Severe Protein-calorie Malnutrition Research Articles

Enteral nutrition in intensive care patients: a practical approach.

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Gastric motility disorders: management that optimizes nutritional status.

Gastric motility disorders are relatively common, and treatment is often challenging. Various etiologies account for numerous clinical sequelae, with weight loss and severe protein-calorie malnutrition often seen in advanced stages of these disorders. In addition to gastrointestinal motor function, an appreciation of visceral sensation is essential to better understand the symptoms found in these patients, as well as possible therapeutic alternatives. This article provides an overview of gut motor and sensory function, techniques available for diagnosing motor disorders, and the principles of nutritional and medical management. Specific nutritional recommendations and a review of pharmacologic agents and novel treatment modalities are provided.

Severe protein-calorie malnutrition after bariatric procedures.

Serious nutritional complications after Roux-en-Y gastric bypass (RYGBP) are infrequent. In a retrospective study of patients operated during a 68-month period, malnutrition was investigated to analyze circumstances associated with nutritional failure. In 236 consecutive RYGBPs, 11 patients with severe malnutrition were identified (4.7%) with age 45.1 +/- 10.6 years (10 females/1 male) and initial BMI 54.6 +/- 8.4 kg/m(2). In these 11 patients, the derangement was diagnosed 17.9 +/- 15.8 months after RYGBP, following defined events in 63.6% (gastric stenosis, associated diseases ) or mostly exaggeration of expected symptoms in 36.4% (vomiting without endoscopic abnormalities). BMI then was 31.4 +/- 8.6 kg/m(2) (42.5 +/- 9.9% total reduction, or 2.4 +/- 2.1% decrease/month), and serum albumin and hemoglobin were 24.0 +/- 8.2 g/L and 97.0 +/- 23.0 g/L respectively. Edema was present in 45.4% (5/11), hospitalization was required in 54.5% (6/11), and 18.2% (2/11) eventually died. Serious malnutrition was unusual but not exceedingly rare in this series. Exogenous precipitating factors were clearly identified in 63.6% of the patients. Careful clinical and nutritional follow-up is recommended to prevent these uncommon but potentially dangerous complications.

Severe protein-calorie malnutrition after bariatric intervention

Severe protein-calorie malnutrition after bariatric intervention

Severe villus atrophy and chronic malabsorption induced by azathioprine

Azathioprine is commonly prescribed for autoimmune hepatitis and inflammatory bowel disease. An acute gastroenteritis-like syndrome has been ascribed to azathioprine use, but chronic diarrhea has not. We report a patient with autoimmune hepatitis who developed severe small-bowel villus atrophy and chronic diarrhea after azathioprine was initiated (50 mg/day). We present a case report of a patient followed up prospectively. Duodenal mucosal histology and expression of brush border enzyme dipeptidyl peptidase IV and peptide transporter PepT1 messenger RNA levels were determined before and after azathioprine discontinuation. Chronic diarrhea developed several weeks after the initiation of azathioprine and resulted in micronutrient depletion and severe protein-calorie malnutrition, which was unresponsive to oral pancreatic enzyme therapy or a gluten-free diet. Severe malabsorption required parenteral nutrition support for longer than 1.5 years; this was complicated by unstable blood glucose control, acute calculous cholecystitis, catheter sepsis, and severe venous thrombosis. When the temporal association between azathioprine and diarrhea was identified, the drug was tapered while the patient consumed an unrestricted diet. Within 2 weeks after azathioprine was discontinued, diarrhea had completely resolved, and parenteral nutrition was discontinued. Mucosal biopsies obtained before and 4 months after azathioprine discontinuation showed complete reversal of severe duodenal villus atrophy and marked up-regulation of mucosal dipeptidyl peptidase IV and PepT1 messenger RNA. The patient has subsequently maintained normal liver function tests on low-dose prednisone alone, with normal stools and stable nutritional status for longer than 4 years. Azathioprine can induce severe small-bowel villus atrophy, diarrhea, and malabsorption that is reversible with drug discontinuation.

