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Rapid Responses: Rapid Responses published:
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Hyponatremia and the "TUR" syndrome
- William H Konarzewski (24 March 2006)
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Hypothyroidism and hyponatraemia: an old wives' tale?
- Eric S. Kilpatrick (27 March 2006)
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Iatrogenic hyponatraemia- vital learning point
- jane e milton (27 March 2006)
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Hypernatraemic Dehydration in Children, management differs
- Jarlath McAloon (28 March 2006)
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Teaching Hyponatraemia
- Robert Lord (28 March 2006)
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Iatrogenic hyponatraemia
- John A W Wildsmith (28 March 2006)
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Hyponatreamia and drug use (and abuse)
- Gerard McDade (28 March 2006)
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Pseudohyponatraemia: Forgotten but not gone?
- William G Simpson, Patrick J. Twomey, and Utkarsh V. Kulkarni. (29 March 2006)
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Re: Iatrogenic hyponatraemia - 3 litres a day is not too much!
- William H Konarzewski (29 March 2006)
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There is some guidance
- Kolja Stille (31 March 2006)
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Treatment of Hypernatraemia
- Anthony O Oke (1 April 2006)
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Causes of Hyponatraemia
- Hannah L Delaney, Caje Moniz, Simon Harris (11 April 2006)
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Cerebral Salt Wasting Syndrome
- Martin M Tisdall, Martin Smith (12 April 2006)
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Dysnatraemia: Balance or Concentration?
- Eric J Will (28 April 2006)
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Disorders of Sodium "concentration"
- Gerardo O. Mogni (25 July 2006)
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Re: disorders of sodium concentration
- Richard G Fiddian-Green (26 July 2006)
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William H Konarzewski, Consultant Anaesthetist Colchester General Hospital, Colchester CO4 5JL
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I much enjoyed reading the article "Disorders of sodium balance" and found it particularly helpful that the authors have stated that acute onset hyponatremia should be rapidly corrected without fear of pontine complications. The article does not specifically mention the acute hyponatremia of "TUR" syndrome which is seen quite commonly in the course of transurethral resection of the prostate. The syndrome may present dramatically with pulmonary oedema, convulsions and, occasionally, cardiac arrest when the plasma sodium falls below 100 mmol/litre. It is, in my opinion, essential to correct the sodium urgently in such situations otherwise the patient may die. I personally give 200 ml of 8.4% sodium bicarbonate (ie 200 mmol of sodium) as soon as I have made the clinical diagnosis of "TUR" syndrome and taken a blood sample to confirm the sodium level. I then correct the sodium level to 120 mmol with further boluses of 8.4% sodium bicarbonate. Once the sodium level is above 120 mmol, there is little clinical urgency and the sodium level can be allowed to rise more slowly with the help of normal saline and furosemide 20 mg intravenously. I have treated 18 patients in this way without any deaths and without any evidence of brain damage. The transient metabolic alkalosis that accompanies this treatment does not appear to cause any problems to the patient. Competing interests: None declared |
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Eric S. Kilpatrick, Consultant in Chemical Pathology Hull Royal Infirmary, Hull, UK, HU3 2JZ
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Reynolds et al give an excellent description of the causes and latest opinions on the treatment of the poorly understood clinical conditions of hypo-and hypernatraemia.1 Their article will hopefully reduce the incidence of iatrogenic central pontine myelinolysis still commonly found due to over-aggressive treatment of hyponatraemia. Like many other sources, the authors include hypothyroidism as a secondary cause of hyponatraemia. However, the evidence supporting this association is extremely poor. Studies in babies with severe congenital hypothyroidism have found no change in serum sodium concentrations after treatment with levothyroxine.2 This has repeatedly been found to be the case in adults too.3,4 A study performed by our group found no difference in sodium concentrations between 999 patients newly diagnosed by their family doctor as having hypothyroidism and 4,875 controls with normal thyroid function.5 Indeed, none of the hypothyroid patients had a serum sodium concentration <120mmol/L at diagnosis, while this was present in 2 of the controls. Hypothyroidism is a common condition, and so is hyponatraemia in acutely unwell hospital admissions. However, when hyponatraemia and hypothyroidism are found to co-exist, the former is not necessarily a consequence of the latter and so other causes of low sodium concentrations should still be sought. Future guidelines could be helpful in clarifying the misconception of this association. 1. Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332:702-705. 2. Asami, T, Uchiyama, M. Sodium handling in congenitally hypothyroid neonates. Acta Paediatr 2004. 93:22-24 3. Croal BL, Blake AM, Johnston J, Glen AC, O’Reilly DS Absence of relation between hyponatraemia and hypothyroidism. Lancet. 1997 350:1402 4. Baajafer FS, Hammami MM, Mohamed GED Prevalence and severity of hyponatremia and hypercreatininaemia in short-term uncomplicated hypothyroidism. J Endocrinol Invest 1999 22:35-39 5. Warner MH, Holding, S, Kilpatrick ES. The effect of newly diagnosed hypothyroidism on serum sodium concentrations: a retrospective study. Clin Endo 2006 (online early doi:10.1111/j.1365-2265.2006.02489.x) Competing interests: None declared |
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jane e milton, psychiatrist in private practice 6 narcissus road, london NW6 1TH
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The article by Reynolds, Padfield and Seckl on Disorders of Sodium Balance fails to make a vital clinical learning point on iatrogenic hyponatraemia. In spite of the fact that their 4th 'Summary Point' on page 702 states 'The causes of sodium balance are often iatrogenic and therefore avoidable' this is not properly expanded upon in the text. This is unfortunate in an otherwise thorough and scholarly article, as there is an opportunity here to pre-empt the needless loss of a number of lives. As a number of the papers the authors refer to point out, hyponatraemia is a significant, probably greatly underreported cause of mortality in healthy older women undergoing elective surgery, where routine post operative fluid replacement is hypotonic. This appears to be due to an increased incidence of inappropriate antidiuretic hormone secretion in response to surgical stress in this group. The routine use of 5% dextrose or dextrose/saline rather than 0.9% saline in these patients (particularly when combined with poor serum electrolyte monitoring) is potentially lethal, but worryingly still often occurs. Competing interests: None declared |
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Jarlath McAloon, consultant paediatrician Antrim Hospital, 45 Bush Road, Antrim, BT41 2RL
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Reynolds and colleagues recommend rapid correction of plasma Sodium when hypernatraemia has developed acutely and the option of administering 5% Glucose intravenously (IV) or possibly water orally. The authors have introduced a paediatric link by correctly identifying infants as being a particular risk group for this problem but they have then either ignored or completely failed to recognise that their recommendation for treatment is the opposite to what is considered in current paediatric literature to be safest practice for management of hypernatraemic dehydration (1). In a paediatric patient with hypernatraemic dehydration, once shock if present is treated, the hypernatraemia would actually be corrected slowly and using 0.45% NaCl IV or a commercial oral rehydration solution if possible. Deliberately rapidly correcting hypernatraemia and using a sodium free glucose solution or water would be considered to be potentially dangerous practice, creating an increased risk for the development of cerebral oedema. This Journal should urgently take steps to ensure that the authors' recommendations do not lead to confusion in the paediatric management of this relatively uncommon but serious condition. (1) Haycock GB. Hypernatraemia: diagnosis and management. Arch Dis Child Educ Pract Ed 2006; 91 (1) ep8. Competing interests: None declared |
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Robert Lord, Consultant Chemical Pathologist Rotherham Hospital S60 2UD
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I thoroughly enjoyed reading the article on Disorders of sodium balance. Hyponatraemia is the commonest electrolyte abnormality encountered in hospital and so I make a special point in teaching medical students about it. It is good to point out at the start that they will encounter hyponatraemia as part of their job ie this is useful knowledge unlike most of what is crammed into their heads! So stress that hyponatraemia is common and that low sodium (and its treatment) may be dangerous - sodium and water go together, ie fluid shifts in and out of brain. I also stress at the outset that many causes are preventable and iatrogenic. I keep it as simple as possible (even though the theory may be wrong!) I tell them that it can all be remembered by the letter 'D'! I do a little experiment with