Re: FW: Hospital chain, under scrutiny, reports rare illness

[Guest guest]

Thanks for your comments Pam,

I'll continue to look into kwashiokor, but edematous PCM doesn't need to be

tropical or infantile. Dietitians do need to step up with evidence regarding

what is and is not a nutritional problem.

The reason I mentioned the B1 is more to point out that malnutrition is due to a

variety of things (and that day the magazine seemed like a house call by a

friendly dietitian). Refeeding can make things worse - more sick to the stomach.

If giving 'protein and electrolytes' often increases mortality, then I wonder

what balance of electrolytes were given and how. Magnesium isn't even in the

IOM's " water and electrolytes " report. Just potassium and sodium.

I hope the doctor and hosptial chain aren't just billing more and doing the

standard care of practice. Edematous PCM is occurring in our hospitals and

nursing homes. I don't know the billing, coding permutations. $2700 extra

dollars for a Dx does seem ridiculous (50% more than $5300).

Nephrologists seem to know the most about hydration. I had already been doing a

variety of reading on this.

http://onlinelibrary.wiley.com/doi/10.1111/j.1525-139X.2010.00705.x/abstract

Effect

of Diabetes Mellitus on Protein–Energy Wasting and Protein Wasting in

End-Stage

Renal Disease, Nazanin Noori1, D. Kopple1,2Article first published online:

13 APR 2010DOI: 10.1111/j.1525-139X.2010.00705.x

http://www.ncbi.nlm.nih.gov/pubmed/19121473 Semin Nephrol. 2009

Jan;29(1):39-49.Causes and prevention of protein-energy wasting in chronic

kidney failure.Dukkipati R, Kopple JD.

Division of Nephrology and Hypertension, Los Angeles Biomedical Research

Institute at Harbor-UCLA Medical Center, Torrance, CA 90509, USA.

http://www.ncbi.nlm.nih.gov/pubmed/19121477

Semin Nephrol. 2009 Jan;29(1):75-84.Nutrition support for the chronically wasted

or acutely catabolic chronic kidney disease patient.Ikizler TA.Department of

Medicine, Division of Nephrology, Vanderbilt University School of Medicine,

Nashville, TN 37232-2372, USA. alp.ikizler@...

http://www.ncbi.nlm.nih.gov/pubmed/16129200

Am J Kidney Dis. 2005 Sep;46(3):387-405.Multinutrient oral supplements and tube

feeding in maintenance dialysis: a systematic review and meta-analysis.Stratton

RJ, Bircher G, Fouque D, Stenvinkel P, de Mutsert R, Engfer M, Elia M.Institute

of Human Nutrition, University of Southampton, UK. r.j.stratton@...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891019/?tool=pubmed

New Insights into the Role of Anabolic Interventions in Dialysis Patients with

Protein Energy Wasting

Jie Dong and T. Alp Ikizler1 Curr Opin Nephrol Hypertens. Curr Opin Nephrol

Hypertens. 2009 November; 18(6): 469–475.doi: 10.1097/MNH.0b013e328331489d.

" Economic Implications of Nutritional interventions

It is also important to assess the impact of nutritional supplements not only

in terms of changes in nutritional parameters, but to extrapolate these

observations to potential improvements in hospitalization, mortality, and

cost-effectiveness. In a recent study, Lacson et al showed that a hypothetical

increase in serum albumin concentration in the order of 2 g/L in 50% of the

United States dialysis population would be associated with projections of

approximately 1400 lives saved, approximately 6000 hospitalizations averted,

and approximately $36 million in Medicare cost savings resulting from a

reduction of approximately 20,000 hospital days over one year[68]. This is a

reasonable estimation since 2 g/L increase in serum albumin is the average

improvement reported in most nutritional intervention studies. "

***The above paper is suggesting that giving them growth hormones and other

anabolic steroids along with protein will help them to stop catabolizing. They

have had success with the strategy, but wouldn't magnesium plus protein be

cheaper than hormones and protein. One chart that I reviewed was for an anemic

woman who is getting erthropoetin hormone injections and CBC blood draws

biweekly to monthly. Her hemoglobin goes up temporarily and then falls again and

they repeat the expense and needle sticks. If she was nourished, then her bone

marrow might want to make blood cells spontaneously instead of by force. The

irony is that her body is being forced to produce a few extra blood cells and

then we take them out with a blood draw - net result - wasted money and further

depletion of her poor body stores.

The seniors and other catabolic patients aren't going to heal quickly if we

can't get their bodies to retain nutrients in their cells.

