hypophosphataemia phosphorus requirements during · secondary to infection. on day 31 her serum...

Postgraduate Medical Journal (June 1977) 53, 289-297.

Hypophosphataemia and phosphorus requirements during intravenous nutrition

S. J. TOVEY* K. G. F. BENTONtM.B., B.S. M.B., B.S.

H. A. LEE.B.Sc., M.B., B.S., F.R.C.P.

*Chemical Pathology Department, Bristol Royal Infirmary, Bristol BS2 8HW,t Wessex Regional Renal Unit, St Mary's Hospital, Portsmouth, and

$Department of Nephrology, University of Southampton, and Wessex Regional Renal Unit, Portsmouth

SummarySeven patients with acute illnesses developed hypo-phosphataemia whilst receiving intravenous nutritionwhich included a fat emulsion, Intralipid, a possiblesource of phosphorus. The authors' observations castdoubt on the bio-availability of the phosphoruscontained in the phospholipid content of the fatemulsion. The currently recommended allowance ofphosphorus for this type of patient appears to be toolow and it is suggested that 0-5-0-75 mmol/kg body-weight be provided, preferably as a neutral phosphatesolution. Since hypophosphataemia can occur atvarious time intervals after starting intravenousnutrition and precede clinical sequelae it is recom-mended that routine serum phosphate measurementsare made in all patients receiving this treatment.

IntroductionHypophosphataemia complicating total intra-

venous nutrition has previously been observed(Travis et al., 1971; Silvis and Paragas, 1972;Woods and Alberti, 1972; Prins, Schrijner andStaghouwer, 1973; Betro and Pain, 1972; Sheldonand Gryzb, 1975). Most of the patients reported whodeveloped hypophosphataemia were receiving intra-venous nutritional regimes obviously deficient inphosphorus. The daily recommended requirementof phosphorus for adults is 0.15 mmol/kg body-weight and for infants, between 0.4 and 0-8 mmol/kg(Recommended Dietary Allowances, 1968). With theincreasing application of complete parenteralnutrition to critically ill patients, it becomes in-creasingly important to be aware of possiblecomplications. Often intravenous nutritional regimesappear to provide all the necessary elements and yetstill the deficiencies may occur. This raises thequestions as to whether such measurements re-present true deficiencies or an induced redistribution.If a redistribution-does this require any correction,and if so, when and by what means?

Reprint requests: Professor H. A. Lee, St Mary's Hospital,Portsmouth.

A series is now reported of patients in whomhypophosphataemia complicated intravenous nu-tritional regimes although the phosphorus intakeexceeded 0-15 mmol/kg/day. The importance ofhypophosphataemia is particularly related to itseffect on the red cell affinity for oxygen where itcauses a displacement of the oxygen dissociationcurve to the left. This means that, in critically illpatients where there may already be a tendency forperipheral anaerobic glycolysis, hypophosphataemiawill accentuate this by depletion of red cell 2,3-diphosphoglycerate (2,3-DPG). The relationship ofphosphorus depletion to oxygen transport hasrecently been reviewed by Sheldon and Gryzb(1975).

Case reportsCase 1A 19-year-old female, weight 65 kg, with a 2-year

history of Crohn's disease was admitted in oligaemicshock following 2 weeks of profuse diarrhoea. Onadmission her blood urea was 100 mmol/l. Treatmentwith intravenous dextrose and saline, gentamicin andfrusemide was given but her urine output fell below200 ml/day. On the fourth day of admission a legshunt for haemodialysis was inserted and intra-venous nutrition (amino acids (Vamin-Glucose),Intralipid and glucose-insulin) via a subclavianvein begun. Although 10 mmol of phosphorus perday were provided from Intralipid, hypophos-phataemia occurred 4 days later (Fig. 1). A chestX-ray showed right middle lobe pneumonia. Bloodgases whilst breathing air gave an arterial blood pHof 7-5 and a Po2 of 7 kPa (50 mmHg). A neutralphosphate solution (0-1 mol/l KH2PO4..Na2HPO4)providing 35 mmol of phosphorus was infused andthe serum inorganic phosphate rose to 0-84 mmol/l.However, 24 hr later (day 10) hypophosphataemia0-45 mmol/l recurred. Hypokalaemia was notassociated with hypophosphataemia in this patient.A further 75 mmol of phosphorus were given asneutral phosphate solution over the next 48 hr,

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during which time calcium gluconate had to begiven to control carpo-pedal spasm (serum calcium1-95 and magnesium 1-0 mmol/l). Insulin was addedto the i.v. regime from day 9 to 12 to control hyper-glycaemia. Hypophosphataemia recurred on day 16even though more than 15 mmol of phosphorus werebeing given per day as Intralipid phospholipid. Onday 22 a further 40 mmol of phosphorus as neutralphosphate solution was infused, when the serumphosphate rose to within the normal range. There-after there was a steady improvement in generalcondition and the patient was discharged on day 41.