Current nutrition in liver disease

Malnutrition is common in severe liver disease. Assessment of malnutrition usually requires a subjective global assessment of the patient with a few additional tests that often include handgrip strength and arm-muscle circumference. The severity of liver disease correlates well with the severity of malnutrition, which has prognostic value. Malnutrition is multifactorial, is difficult to correct, and occurs in liver disease independently of the etiology of hepatic injury. Patients who have severe protein-calorie malnutrition require diets with high calorie and protein intake, even in the presence of hepatic encephalopathy. Some forms of complementary and alternative medicine are frequently used in patients with advanced liver disease, but supporting scientific data is needed. Obesity is detrimental to patients with advanced liver disease and is of greater concern in liver transplant candidates because it increases transplant-related morbidity. Data detailing the effects of aggressive nutritional support before transplantation are scarce, and more studies are needed.

Severe protein calorie malnutrition as a late complication post bariatric surgery: a case report

Severe protein calorie malnutrition as a late complication post bariatric surgery: a case report

Plasma fatty acid status in Moroccan children: increased lipid peroxidation and impaired polyunsaturated fatty acid metabolism in protein-calorie malnutrition

In previous studies on plasma fatty acid and antioxidant status in 29 malnourished Moroccan children (12 with mild protein-calorie malnutrition, 17 with severe protein-calorie malnutrition) compared to 15 healthy control children from the same area, we pointed out that these populations were heterogeneous in terms of their essential fatty acid and antioxidant status. The aim of the present study was to classify the children using the Waterlow classification and their essential fatty acid status. The discrepancies in lipid parameters, nutritional and inflammatory markers, blood oxidative indexes, antioxidant micronutrients or trace elements (selenium, zinc, vitamin E) related to polyunsaturated fatty acids were checked in these populations. Eight of the control subjects and nine of the severe protein-calorie malnutrition children were essential fatty acid-deficient, compared to only one of the mild protein-calorie malnutrition group. Examination of the essential fatty acid-sufficient subjects with mild protein-calorie malnutrition, compared to the essential fatty acid-sufficient control subjects, showed only a decrease in Z scores and a non-significant decrease in selenium and vitamin E. In severely malnourished children, albumin, cholesterol and low density lipoprotein (LDL) cholesterol, plasma selenium, vitamin E and zinc were low, whereas inflammatory proteins and triglycerides were high. These features worsened with essential fatty acid deficiency. In all protein-calorie malnutrition subjects, there was oxidative stress (increase in thiobarbituric-acid reactants, imbalance between plasma polyunsaturated fatty acid, vitamin E and selenium levels), even in the absence of essential fatty acid deficiency. Monounsaturated fatty acids, oleic acid/stearic acid (C18:1 n-9/C18:0) Δ9 desaturase and n-3 and n-6 elongase activity indexes increased. The C18:1/C18:0 Δ9 desaturase activity index was negatively correlated to Z scores (r = –0.44, P < 0.01 for Z score weight, r = –0.39, P < 0.01 for Z score height), albumin (r = –0.82, P < 0.01) and zinc (r = –0.51, P < 0.01) levels. In essential fatty acid-deficient, severe protein-calorie malnutrition subjects, Δ6 desaturase activity was impaired, and there was a non-significant decrease in arachidonic acid. Essential fatty acid deficiency is a type of malnutrition, and is associated with an aggravation of all parameters in severe protein-calorie malnutrition. The increase in the C18:1/C18:0 Δ9 desaturase activity and enhanced lipid peroxidation without any essential fatty acid deficiency could be early markers of protein-calorie malnutrition.

Dendritic spine pathology in infants with severe protein-calorie malnutrition.