So lesson for me to take home if I want magnesium to get a fair hearing

eventually - get all odd references out of my bibliography and mainly use the

Pubmed type - Correct Pam?

http://asheducationbook.hematologylibrary.org/cgi/content/full/2010/1/271 Marrow

Responses to Aging and Inflammation,Anemia in Elderly Patients: An Emerging

Problem for the 21st Century, J. Vanasse1,2 and Berliner2 " It is

estimated that more than 3 million Americans aged 65 yearsand older are anemic.

Of the anemic patients, one-third wereidentified to have nutritional deficiency,

one-third were diagnosedon the basis of iron studies to have anemia of

inflammation,and one-third were diagnosed with " unexplained " anemia.3A

wideethnic disparity was also noted, with non-Hispanic blacks havinga rate of

anemia that was three times that of non-Hispanic whites;a finding that is

consistent with the results seen in otherstudies.4,5 " " Anemia and inflammation

are strongly associated with, and maycontribute to, the development of

" frailty, " a poorly definedsyndrome of the elderly population associated with

weight loss,impaired mobility, generalized weakness, and poor balance.24Some

studies have suggested that elevated proinflammatory markersare associated with

development of frailty.24 Furthermore, anemiais associated with an increase in

nearly all markers of frailtyin elderly populations, suggesting that there may

be a linkbetween the pathogenesis of the two syndromes.25 "

" Anemia of inflammation (AI) has historically been termed the " anemia of chronic

disease " and is most commonly seen in associationwith infection, rheumatologic

disorders, malignancy, and otherchronic illnesses. On a biochemical level, it is

classicallycharacterized by low serum iron and low iron binding capacityin the

setting of an elevated serum ferritin. Although the etiologyof classical AI has

been attributed to decreased red cell survival,disordered iron-limited

erythropoiesis, and progressive EPOresistance of erythroid progenitors, the

relative role and interplayof these three mechanisms in the development of

anemia remainunknown, as are the potential common pathways that may linkthem. "

" In phases 1 and2 of NHANES III, we examined the association between anemiaand

vitamin D levels in men and women older than age 60 years(n = 5100) and found

that vitamin D deficiency was associatedwith anemia independent of age, sex,

race/ethnicity, with theodds for anemia being increased approximately 60% in the

presenceof vitamin D deficiency (odds ratio [OR] 1.6; 95% CI [1.37;1.95];P <

..05). Using phase 2 data, we next examined the prevalenceof vitamin D deficiency

in anemia subtypes in men and womenolder than age 60 years (n = 2657) and found

that, among thosewith anemia, vitamin D deficiency was most prevalent among

thosewith AI. The risk of AI was significantly increased in vitaminD-deficient

versus nondeficient participants (OR 1.85; 95% CI[1.64;2.07]; P < .05). These

are the first population-basedstudies demonstrating an association between

vitamin D deficiencyand anemia, particularly AI, in an older adult cohort (T.

Perlsteinand G. Vanasse, manuscript submitted, 2010) and provide

compellingevidence that vitamin D deficiency may be a previously

unrecognizedcontributor to the development of anemia in relatively healthyolder

individuals and is particularly prevalent among thosewith AI. The potential

efficacy of vitamin D in amelioratinginflammatory anemia in elderly patients and

the physiologicmechanisms by which vitamin D may abrogate anemia remain tobe

studied. " (AI = anemia of inflammation)

**trust me - vitamin D not effective at reducing anemia - seen a number of

charts - 1000 IU to 4000 IU started a year ago - all still anemic if not worse.

R Vajda, R.D.

www.GingerJens.com

________________________________

To: rd-usa

Sent: Mon, February 21, 2011 11:35:08 AM

Subject: Re: FW: Hospital chain, under scrutiny, reports rare illness

,

With all due respect, one should not use Today's Dietitian as the

place to learn the latest science. The information published there is

not peer reviewed, nor is it systematic. It's what we call a

" journalistic review " . That's not a bad thing, I've written for them

myself, it's just that you should know the difference.

I know you like magnesium as the perpetrator for a number of health

conditions, based on your recent posts here. However, kwashiorkor is

not protein and electrolyte imbalance, at least not at the root cause.

In fact, in some research, when you give folks with (real) kwashiorkor

protein and electrolytes without considering co-morbid conditions, you

often end up increasing mortality, which we really don't want to do.

What's going on here is much more complex; it's a mix of facilities

trying to pull as much medicare money their way and RDs not stepping

up with evidence to show what is and what is not truly a nutrition

problem.

I'd urge you to search PubMed for some of the more recent papers on

kwashiorkor. Golden from the UK had published some that are

very readable. There are others in the tropical medicine journals that

also talk about some other purported etiologies for kwashiorkor.