Case 2A previously healthy female aged 34 years, weight

55 kg, developed intestinal ileus and pyrexia (41°C)after ovarian cystectomy and a cholecystectomy forchronic cholecystitis with cholelithiasis. On the fifthpostoperative day she was oliguric, collapsed anduraemic. Treatment with intravenous fluid, electro-lyte replacement and intravenous nutrition (aminoacids (Vamin-Glucose), Intralipid and glucose-insulin) was begun. Two days later even with aphosphorus intake of 18-5 mmol/day derived fromIntralipid phospholipids the serum inorganic phos-phate fell to 0-74 mmol/l (Fig. 2). Forty-eight hourslater when the mean phosphorus provision fromIntralipid phospholipid was 26-5 mmol/day theserum inorganic phosphate fell to 0-32 mmol/l.Insulin, 20-160 u./day, was added to the i.v. regime



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Hypophosphataemia and phosphorus requirements 291

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FIG. 2. Case 2, female aged 34 years. Hypophosphataemiadeveloped without concurrent phosphaturia, but was related toonset of intravenous nutrition. It was rapidly corrected by neutralphosphate infusion. Blood urea correction for nitrogen balanceaccording to Lee and Hartley (1975) formula. Nitrogen balanceimproved with additional nitrogen provision after day 21.

for control of hyperglycaemia. Marked respiratoryinsufficiency occurred owing to bilateral broncho-pneumonic change and even with 40% added oxygenthe arterial Po2 was 6-5 kPa. With intermittentpositive pressure ventilation the arterial pH was 7.55.Following 40 mmol of phosphorus intravenously asneutral phosphate solution the serum inorganicphosphate rose to 1-2 mmol/l (day 12). From day 6to 21 the mean insulin requirement was 100 u./dayto maintain normoglycaemia. On day 15 a furtherlaparotomy disclosed an acute pancreatitis. Follow-ing this operation there was a further slight fall inserum inorganic phosphate but the patient continued

to improve and with the recommencement of normaloral nutrition her serum inorganic phosphatereturned to the upper limits of normal. Whendischarged home on the thirty-third day she was 2 kgabove her pre-operative weight.

Case 3A 70-year-old female, weight 66 kg, with a history

of diverticulitis, was admitted with a 5-day historyof recurrent lower abdominal pain accompanied byvomiting and diarrhoea. An exacerbation of di-verticular disease was diagnosed and her subsequentmetabolic progress is shown in Fig. 3. Laparotomy 5



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FIG. 3. Case 3, female aged 70 years. Note in-appropriate delay in starting intravenous nutritionallowing appreciable cumulative negative nitrogenbalance to occur. Note considerable gastrointestinaltract losses of nitrogen, measured by micro-Kjeldahlmethod. From days 8 to 26 amino acid solutions usedwere aminosol 10% and amino-fructose-ethanol.Thereafter Vamin-Glucose was used. On two widelyseparated occasions hypokalaemia, hypophosphataemiaand alkalosis were associated. Blood urea correction fornitrogen balance as in Fig. 2.

days after admission revealed an infarcted rightcolon with small bowel infarction involving all but 35cm of the jejunum. Resection of most of the smallbowel together with a right hemi-colectomy wasundertaken. Septicaemia occurred 2 days post-operatively and a complete intravenous nutritionregime was begun 24 hr later. Hypophosphataemiaoccurred on days 11 and 26 with associated hypo-kalaemic metabolic alkalosis. On day 22 the patientdeveloped orthopnoea and generalized oedemawhich responded to intravenous frusemide. Thefollowing day she was found to have a hypokalaemicmetabolic alkalosis, arterial pH 7-53, Pco2 3-2 kPa,

Po2 7.2 kPa, standard bicarbonate 22-2 mmol/land a base deficit of 2-3 mmol/l. Two days laterwith a deterioration in her general condition aStreptococcus faecalis septicaemia complicating anintestinal fistula was diagnosed. Intravenous nu-trition was continued and resulted in a generalizedclinical improvement. Blood, total five units (pints),was transfused over the next 3 days to correctanaemia due to toxic suppression of the bonemarrow combined with an episode of haemolysissecondary to infection. On day 31 her serummagnesium was 0-78 mmol/l (normal range 0-65-1-10 mmol/l) and serum calcium was 2-26 mmol/l(normal range 2-1-2-7 mmol/l).

