Salah Gariballa

Dying trajectories in heart failure

Objectives: To explore dying trajectories in heart failure. Design: Prospective, longitudinal study. Setting: Sixteen GP surgeries in four demographically contrasting areas of the UK. Participants: A total of 27 heart failure patients, >60 years of age, who completed questionnaires for at least five time-points before death. Main outcome measures: Kansas City Cardiomyopathy Questionnaire Physical Limitation Scale. Results: No ‘typical’ dying trajectory could be identified, and only a minority of patients conformed to the theoretical trajectory of dying in heart failure. Conclusions: This study provides the first prospective data regarding physical decline prior to death in heart failure. Findings challenge current efforts to plan and deliver palliative care services on the basis of the theoretical heart failure dying trajectory.

Nutritional status of hospitalized acute stroke patients

The nutritional status of 201 hospitalized stroke patients was assessed from anthropometric, haematological and biochemical data in an observational prospective study. On admission, sixty-two (31%) stroke patients had BMI < 20, ninety-nine (49%) had a triceps skinfolds thickness below the 25th centile, twenty-five (12%) had a mid-arm circumference below the 25th centile and thirty-eight (19%) had a serum albumin concentration below 35 g/l. Baseline nutritional status was worse among those who later died or remained in hospital compared with those discharged and most patients who remained in hospital showed marked and significant deterioration in all measures of nutritional status within 4 weeks of hospitalization. After adjusting for age, stroke severity and co-morbidity, low serum albumin concentrations of these patients in hospital were a strong and independent predictor of death following acute stroke (odds ratio 1.13 (95% CI 1.01-1.27) for 1 g/l lower serum albumin concentration).

A Randomized, Controlled, Single-Blind Trial of Nutritional Supplementation After Acute Stroke

BACKGROUND Although stroke patients who do not have difficulty swallowing may be at risk of undernutrition and worsening nutritional status during hospitalization, optimum methods for nutrition intervention in stroke patients have not been established. AIM To examine the feasibility of enteral sip feeding as an effective nutrition intervention after acute stroke. METHODS Forty-two acute ischemic stroke inpatients with impaired nutritional status who did not have difficulty swallowing within 1 week after the stroke were entered into a single-blind, randomized, controlled, prospective study of enteral sip feeding. Twenty-one patients were randomized to receive daily oral food supplements for 4 weeks in addition to the hospital food, and 21 patients received only the hospital food for the same period. Main outcome measures were energy and protein intakes during the intervention period, change in nutritional status, disability, infective complications, length of stay, and mortality during hospitalization and at 3 months. RESULTS Two patients, one from each group, were lost to follow-up immediately after randomization. Twenty patients received oral nutritional supplementation. The energy intake was significantly greater in the supplemented group: 1807 +/- 318 vs 1084 +/- 343 kcal/d (mean +/- SD; p < .0001) (estimated treatment effect, 723 kcal/d; 95% confidence interval [CI], 498 to 947), as was protein intake: 65.1 +/- 13.8 vs 44.1 +/- 12.8 g/d (p < .001) (estimated treatment effect, 21.0 g/d; 95% CI, 11.7 to 30.3). There also were significant differences between the two groups in the changes in serum albumin and serum iron concentrations between randomization and at follow-up. There was a trend to lower mortality at 3 months in the supplemented group with two deaths (10%) compared with seven deaths (35%) in the control group (p = .127, relative risk, 0.29; 95% CI, 0.07 to 1.21). CONCLUSIONS This study suggests that enteral sip feeding is effective in improving nutritional intake and status in stroke patients who do not have swallowing difficulties. There also may be some beneficial effects on clinical outcome, but larger studies are required to confirm this observation and define more precisely the magnitude of any favorable effects.

Age as a determinant of nutritional status: a cross sectional study.