Experimental undernutrition in animals, during the critical brain development period, produces retardation of brain growth as well as a number of different morphologic and functional abnormalities in neurons, mainly in the dendritic synaptic apparatus. These alterations are the cause of the poor neurointegrative development that occurs in experimental malnutrition. Severe malnutrition during early postnatal life in humans is known to produce similar neurointegrative disorders as well as mental retardation, but there are very few studies describing the morphology of the dendritic apparatus in infants suffering from this condition. To study the dendritic spine density and morphology in dendrites from cortical neurons in infants dying from severe malnutrition. Brain sections from the somestesic, motor, and occipital cortical areas of 13 infants who died of severe malnutrition and 7 eutrophic infants who died of other causes were studied by means of the rapid Golgi method. Apical dendritic spines from neurons of the fifth cortical layer were studied and counted in all sections. Apical dendrites were significantly shorter in malnourished infants than in the control group (581.54 +/- 54.32 microm in severe malnutrition vs 846.3 microm in normal infants). The number of dendritic spines per dendrite was also significantly diminished (185.3 +/- 36.1 in malnourished vs 374.3 +/- 41.6 in eutrophic infants). There were marked morphologic abnormalities in the dendritic spines of infants dying of severe malnutrition that were classified as dysplastic. Short apical dendrites, fewer spines, and dendritic spine abnormalities occur in severe infant malnutrition. These anatomic anomalies might be related to the neuropsychological deficits that occur in these children.

Enteral nutrition in intensive care patients: a practicalapproach

Severe protein-calorie malnutrition is a major problem in many intensive care (ICU) patients, due to the increased catabolic state often associated with acute severe illness and the frequent presence of prior chronic wasting conditions. Nutritional support is thus an important part of these patient's management. Over the years, enteral nutrition (EN) has gained considerable popularity, due to its favorable effects on the digestive tract and its lower cost and rate of complications compared to parenteral nutrition. However, clinicians caring for ICU patients are often faced with contradictory data and difficult decision-making when having to determine the optimal timing and modalities of EN administration, estimation of patient requirements and choice of formulas. The purpose of this paper is to provide practical guidelines on these various aspects of enteral nutritional support, based on presently available evidence.

Importance of milk and diet on the ontogeny and adaptation of the intestine.

Importance of milk and diet on the ontogeny and adaptation of the intestine.

Effects of Recombinant Human Insulin‐like Growth Factor‐1 and Recombinant Human Growth Hormone on Anabolism and Immunity in Calorie‐Restricted Alcoholic Rats

Patients with severe alcoholic liver injury exhibit very low serum insulin-like growth factor-1 (IGF-1) concentrations, along with many of the symptoms that might occur with an IGF-1 deficiency state (including severe protein calorie malnutrition and immunosuppression). This study was performed to assess the effects of recombinant human (rh) IGF-1 and/or rh growth hormone (rhGH) on anabolism and immunity in the calorie-restricted, immunosuppressed alcoholic rat. Undernutrition was induced by calorie restriction such that each animal consumed 40% of ad libitum-fed controls. Alcohol was administered orally in the diet such that the mean daily intake was 9.4 g/kg/day. rhIGF-1 was administered by continuous subcutaneous infusion (380 micrograms/day) using a 14-day miniosmotic pump; rhGH was given by subcutaneous injections (400 micrograms/day). Matching placebo groups were also studied. On this regimen, ad libitum-fed controls were well nourished and increased body weight 34%, whereas Restricted controls lost 7.7% and Restricted alcohol-fed rats lost 15.2%. Significant but incomplete reversal of undernutrition was achieved with hormone therapy. Best improvement was obtained with combined therapy: rhIGF-1 + rhGH (p < 0.005; placebo versus active treatments). Immunologic impairment was observed to be severe in both thymus and spleen. The most severe changes were seen in thymi of the calorie-restricted, alcohol-fed rats, wherein 98% of the T lymphocytes were lost. rhIGF-1 treatment, but not rhGH, produced significant improvements in thymus. This was most pronounced in control rats (p < 0.005). Splenic T lymphocytes were less impaired and were more responsive to rhIGF-1 treatment; there was a maximum loss of 71% of T cells in Restricted, alcohol-fed rats. rhIGF-1 treatment completely restored splenic cellularity, as well as each of the T lymphocytes studied: CD5, CD4, and CD8. Functional status of splenic T lymphocytes was assessed by blast transformation after concanavalin A stimulation. Calorie restriction did not impair significantly this function in controls [Lieber-DeCarli control diet (LCD)]. However, it was significantly impaired in the Restricted, alcohol-fed rats (p = 0.003). In the presence of continued calorie restriction and alcohol, this function was not restored with either hormone (rhIGF-1 and/or rhGH). Their role in facilitating functional recovery after calories is restored, and alcohol is discontinued is under investigation.