Case 4A 20-year-old female, weight 62-5 kg, was admitted

at 32 weeks' pregnancy with a 3-day history of severepersistent vomiting which had not responded toprochlorperazine or promethazine theoclate. Overthe first 2 days of admission she was given intra-venous saline and dextrose with potassium supple-mentation and a full intravenous nutritional regimebegun on the third day. This provided 9-4 g nitrogen(Vamin-Glucose) and 2400 kcal daily as 50%/ glucosewith 120 u. of soluble insulin added per litre.Although vomiting persisted there was a generalclinical improvement. On day 4 hypophosphataemia0-25 mmol/l occurred. Phosphorus 50 mmol, as aneutral phosphate solution was infused and thenutritional regime modified to provide a total of 14-1g nitrogen and 2600 kcal daily of which 2000 kcalwere derived from Intralipid. Even on the day whenthe phosphorus provision exceeded 1 mmol/kgbody-weight the hypophosphataemia was notcorrected. Over subsequent days when 0-24 mmol ofphosphorus/kg was provided hypophosphataemiacontinued for another 4 days. This patient's hypo-phosphataemia was not associated with hypo-kalaemia or alkalosis. On day 7 the patient developedhaematemesis and melaena complicated by a severeurinary tract infection. The latter was treated withantibiotics and an emergency oesophagoscopyrevealed extensive oesophageal ulceration andbleeding due to an hiatus hernia. On day 8 a livefemale infant weighing 2-26 kg was delivered byCaesarian section. On the second postoperative daythe patient developed hypernatraemia, hyper-chloraemia and hypokalaemia which were correctedby 6 1 of intravenous 5%/ dextrose and 200 mmol ofpotassium chloride.

Case 5A 28-year-old female, weight 47-8 kg, was admitted

with a 6-week history of vaginal bleeding. Examina-tion revealed an exophytic tumour of the cervixinvading the anterior vaginal vault and the uterine



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endometrium. There was no evidence of metastases.Radium was applied and 9 and 10 days later ir-radiation of 6000 rad was given to the pelvis. Fourmonths later her condition was good, weight 50-4 kg,but examination revealed a raised edge of a cervicalulcer. Another 6 weeks later she underwent aradical hysterectomy but 2 months afterwards shehad developed large vesico-vaginal and recto-vaginal fistulae with continual vaginal leakage.After 10 days, this emaciated, depressed andanorexic patient weighed 34 kg. A full intravenousnutritional programme was begun providing 2625kcal (975 as glucose and 1650 as fat emulsion) and14-1 g of nitrogen (Vamin-Glucose). All elements,trace elements and vitamins were provided inclusiveof phosphorus 0-66 mmol/kg body-weight derivedfrom Intralipid phospholipid. Her condition steadilyimproved on this regime and within 4 weeks sheweighed 39-5 kg. This patient developed markedhypophosphataemia on the second day of intra-venous nutrition in spite of provision of apparentlyadequate amounts of phosphorus. A further slighttendency towards hypophosphataemia occurred onthe fifteenth day of intravenous nutrition when thepatient had an intercurrent infection.

Case 6A 13-month-old male infant, weight 7-4 kg, was

admitted with a 1-month history of general malaiseand 7 days' diarrhoea. A feeding history suggested adiagnosis of rumination. Three days after admissionhis condition deteriorated and he developed septi-caemia secondary to urinary tract infection. Heresponded to vigorous therapy with intravenousfluids and antibiotics. Subsequent progress washampered by persistent rumination. Intravenousfeeding via a femoral vein was then started providing438 mg of nitrogen and 120 kcal/kg body-weightdaily. The phosphorus provision in this regime wasderived from Intralipid phospholipids yielding 0-4mmol/kg. Hypophosphataemia occurred on the fifthday of this regime. After 9 days of intravenousfeeding he developed a septicaemia from the i.v.feeding catheter which was then removed.