BackgroundUndenutrition is known to be prevalent and largely unrecognised in older patients; however, aberrations in indicators of nutritional status may simply reflect effects of age and/or functional disability.ObjectiveThe aim of this study was to measure the effect, if any of age on nutritional status in older patients.Design445 randomly selected hospitalised patients consented to nutritional status assessment derived from anthropometric, haematological, and biochemical data within 72 hours of admission. Nutritional status was compared between those age < 75 years and those aged 75 years or more. Using multiple regression models, we measured the association between age and nutritional assessment variables after adjusting for disability, chronic illness, medications, smoking and tissue inflammation.ResultsBody weight, body mass index, mid-upper arm circumference, haemoglobin, serum albumin and plasma ascorbic acid were all significantly lower in people aged ≥ 75 years compared with those < 75 years of age. Although riboflavin (vitamin B2), 25OH VitD3, red-cell folate and vitamin B12 concentrations were lower in those aged ≥ 75 years, differences were not statistically significant. After adjusting for disability and co-morbidity in a multivariate analysis, age alone had a significant and independent effect on important anthropometric and biochemical nutritional assessment variables.ConclusionIncreasing age is independently associated with poor nutritional status. This may partly explain the poor clinical outcome in older patients.

B-group vitamin supplementation mitigates oxidative damage after acute ischaemic stroke

Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately following acute stroke and that endogenous antioxidant defences are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated plasma tHcy (total homocysteine). In the present study, we assessed whether supplementary B-group vitamins during this critical period will enhance antioxidant capacity and mitigate oxidative damage. Forty-eight patients with acute ischaemic stroke within 12 h of symptom onset were assigned to receive daily oral supplements of B-group vitamins comprising 5 mg of folate, 5 mg of vitamin B2, 50 mg of vitamin B6 and 0.4 mg of vitamin B12 (n=24) or no supplements (n=24) for 14 days. The treatment group and controls were matched for stroke subtype and age. Blood samples were obtained before intervention and also at 7 and 14 days post-recruitment for measurement of the following biomarkers: red cell folate (whole blood folate corrected with haematocrit), erythrocyte glutathione reductase activity coefficient (EGRAC; measure of vitamin B2 status), plasma pyridoxal phosphate (vitamin B6 status), plasma vitamin B12, plasma alpha-tocopherol, plasma ascorbic acid, plasma TAOC (total antioxidant capacity), plasma MDA (malondialdehyde), plasma tHcy and CRP (C-reactive protein). Supplementation for 14 days with B-group vitamins significantly increased the plasma concentrations of pyridoxal phosphate and red blood cell folate and improved a measure of B2 status compared with the control group (P<0.05). Plasma tHcy decreased in both groups albeit less in the control group, but differences in cumulative changes were not significant. There was, however, a decrease in plasma MDA concentration in the treatment group, in contrast with the increase seen in the control group and these differences were significant (P=0.05). CRP concentration, a marker of tissue inflammation, was significantly lower in the treatment group compared with controls (P<0.05). In conclusion, B-group vitamin supplementation immediately post-infarct may have antioxidant and anti-inflammatory effects in stroke disease independent of a homocysteine-lowering effect.

Antioxidant supplementation with or without B-group vitamins after acute ischemic stroke: a randomized controlled trial.

BACKGROUND Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately after acute ischemic stroke and that endogenous antioxidant defenses are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated total plasma homocysteine (tHcy). METHODS To test whether supplementary antioxidants with or without B-group vitamins during this critical period enhance antioxidant capacity or mitigate oxidative damage, ninety-six acute ischemic stroke patients within 12 hours of symptom onset were randomly assigned to receive either daily oral 800 IU (727 mg) vitamin E and 500 mg vitamin C (n = 24), or B-group vitamins (5 mg folic acid, 5 mg vitamin B(2), 50 mg vitamin B(6), and 0.4 mg of vitamin B(12); n = 24), both vitamins together (n = 24), or no supplementation (n = 24) for 14 days. Treatment groups and controls were matched for stroke subtype and age. Blood was obtained before treatment, at day 7, and day 14 for measurements of plasma or blood vitamin status, plasma total antioxidant capacity (TAOC), malondialdehyde (MDA), tHcy and C-reactive protein (CRP). RESULTS Supplementation with antioxidant vitamins and B-group vitamins separately or together significantly increased the plasma concentration of vitamin C, E, pyridoxal phosphate (B(6) status), red blood cell folate, and improved a measure of B(2) status (red cell glutathione reductase activation coefficient [EGRAC]), compared with the control group. Plasma TAOC increased significantly in the antioxidant treatment groups compared with the nonsignificant decline seen in the control group. tHcy concentrations decreased in subjects who received B-group vitamins and the control group compared with the rise seen in those who received antioxidants alone. There was a significant reduction in plasma MDA concentration in the 3 treatment groups, in contrast to the increase seen in the control group; however, the changes were most evident in antioxidant groups. CRP concentrations (a marker of tissue inflammation) were significantly lower in the 3 treatment groups compared with the control group. There were no additive or synergistic effects of antioxidants and B-group vitamins together on any outcome measure. CONCLUSIONS Antioxidants supplementation with or without B-group vitamins enhances antioxidant capacity, mitigates oxidative damage, and may have an anti-inflammatory effect immediately postinfarct in stroke disease.