Sister-chromatid exchange (SCE) and cell proliferation in lymphocytes from infected and non-infected children with severe protein calorie malnutrition (PCM)

The frequency of sister-chromatid exchanges (SCE) and the rate of cell proliferation were evaluated through differential staining of sister chromatids in mitogen-stimulated cultured lymphocytes sampled from five well-nourished children, from seven severely malnourished children infected with bacterium, and from 10 severely malnourished children following treatment for infection with antimicrobial drugs 2 weeks before blood sampling. The replication indices at 48 h of culture were higher in both groups of malnourished children than in the well-nourished children, indicating either a faster response to PHA and/or a shorter cell cycle in lymphocytes of these patients. The average frequency of SCE per mitosis was also significantly higher than in the control group. The mitotic index was similar in the three groups of children. The lack of significant difference in response between the two groups of malnourished children suggests that the effects observed at the cytogenetic level are caused by severe malnutrition per se, and not by any associated infection.

Nutrition and infection.

The papers presented at this session again emphasize the interactions between the nutritional status of the host and the occurrence and severity of infectious diseases. For many infections, malnourished subjects are more likely to develop severe clinical manifestations, are at greater risk of complications, and take much longer to recover than well-nourished persons. However, there are exceptions to the general rule that undernourished subjects are more susceptible to infections; malnourished subjects are more resistant to some viral and protozoan infections or they show less severe manifestations of disease. The effects of acute and chronic infections on the nutritional status of the host are also well-known. For example, an attack of measles is often the precipitating cause of acute manifestations of severe protein-calorie malnutrition in children who are marginally undernourished.

Interrelationship between protein-energy malnutrition and essential fatty acid deficiency in nursing infants

The influence of severe protein-calorie malnutrition on essential fatty acid (EFA) status was evaluated in nursing infants aged 2-5 mo. A control group of the same age and with normal weight-for-height was also selected for this study. The fatty acid pattern of total phospholipids from plasma and red blood cells (RBCs) was determined and then used as a biochemical variable for evaluating EFA status. A sharp fall in the relative percentage of n-6 (omega-6) fatty acids concomitant with an increase in the n-9 fatty acids in plasma and RBC phospholipids was observed. These results are consistent with the picture of EFA deficiency and showed that the deficiency state is well correlated with the severity of malnutrition. Calculation of the product-precursor ratio of polyunsaturated fatty acids derived from linoleic acid (18:2n-6) in RBC phospholipids provides evidence for an impairment in the elongation-desaturation pathway promoted by the protein-calorie malnutrition.

Inadequacy of Urinary Urea for the Estimation of Nitrogen Balance during Total Parenteral Nutrition

Measurement of urinary urea has been proposed as a convenient means to estimate urine nitrogen excretion, as the basis for prescription of amino acid nitrogen in parenteral feeds.l-? The validity of this procedure was investigated. Seven in-patients each with moderate to severe protein-calorie malnutrition (~80% ideal body weight and/or 0·3 giL protein. Plasma urea and C-reactive protein (CRP) were measured at 1-2 day intervals by the ophthaldehyde reaction, on a Parallel analyser (American Monitor, Burgess Hill, UK), and by end point immunonephelometry using a Hyland Laser Nephelometer PDQ (Travenol Laboratories, Norfolk, UK), respectively. The betweenbatch CV was < 5% in each case. If a rise in plasma urea occurred during the period of urine collection, the retained nitrogen was calculated and added to the estimates of total and urea nitrogen excretion.' The 24-hour urinary total and urea nitrogen excretions are shown in Table 1. They are closely correlated (Kendall's rank correlation coefficient = 0·80, P < 0,0001) and the mean fractional nitrogen excretion as urea is 0·79 (n = 49). The

Alveolar macrophage function in rats with severe protein calorie malnutrition. Arachidonic acid metabolism, cytokine release, and antimicrobial activity.