Case 7A 42-year-old male, weight 72 kg, was transferred

to this hospital with oliguric renal failure. Thirty-twodays earlier he had had an ante-colic Polya recon-struction for pre-pyloric ulceration. Previously therehad been a left nephrectomy for hypernephroma, butno evidence of metastases had been found. A smallbowel fistula developed 4 days after operation.Parenteral nutrition was begun on the seventh post-operative day and continued over the next 12 daysuntil transferred, providing 0 15 g nitrogen and 17-6kcal/kg body-weight daily. Phosphorus provision

over this time derived from Intralipid phospholipidand phosphorus contained in casein hydrolysate(Aminosol 10%) amounted to 0-14 mmol/kg.Serum phosphate was not checked during thisperiod. Hydration was good throughout but on day15 he became jaundiced and the blood urea waselevated. Closure of the fistula by local suturesfailed, and formal closure was undertaken on day 31.Oliguria had been noticed over the previous 2 daysand during the operation a short cardiac arrestoccurred. Assisted ventilation was required duringthe next 24 hr. The patient remained anuric and wastransferred on day 32 for haemodialysis. He wasnow seriously ill, pyrexial, deeply jaundiced andgrossly fluid overloaded. Cardiac output and peri-pheral perfusion were good with adequate spon-taneous respiration. The anterior abdominal wallwound was gaping and bile was draining via a drainin the superior subphrenic space. Blood-stained fluidwas still draining from the fistula area. On arrival,the blood urea was 33-7 mmol/l with a serum phos-phate of 2-14 mmol/l. He was immediately hae-modialysed and started on a complete intravenousnutrition regime which included albumin and humanplasma protein fraction. At this time the aminoacid solution used was Vamin-Glucose and provided0-15 g nitrogen and 53 kcal/kg. Although Intralipidphospholipids provided a phosphorus intake of 0-12mmol/kg, hypophosphataemia occurred after 3 days.The phosphorus intake was increased by the additionof neutral phosphate solution to 0.49 mmol/kg butsevere hypophosphataemia (0-14-0-18 mmol/l) re-curred. The patient died on day 40 from intra-abdominal sepsis and associated septicaemia.

TABLE 1. Phosphorus content ofUK intravenousnutrition solutions

ContentSource (mmol/l)Aminosol 10% 15Aminosol-glucose 6Aminosol-fructose-ethanol 6Travasol (Baxter) 15Freamine II (McGaw) 20Intralipid 10% and 20% (KabiVitrum) 15Neutral phosphate solution (Boots)* 100

* Provided as 500 ml Polyfusor packs whichcontain in addition to phosphorus, 162 mmolsodium/l and 19 mmol/l potassium.

DiscussionHypophosphataemia is associated with a decrease

in the erythrocyte glucose 6-phosphate, fructose6-phosphate, 3-phosphoglyceric acid, 2-phospho-glyceric acid, phosphoenolpyruvate, 2,3-DPG andadenosine triphosphate (ATP) with an increase intotal triophosphates (Travis et al., 1971). This



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altered metabolic environment of the erythrocyte isassociated with a displacement of the oxygendissociation curve to the left, i.e. an increasedaffinity of red cells for oxygen and consequentimpairment of tissue oxygenation (Sheldon andGryzb, 1975). This may be of particular significancein critically ill patients with compromised pulmonaryfunction and a low arterial oxygen tension, especiallyif there is an associated alkalosis. Impairment oftissue oxygenation is thought to be the cause of thecentral nervous system symptoms associated withhypophosphataemia (Prins et al., 1973; Ricour,Millot & Balsan, 1975), although the time course ofthe symptoms does not strictly correlate with therate of serum phosphate depletion or the duration ofintravenous nutrition.