one of the students as a 'volunteer'. Get them to put some salt in a cup. Add a little bit of water. Then get them to add some more water. What has happened to the sodium concentration. It has gone down! A useful illustration of DILUTION (The first D). I then give another student a bag of 5% dextrose and ask them what it contains. What does the body do with it? Takes the sugar. What's left? Water. So if you give just this post op then you will dilute the sodium - and the op will have increased ADH so making it difficult for the body to get rid of the water ie DEXTROSE (The second D). I then present really weird biochemistry which shows hyponatraemia due to a DRIP ARM SAMPLE (The third D) which is a useful point to emphasise the principle of 'if its a weird result, check'! I then pass round some medicine bottles containing pills (actually, vitamin tabs!) labeled with different drugs eg diuretics to get across that DRUGS must be checked thoroughly - I always run the list past Pharmacy Drugs Info (The fourth D). I then move on to look at fluid status - oeDema, volume Depletion, and SIADH (normovolaemic) - to include some more D's! I then put up a cartoon to show that they must DEMAND (another D) a urine sample to check urine osmo and sodium. I then go on to talk about interpretation of the urine osmo is on the basis of the plasma osmo ie is it appropriate (this is often the hardest part for students to get their heads round!). We go through a case of SIADH to illustrate this. Finally I mention that they must also check enDocrine causes (yet another D!) since cortisol and thyroxine required to excrete a water load ie check TSH, fT4 and cortisol (ideally with SST). Hopefully, they'll remember a bit of this at the bedside! Competing interests: None declared |
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John A W Wildsmith, Professor of Anaesthesia Ninewells Hospital, Dundee DD1 9SY
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I was pleased to see an article (Disorders of Sodium Balance) addressing an important, every day clinical problem, and including the clear statement that most cases of hyponatraemia are iatrogenic. However, I was disappointed that this statement was not followed by any real indication of the reasons for iatrogenic hyponatraemia: usually a combination of water overload and inadequate potassium replacement. Too many doctors believe that a 'normal 24 hour requirement' for water is 3 litres or more (I challenge anyone who thinks that this is correct to drink that much over 24 hours and experience the effect on urine output!) so they prescribe that volume to patients receiving iv fluids. If the iv fluid used is saline, volume overload can occur rapidly; if it is dextrose solution, the dextrose is metabolised leaving the water to dilute extracellular fluid. More importantly, this practice is often accompanied by a failure to provide adequate potassium replacement. The nephron is dedicated to the re -absorption of sodium, but only by exchange excretion of either potassium or hydrogen. The potassium is leached from intracellular fluid to be replaced by sodium to maintain the cation/anion balance. The hydrogen ions are generated by carbonic anhydrase, with the bicarbonate diffusing 'back' into the plasma. The overall result is a decrease in plasma sodium and an increase in plasma bicarbonate, with the treatment being proper replacement of potassium. Arguably, the real failure of the paper was to ignore (like too many clinicians) the basic physiology of water, sodium and potassium balance. These balances are very closely inter-related and should have been set out at the start of the review. Should they should be printed at the top of every fluid balance chart to remind prescribers of the relevant normal physiology? Competing interests: None declared |
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Gerard McDade, Consultant Psychiatrist Tameside General Hospital
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I enjoyed this review but was struck that no mention was made of the role of prescribed medication, particullarly under the mantle of 'iatrogenic causes', (and indeed illict drug use), despite the references to the former in the article, 1,2. A Large numbers of drugs are implicated in inappriate ADH secretion, including most of the Selective Serotonin Re-uptake Inhibitors (Prozac like drugs), which can present with life threatening seizures. It would have been usefull to gently remind a general readership of this, and the need to take a drug history. 1. Adrogué, HJ, Madias NE. Hyponatraemia. N Engl J Med 2000;342: 1581 -9. 2.Matthai SM, Davidson DC, Sills JA, Alexandrou D. Cerebral oedema after ingestion of MDMA ("ecstasy") and unrestricted intake of water. BMJ 1996;312:1359. Competing interests: None declared |
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William G Simpson, Consultant Chemical Pathologist Aberdeen Royal Infirmary, ABERDEEN, AB25 2ZD, Patrick J. Twomey, and Utkarsh V. Kulkarni.
