinstitute e.V. Jahre alt und zur Zeit kein Erwachsener anwesend ist: (ADM) – arbeitet nach den Vorschriften d

© 2010-2018 Modern Medicine