It is generally agreed that phosphorus must begiven as an integral part of total parenteral nutritionand meet the minimal requirements quoted. It hasbeen shown in the rat that when inorganic phos-phorus and ATP depletion of the liver is induced byfructose infusion, incorporation of leucine into liverprotein synthesis is less than 10% of normal(Maenpaa, Rairo and Kekomaki, 1968). Thissuggests that phosphate depletion may have evenmore widespread implications, e.g. enzyme pro-duction and consequently impaired immunocom-petence. In support of this, acquired phagocytedysfunction has been reported as a complication ofhypophosphataemia in man (Craddock et al., 1974)and the treatment of hypophosphataemia whichdevelops during septicaemia in guinea-pigs results inan improved survival (Garner, Huebner and O'Dell,1967). Riedler and Scheitlin (1969) concluded Gram-negative septicaemia to be a common cause of hypo-phosphataemia and such a septicaemia was a featurein four of the present cases (Nos 2, 3, 6 and 7). Inother patients with septicaemia more recentlyobserved, however, Tovey (1976, unpublishedobservations) noted that hypophosphataemia pre-ceded all clinical signs of septicaemia and suggeststhat prophylactic replacement therapy with phos-phate solution may be of importance for preventionor management of septicaemia in man.There is also evidence that phosphate depletion

impairs intracellular glucose metabolism with aresultant increase in intracellular osmolarity asmeasured by increased red cell volume and in somecases associated with haemolytic anaemia (Jacob andAmsden, 1971). Paradoxically, the impairment ofglucose metabolism may have contributed in part tothe reports of an association of hypophosphataemiawith the use of insulin (Wright, 1973; Allison, 1976).The occurrence of hypophosphataemia when the

major source of intravenous energy has been derivedfrom carbohydrate, especially when concomitantinsulin is used, has been attributed to the phosphate

accompanying the entry of glucose into the cells andsubsequent phosphorylation processes. The presentobservations have confirmed an earlier report thatsuch depletion may occur when the major source ofenergy is a fat emulsion (Intralipid) even though thispreparation contains phosphorus as phospholipids(Baum and Aynsley-Green, 1975). With the adventof the modern crystalline amino acid solutions,many of which do not contain phosphate where thecasein hydrolysates do (Table 2) and where glucose/insulin regimes may be used for energy provision,then the risk of hypophosphataemia is considerable.Although hypokalaemia has often been associated

with hypophosphataemia this was not uniformlyseen in our patients. Like potassium and magnesium,phosphate is mainly an intracellular ion and factorscausing a shift of any one of these will affect theothers. When hypokalaemia accompanies hypo-phosphataemia it has been postulated that excessiveloss of phosphate via the urine is the result of thehypokalaemic effect on renal tubular function (Betroand Pain, 1972). This is unlikely, because when apatient becomes anabolic a considerable shift ofpotassium into the intracellular space will occur.At least 5-6 mmol of potassium are required for theeffective anabolism of each gramme of nitrogenprovided (Frost and Smith, 1953). Case 3 exemplifiesthe association of hypophosphataemia with hypo-kalaemic alkalosis. A shift of phosphates may occurinto red cells in association with a buffering ofextracellular alkalosis. This would not necessarilymilitate against a low red cell 2,3-DPG level,however, as high levels of intracellular phosphatemay also inhibit the normal metabolic pathways.

Patients in negative nitrogen balance followingstarvation or injury have increased urinary losses ofphosphate but maintain normal serum inorganicphosphate levels (Cuthbertson, 1932). Thus, pre-viously malnourished patients receiving intravenousnutrition are particular candidates for hypophos-phataemia. Since, as their metabolism is shiftedtowards anabolism with the formation of phos-phorylated intermediary compounds and the for-mation of ATP together with an overall increase incell protoplasm, extracellular phosphorus depletionwill become highlighted. In such cases the finding ofa low red cell phosphate may indicate a differentialshift of emphasis to anabolic processes for examplein muscle and hepatic cells (Miller et al., 1952) asopposed to erythrocytes which have a metabolismindependent of insulin.Two of the present patients developed hypo-

phosphataemia even though they had acute renalfailure and required haemodialysis. Previous reportshave shown that essential amino acid therapyreduces serum phosphorus levels in acute renalfailure (Abel, Abbott and Fischer, 1972) and in



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chronic renal failure (Heidland and Kult, 1975)by presumed incorporation of inorganic phosphorusinto intracellular protein synthesis. Coupled withthis it must be appreciated that dialysis losses (Fig. 1)will accentuate any tendency to a hypophosphatae-mia in such cases.