Regards,

pam

Pam Charney, PhD, RD

Pamela Charney and Associates, LLC

consultants in nutrition informatics

Transforming Nutrition Care With Informatics

pcharney@...

http://www.linkedin.com/in/pamcharney

> Marasmus is starvation, kwashiorkor is protein starvation and

> electrolyte

> imbalance. A Today's Dietitian article a few months age directed me

> to B1 for

> refeeding anorexia - it worked - I was so disoriented, and my heart

> was fluttery

> and weird. The magazine had flipped open to that page and it was a

> life saver.

> When you are that underfed, there really is no appetite - zinc

> deficiency

> worsens appetite I believe. The magnesium deficiency adds to the

> edema problem

> that the lack of albumin causes. Loss of muscle tone, alopecia, and

> dermatologic

> symptoms would all relate to protein deficiency. Getting rehydrated

> was

> necessary before I could swallow much food. When one or two bites

> feels like

> sawdust it is easy to give up eating and not figure out how to start

> again.

> Rehydration requires magnesium as well as sodium and potassium. Many

> major

> electrolyte brands don't even have magnesium - it was regulated out

> sometime in

> the 20's - 30's.

>

> I think that that doctor and hospital system is recognizing the

> problem I've

> been working on - we can't heal and regenerate tissue if we don't

> have the

> nutrients. As for increased Medicare billing I hope the hospital/

> doctor is

> figuring out how to use that money to actually nourish the starving

> seniors and

> isn't just bonusing it out to executives.

>

> Kwashiorkor was more prevalent in starving children countries -

> edamatous belly

> - but I just saw that in my father-in-law. I couldn't find a formula

> that didn't

> have the high calcium level that throws off absorption. Our enteral

> feedings

> are not based on ratios that the chronically ill can absorb. The

> feeding made

> him worse, 40 pounds edamatous. So painfully swollen with water and

> skin

> integrity you could poke a fingernail through (it seemed). He is

> getting better

> finally.

>

> Providing " Health Shakes " and supplemental formulas that are high in

> calcium

> isn't helping. The problem is not that there is no protein in the

> diet or even

> in the body - the problem is keeping the protein in the cells and

> blood vessels

> where it can do some good. Magnesium is what is needed to prevent

> the leaky

> membranes and in the chronically ill calcium is being preferentially

> absorbed.

>

> I want to make sweet potato ginger smoothies boosted with garbanzo

> bean puree

> for everybody.

>

>http://www.nutritionmd.org/health_care_providers/general_nutrition/protein_maln\

utrition.html

>l

>

> Protein-Calorie Malnutrition: Overview and Treatment

> Protein-calorie malnutritionresults in 2 similar but distinct

> diseases, marasmus and kwashiorkor.

>

> Marasmus is defined simply as chronic deprivation of energy needed

> to maintain body weight. Its extreme form is characterized by severe

> weight loss and cachexia.1 Marasmus is further characterized by

> subnormal body temperature, decreased pulse and metabolic rate, loss

> of skin turgor, constipation, and starvation diarrhea, consisting of

> frequent, small, mucus-containing stools.2

> Kwashiorkor is a somewhat more complex disease. It is characterized

> by edema, low capillary-filtration rate, hypoalbuminemia, and

> dermatitis.

>

> Derived from an African term meaning " the disease that occurs when

> the next baby is born " , kwashiorkor was initially thought to result

> from a diet high in calories (mainly carbohydrates, such as maize),

> yet deficient in protein. However, infection, aflatoxin poisoning,

> and oxidative stress may also play causative roles.1,3 Edema, a

> defining

> characteristic of kwashiorkor, resolves with treatment, despite

> continuing hypoalbuminemia, suggesting that the edema is due to

> leaky cell membranes, low capillary filtration rates, high

> concentrations of free iron, and free radicals that increase capillary

> permeability.4 Kwashiorkor is further distinguished from marasmus by

> the following findings:

> * Massive edema of the hands and feet.

> * Profound irritability.

> * Anorexia.

> * Dermatologic symptoms (desquamative rash, hypopigmentation).

> * Alopecia or hair discoloration.

> * Fatty liver.

> * Loss of muscle tone.

> * Anemia and low blood concentrations of albumin, glucose, potassium,

> and magnesium.5,6

> Kwashiorkor may also involve severe, life-threatening hypophosphatemia

> (<1.0 mg/dL), which has been found to triple the mortality rate when

> compared with children who have normal phosphorus levels.7

> Treatment

> Individuals treated for protein-energy malnutrition are at risk for

> refeeding syndrome, in which hypophosphatemia, hypokalemia, and

> hypomagnesemia may lead to disturbances in the cardiac, neurologic,

> gastrointestinal, respiratory, hematologic, skeletal, and endocrine

> systems. Guidelines have been developed to help prevent these

> complications

> and to establish a transition to normalcy. Treatment consists of 2

> phases: stabilization and rehabilitation.