Recruiting older people into a large, community-based study of heart failure

This paper highlights some of the challenges encountered when recruiting older people with heart failure into longitudinal, community-based research. It draws on the experience gained in a study to provide insights into the palliative care needs of older people with heart failure and the timing and need for service interventions. Five hundred and forty-two people with heart failure (New York Heart Association (NYHA) stages II—IV) and 213 of their informal carers were recruited from primary care practices in four areas of the UK. Ethical issues arising around gate-keeping, terminology and participant burden are discussed along with challenges faced during the recruitment process. Strategies to increase general practitioner and patient recruitment are provided. The paper concludes that prospective longitudinal studies are of particular relevance to chronic illness, and the complexity of setting up such research must be acknowledged and appropriately resourced.

Dietary supplementation and quality of life of older patients: a randomized, double-blind, placebo-controlled trial.

OBJECTIVES: To test the effect of nutritional support on older patients quality of life.

Nutritional factors in stroke

Observational studies support the role of modifying lifestyle-related risk factors such as diet, physical activity and alcohol use in stroke prevention. For example, increased Na intake is associated with hypertension, and reduction in salt consumption may significantly lower blood pressure and may reduce stroke mortality. Moderately elevated homocysteine levels may be associated with stroke and are associated with deficiency of dietary intake of folate, vitamin B6 and vitamin B12. Consumption of a diet rich in fruits, vegetables, folate, K, Ca, Mg, dietary fibre, fish and milk may protect against stroke. Regular physical activity may also protect against stroke through its role in controlling various risk factors such as hypertension, diabetes mellitus and obesity. The role of fat intake as a risk factor for stroke remains uncertain, whereas the association between stroke and cholesterol has more convincingly been demonstrated by the recent intervention trials using statins. There is also evidence that a low serum albumin may be causally linked to stroke risk and outcome and that a significant number of stroke patients are undernourished on admission and their nutritional status deteriorates further whilst in hospital. Undernutrition is associated with increasing morbidity and mortality and nutritional supplements may have some beneficial effect on some outcome measures.

Refeeding syndrome: A potentially fatal condition but remains underdiagnosed and undertreated

OBJECTIVE To describe two cases of successfully prevented refeeding syndrome in a high-risk group of patients. METHODS Case 1 was a 70-y-old woman who presented with a 4-mo history of poor dietary intake and ill health due to a connective tissue disease leading to myositis and dysphagia and complicated by respiratory failure needing mechanical ventilation. Twelve hours after starting nasogastric tube feeding, she developed a cardiac arrest from which she was successfully resuscitated. Repeated attempts to wean her from the ventilator failed. Case 2 was a 15-y-old girl who was readmitted after a total colectomy for severe ulcerative colitis with diarrhea and vomiting leading to significant weight loss. Her body mass index was 11.4 kg/m(2). RESULTS In case 1, after consultation by the clinical nutrition team, the diagnosis of refeeding syndrome was made and the patient was duly started on a high-protein, high-fat, low-carbohydrate diet, multivitamin and trace-element supplements, and electrolyte infusion. Subsequently she was successfully weaned from the ventilator. In case 2, further investigation by the clinical nutrition team revealed low baseline electrolyte concentrations including potassium, magnesium, calcium, and phosphate and low serum albumin. Her low body mass index and baseline electrolyte concentrations put her at high risk of developing refeeding syndrome. She was initially started on low-calorie feeding, multivitamin and minerals, and her electrolytes were carefully monitored. She made a good recovery. CONCLUSION Refeeding syndrome is a life-threatening, underdiagnosed, treatable condition but there is a need for a wider awareness of the condition among health professionals.