guidelines for the integrated management of severe acute malnutrition

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ACF-In Guidelines for the integrated management of SAM In-patient: Complications 92 � Unconscious patients should also be given sugar-water by naso-gastric tube. They should then be given glucose as a single intravenous injection (approximately 5ml/kg of a sterile 10% glucose solution 147 ). � All malnourished patients with suspected hypoglycaemia should be treated with second-line antibiotics. � The response to treatment is dramatic and rapid. If a very lethargic or unconscious patient does not respond in this way, then there is another cause for the clinical condition that has to be found and treated (e.g. cerebral malaria, dehydration etc.) 10.Other conditions Children with many other underlying illnesses can first present with severe malnutrition. Initially, they should all be treated according to the standard protocol for severe malnutrition. Those that fail to respond to this treatment need further investigation for an underlying condition (see failure to respond to treatment). For HIV/Aids see separate section. 11.DRUGS Great care should be exercised in prescribing all drugs to severely malnourished patients. They have abnormal kidney and liver function, changed levels of the enzymes necessary to metabolise and excrete drugs, excess enterohepatic circulation (reabsorption) of drugs that are excreted in the bile, a decreased body fat which increases the effective concentration of fat soluble drugs (particularly in the brain) and, in kwashiorkor, there may be a defective blood-brain barrier. Those drugs which have been studied (see references) show abnormal pharmacodynamics and metabolism, as Buchanan says “they are even more vulnerable than an ill neonate” [84,85]. Very few drugs have had their pharmacokinetics, metabolism, side effects or major toxicity examined in severely malnourished patients. Drugs that have known side effects in normal children or adults should be used with great caution. Drugs which affect the central nervous system such as antiemetics, those that affect liver, pancreatic, renal, cardiac or intestinal function adversely and those which cause loss of appetite should not be used, or only used under very special circumstances [86,87]. It is strongly advised that either: � The malnutrition is treated first, before standard doses of drugs are given. Drugs used for HIV and TB 148 can damage the liver and pancreas. These diseases are not usually rapidly fatal (except military TB and TB meningitis) so treatment should normally be delayed for at least one week whilst the nutritional treatment returns the metabolism of the patient towards normal. � If it is critical that drugs that are given at the start of treatment for malnutrition have initially reduced doses where the pharmacokinetics are unknown. � Many drugs should be avoided altogether until there is research to show that they are safe and how the dosage should be adjusted for the malnourished state. Common drugs such as paracetamol do not work in most malnourished children during acute phase and can cause serious hepatic damage. � Drugs can usually be given in standard doses to patients that are in the later stages of treatment in OTP or have lesser degrees of malnutrition. 147 Do not use the concentrated glucose straight from a vial of 50% glucose – it is very hypertonic and will cause damage and clotting of the vein. 148 In particular isoniazid, but the other anti-TB drugs are toxic in the malnourished [33,88]
ACF-In Guidelines for the integrated management of SAM In-patient: Complications 93 12.Re-feeding syndrome A rapid increase in the intake of food given to malnourished patients is dangerous (either long standing malnutrition of those who have had minimal intake for more than five days). The patients can develop acute weakness, “floppiness”, lethargy, delirium, various neurological symptoms [89], acidosis[90] muscle necrosis, liver and pancreatic failure [91-93], cardiac failure and sudden unexpected death. - This condition is commonly termed “re-feeding syndrome”. There is an extensive literature on refeeding syndrome in adults and those receiving artificial feeding in developed countries (see references in [94-99]); the syndromes also occur in children [92,100-102]. Although this syndrome is usually unrecognised, even in those with full access to laboratory measurements, a full staff and close patient monitoring and doctors rarely recognise the syndrome or follow established guidelines [103]. The induction of this syndrome is clearly a danger for all those treating the severely malnourished child and clinical awareness is of paramount importance: all staff should be taught to look for and recognise re-feeding syndromes. The syndrome appears to be due to rapid consumption of key nutrients for the metabolism of protein, carbohydrate and lipid as well as the movement of electrolytes between the compartments of the body. There is frequently rapid reduction in plasma phosphorus, potassium and magnesium. Other problems during re-feeding include re-feeding-oedema 149 and re-feeding-diarrhoea (see separate section). - The most consistent finding is a rapid reduction in plasma phosphorus. Phosphorus levels are low in SAM children [104] and there is a close relationship between phosphate depletion and death [105,106]. The plasma phosphorus is also related to death during the initiation of treatment of HIV in adults [107]. The induced deficiency results in abnormal energy production in muscle [108] and liver [109]. Although there is adequate potassium and magnesium in F75, phosphorus is a limiting nutrient in F75 (all the phosphorus comes from the dried skimmed milk); thus, it is critical that excess F75 is not given to the children during the acute phase of treatment 150 . F100 and RUTF have adequate phosphorus to support catch-up growth 151 ; nevertheless, it is necessary at the start of treatment not to have a sudden jump from the malnourished state to an excess intake 152 . This is the purpose of the transition phase of treatment. - If there is deterioration during the recovery or transition phase of treatment then the child should be returned to the acute phase. - For patients that are in the acute phase the diet should be reduced to 50% of the recommended 149 The aetiology of re-feeding oedema is unknown; it is probably related to the sodium content of the recovery diets used. It should be noted that the biochemical lesions of kwashiorkor take at least two weeks to recover even if oedema resolved within a few days, so that excess Na intake during this time can lead to re-feeding-oedema. It appears not to carry the same poor prognosis as patients presenting with nutritional oedema. However, if it is common then the application of the protocol should be reviewed. The other patients being treated with the same regimen, who do not safely sequester the additional intake of sodium into oedema fluid and remain oedema-free, are at serious risk of heart failure. 150 The appropriate level and salt for phosphorus supplementation of F75 has not been determined. There is anecdotal evidence that choice of the wrong salt or dose could be detrimental [104]. 151 Alternative recipes that have reduced amounts of dried skimmed milk are potentially dangerous unless additional phosphorus is added. 152 Some protocols advocate sudden introduction of intakes as high as 200kcal/kg. It is possible that some of the deaths in OTP are due to caretakers forcing the full ration given in OTP to the malnourished children. Although it would complicate OTP management, it would be sensible to have an initial “transition phase” where the children in OTP were given not more than 130kcal/kg/d for the first one or two weeks of OTP treatment.
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Cover photography: © ACF, Anne-Dom
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guidelines for the integrated management of severe acute malnutrition

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