Possible sources of phosphorus for parenteralnutrition are protein hydrolysates, fat emulsionsand inorganic phosphate solutions. The amountsderived from these sources are shown in Table 2.Intravenous fat emulsions in the form of Intralipid(soya oil emulsion) 10% and 20% supply 15 mmolof phosphorus per litre and when 2 g of fat are givenper kg body-weight this will provide 0-3 and 0-15mmol/kg of phosphate respectively (Wretlind, 1974).The present authors' studies throw some doubt as tothe most useful source of phosphorus to use duringtotal parenteral nutrition. It has hitherto beenassumed that the phosphate content of proteinhydrolysates, e.g. Aminosol 10%, is readily meta-bolically available. It is perhaps interesting that inthe U.K., with the more recent shift of emphasistowards using synthetic crystalline amino acidpreparations, that hypophosphataemia is nowbecoming a problem. The observations here,together with a previous report (Baum and Aynsley-Green, 1975) cast doubt as to whether 'Intralipid'phospholipid phosphate is metabolically available.It would appear that an actual supplement of neutralphosphate should be included during an intravenousnutritional regime to prevent the occurrence ofhypophosphataemia. The time of onset of hypo-phosphataemia varies enormously, sometimes veryearly, other times after a considerable lag. As seenin Fig. 3 hypophosphataemia may recur even whenan earlier episode has been corrected. The timeduration effect may be related to the time taken tochange from a catabolic to an anabolic state. It mustbe emphasized there is no direct correlation betweenthe serum phosphate levels and the onset of symp-toms, particularly with respect to central nervoussystem symptoms. The recommended daily allow-ance of phosphorus of 0.15 mmol/kg may well beacceptable if phosphorus is provided as a neutralphosphate intravenous supplement and also toa patient who has not been severely catabolic. Itwould appear that the same may not be true for thetype of catabolic patients treated here and with thephosphate sources used.

Whilst it may be difficult to be dogmatic about theabsolute amounts of phosphate required duringintravenous regimes it it equally clear that carefulmonitoring of serum phosphate levels is mandatoryduring intravenous nutrition. Other studies havesuggested that the optimum daily intravenousnitrogen and energy intakes for adults are 0-22-0-24g and 45 kcal/kg body-weight (Hartley and Lee,

1976). Using the recommended daily allowance ofphosphorus of 0-15 mmol/kg, the nitrogen: phos-phorus and energy: phosphorus ratios would be1 46-1 6 and 300, respectively. The mean nitrogen :phosphorus and energy : phosphorus ratios obtainedin the patients reported here were 1-16 (range 0-22-1-84) and 174 (range 70-6-441). As a result of theseobservations, the authors recommend that 0-5-0-75mmol of phosphorus/kg body-weight be given toacutely ill adults. Based on the optimum nitrogenand energy requirements referred to above, thiswould provide nitrogen (0-22-0-24): phosphorus(0-5 mmol) ratios of 0-44-0-48 or nitrogen : phos-phorus (0-75 mmol) ratios of 0-29-0-32 and energy:phosphorus ratios of 90-60.For infants the suggested intravenous nitrogen,

energy and phosphorus intakes are 100 kcal, 0-4 gand 1-3 mmol/kg for 24 hr. Thus nitrogen: phos-phorus and energy : phosphorus ratios of 1-3 and 77respectively are recommended. Based on thesefigures sixty-three patients were treated with totalintravenous nutrition for periods varying between 20days and 9 months without hypophosphataemiaoccurring (Ricour et al., 1975).Although it must be assumed, in all the patients

with hypophosphataemia in this study, that aconsiderable store of phosphorus is contained inthe bone depots, it is equally clear that this is notreadily metabolically available. Carpo-pedal spasmoccurred in one of the cases treated with neutralphosphate infusion and this could be related to therate of administration. It is unlikely that the pro-vision of extra phosphorus of the levels suggested canlead to adverse metabolic complications providedone is aware of the implications with regard to cal-cium and magnesium homeostasis. However, it mustbe appreciated that the phosphate solutions normallyused contain additional potassium and sodiumdepending on their formulation (see Table 1).Despite the uncertainty as to the exact mechanismsinvolved in the hypophosphataemia which can occurwith intravenous nutrition, the authors feel there issufficient evidence that it should be avoided and thatthe use of Intralipid as a major energy source doesnot provide sufficient phosphorus for some patients.

AcknowledgmentsWe wish to express our thanks to the surgeons in the

Portsmouth and Bristol Groups of Hospitals who referredthe patients described for metabolic management.

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travenous essential L-amino acids and hypertonic dextrosein patients with acute renal failure. Effects on serumpotassium, phosphate and magnesium. American Journal ofSurgery, 123, 632.



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