>

> The initial (stabilization) phase proceeds from days 1 through 7. It

> consists of treatment and prevention of hypoglycemia, hypothermia,

> dehydration, and infection; correction of electrolyte imbalance and

> micronutrient deficiencies; and a cautious feeding regimen.

>

> http://www.wrongdiagnosis.com/k/kwashiorkor/book-diseases-7a.htm

>

> Protein-calorie malnutrition: Excerpt from Professional Guide to

> Diseases

> (Eighth Edition)

> " Both kwashiorkor (edematous PCM) and marasmus (nonedematous PCM)

> are common in

> underdeveloped countries and in areas in which dietary amino acid

> content is

> insufficient to satisfy growth requirements. Kwashiorkor typically

> occurs at

> about age 1, after infants are weaned from breast milk to a protein-

> deficient

> diet of starchy gruels or sugar water, but it can develop at any

> time during

> the formative years. Marasmus affects infants ages 6 to 18 months as

> a result

> of breast-feeding failure, or a debilitating condition such as chronic

> diarrhea.

>

> In industrialized countries, PCM may occur secondary to chronic

> metabolic

> disease that decreases protein and calorie intake or absorption, or

> trauma that

> increases protein and calorie requirements. In the United States,

> PCM is

> estimated to occur to some extent in 50% of elderly people in

> nursing homes.

> Those who aren’t allowed anything by mouth for an extended period

> are at high

> risk of developing PCM. Conditions that increase protein-calorie

> requirements

> include severe burns and injuries, systemic infections, and cancer

> (accounts

> for the largest group of hospitalized patients with PCM). Conditions

> that cause

> defective utilization of nutrients include malabsorption syndrome,

> short-bowel syndrome, and Crohn’s disease.

>

> Read more at

>

http://www.wrongdiagnosis.com/k/kwashiorkor/book-diseases-7a.htm?ktrack=kcplink

>

> Signs and symptoms

> Children with chronic PCM are small for their chronological age and

> tend to be

> physically inactive, mentally apathetic, and susceptible to frequent

> infections. Anorexia and diarrhea are common.

>

> In acute PCM, children are small, gaunt, and emaciated, with no

> adipose tissue.

> Skin is dry and “baggy,†and hair is sparse and dull brown or

> reddish-yellow.

> Temperature is low; pulse rate and respirations are slowed. Such

> children are

> weak, irritable, and usually hungry, although they may have

> anorexia, with

> nausea and vomiting.

>

> Unlike marasmus, chronic kwashiorkor allows the patient to grow in

> height, but

> adipose tissue diminishes as fat metabolizes to meet energy demands.

> Edema

> often masks severe muscle wasting; dry, peeling skin and

> hepatomegaly are

> common. Patients with secondary PCM show signs similar to marasmus,

> primarily

> loss of adipose tissue and lean body mass, lethargy, and edema. Severe

> secondary PCM may cause loss of immunocompetence.

>

> Diagnosis

> CONFIRMING DIAGNOSIS Clinical appearance, dietary history, and

> anthropometry

> confirm PCM. If the patient doesn’t suffer from fluid retention,

> weight change

> over time is the best index of nutritional status.

>

> The following factors support the diagnosis:

> ①height and weight less than 80% of standard for the patient’s

> age and sex,

> and below-normal arm circumference and triceps skinfold

>

> â‘ serum albumin level less than 2.8 g/dl (normal: 3.3 to 4.3 g/dl)

> â‘ urinary creatinine (24-hour) level used to show lean body mass

> status by

> relating creatinine excretion to height and ideal body weight, to

> yield

> creatinine-height index.

>

> R Vajda, R.D.

> www.GingerJens.com

>

> ________________________________

>

> To: rd-usa ; dhcc@...

> Sent: Sun, February 20, 2011 8:50:58 PM

> Subject: FW: Hospital chain, under scrutiny, reports rare

> illness |

> Local News | PE.com | Southern California News | News for Inland

> Southern

> California

>

> This is a very interesting article. Aside from the fact that our tax

> $$ are

> now going to our neighbor to the North, what is the accurate

> definition of

> Kwashiorkor IYO? And how is it diagnosed?

>

> Digna

>

> Hospital chain, under scrutiny, reports rare illness |

> Local News |

> PE.com | Southern California News | News for Inland Southern

> California

>

> http://www.pe.com/localnews/stories/PE_News_Local_D_malnutrition20.27e2afa.h

> tml

>

>