To investigate the effects of protein calorie malnutrition (PCM) on alveolar macrophage function, we measured antimicrobial activity, IL-1 and TNF production, and arachidonic acid metabolism in alveolar macrophages of infant rats with moderate and severe PCM. Groups of weanling male rats were fed a diet containing 0.8% protein (PCM) or 24% protein (control). A third group (pair fed) was fed limited amounts of the control diet that matched the mean daily dietary intake of the PCM group. After 4 wk on the diets, alveolar macrophages from all three groups functioned similarly with respect to surface adherence, phagocytosis and killing of Listeria monocytogenes, release of hydrogen peroxide and superoxide anion, and production of IL-1 and TNF. In contrast, Listeria-stimulated alveolar macrophages from the PCM group exhibited a marked shift in arachidonic acid metabolism, with impaired production of leukotriene B4 and enhanced release of thromboxane B2 and PGE2. The membrane arachidonic acid content and the uptake of [3H]arachidonate by alveolar macrophages did not differ among the three groups. The shift toward the cyclooxygenase pathway was not seen after 2 wk of dietary restriction and was reversed if PCM animals were fed the control diet for 1 wk. Thus, PCM does not affect the antimicrobial activity or cytokine production of alveolar macrophages, but causes alterations in arachidonic acid metabolism that may interfere with the modulatory functions of alveolar macrophages.

Sternal-Manubrial Separation as a Complication of Marrow Aspiration in a Patient with Protein-Calorie Malnutrition and Osteoporosis

A simple needle aspiration of marrow from the sternum was performed in a middle-aged woman with severe protein-calorie malnutrition and osteoporosis. Though carefully performed, a separation of the sternal-manubrial junction occurred with pain but no other serious sequelae. The subject of complications from marrow aspiration for diagnostic and therapeutic purposes is discussed.

Serum Cortisol Concentrations in Children with Protein-Energy Malnutrition

ABSTRACT We measured basal Cortisol levels in 15 children with kwashiorkor, 15 children with marasmic kwashiorkor, and 21 children with marasmus, before and after nutritional rehabilitation, as wel...

Abnormalities of blood selenium and glutathione peroxidase activity in patients with acquired immunodeficiency syndrome and aids-related complex

Severe protein-calorie malnutrition is common in patients with AIDS and could contribute to the progressive deterioration characteristic of that disease. Selenium deficiency could also have a negative impact on immune function and other organ functions vital for recovery from infectious diseases. Therefore, to assess any role for selenium in AIDS we determined plasma and erythrocyte selenium levels and glutathione peroxidase activity in 13 patients with AIDS compared to 8 patients with AIDS-related complex (ARC) and 14 healthy controls. Plasma selenium levels were significantly reduced in AIDS patients compared to controls (p less than .0001) and to ARC (p less than .02). Erythrocyte selenium levels in both AIDS and ARC were also reduced compared to controls (p less than .02), but not to each other. Glutathione peroxidase activity in AIDS was 28.9 +/- 1.4 U/g Hb vs 38.4 +/- 6.9 in ARC (p = NS) and 52.3 +/- 1.7 in controls (p less than .0001 vs AIDS; p less than .02 vs ARC). When all groups were combined, there were significant correlations between total lymphocyte count and both plasma selenium (r = .53; p less than .002) and erythrocyte glutathione peroxidase activity (r = .65; p less than .0001). In addition, strong correlations were noted between plasma selenium and serum albumin (r = .68; p less than .0001), plasma selenium and glutathione peroxidase (r = .77; p less than .0001), and glutathione peroxidase and hematocrit (r = .66; p less than .0001). In AIDS or ARC, no correlations between selenium with disease duration or weight loss were present. We conclude that, in comparison to normals, patients manifesting infection with human immunodeficiency virus have evidence of selenium deficiency as determined by diminished plasma and erythrocyte levels and glutathione peroxidase activity. These abnormalities are most marked in patients with AIDS, but are also present in patients with AIDS-related complex. Selenium deficiency has important implications for the progression and pathogenesis of clinical disease in AIDS.