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Reynolds et al provide a very useful overview of the causes and treatment of hypo-and hypernatraemia.1 However, the not uncommon artefactual causes of abnormal serum sodium levels might have had greater representation. In particular, the authors state: “Pseudohyponatraemia ... should no longer be seen with the measurement of sodium by ion specific electrodes” needs to be interpreted with caution. The authors dismiss pseudohyponatraemia, but in our view this remains an important cause of apparently abnormal levels. Whilst Ion Selective Electrodes (ISEs) are almost universal now, there are two types namely direct and indirect ISEs. The distinction is important as the indirect ISEs are affected by pseudohyponatraemia. In the latest round of the National External Quality Assurance Scheme (NEQAS), 534 (397 from UK labs) respondents employed indirect compared to only 31 (30 from UK) employing direct ISE measurement. (Source: Finlay MacKenzie, UKNEQAS, personal communication). With more than 90% of labs still potentially experiencing pseudohyponatraemia, we believe that this issue should not be forgotten! 1. Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332:702-705. Competing interests: None declared |
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William H Konarzewski, Consultant Anaesthetist Colchester General Hospital, Colchester CO4 5JL
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Professor John Wildsmith suggests that 3 litres of fluid a day is too high an intake and may lead to frequency of micturition. Whilst urine output certainly is commensurate with fluid ingestion, I would challenge the premise that a high (but not excessive) daily intake is likely to be harmful in any way for healthy adults with healthy kidneys. Most of us consume far more sodium than we need - government figures suggest that most adults consume about 10 grams a day, whilst our daily requirement is actually only about 0.5 grams a day. I am sure a high fluid intake helps flush out some of this surplus and harmful sodium. The risks of hyponatremia are low as the kidneys are very effective at retaining sodium. Of course, most of us who practice this simple form of "detox" have learned to ingest fluids early in the day rather than late at night. Competing interests: None declared |
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Kolja Stille, SHO Gen Med/Gastro Lister Hospital Stevenage, SG1 4TY
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Thank you for the well written and easily understandable review about dysnatraemias! Many junior doctors will benefit from this. I would like to add that there is some help available to estimate the correction of dysnatraemias by intravenous fluids. In 2000 HJ Androuge and NE Madias published their reviews about dysnatraemias in the NEJM (1,2). They included a formula to predict what effect a given intravenous solution will have on the serum-sodium level. The aim was to use this formula to avoid too rapid changes and therefore complications of sodium correction. In January 2006 G Liamis et al. published a paper where it was verified that this formula (Adrogue-Madias formula) is indeed useful in the real world and can fairly accurately predict the effect of intravenous fluids (though it tends to underestimate the result by a few milimol)(3). Care has to be taken to use an adequate total body weight. The formula was not very good to estimate sodium correction in patients with hypernatraemia, severe dehydration and marked renal impairment. (1) Androgue HJ, Madias NE. Hyponatremia. N Engl J Med 2000;342; 1581 -1589 (2) Androgue HJ, Madias NE. Hypernatremia. N Engl J Med 2000;342; 1493- 1499 (3) Liamis G et al. Therapeutic approach in patients with dysnatemias. Neprol Dial Transplant 2006; doi:10.1093/ndt/gfk090 Competing interests: None declared |
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Anthony O Oke, Consyltant Physician/Geriatrician Staffordshire General Hospital, Weston Road, Stafford. ST17 3SB
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When the duration of hypernatraemia is unknown, and the patient has only mild to moderate neurological symptoms but unable to drink, there is no justification for using hypotonic saline or any dextrose iv infusion. 0.9% (normal) saline would suffice. Its sodium concentration at 150mmols per litre, is still lower than the serum sodium concentration in such patients. As the vascular volume expands there would be gradual correction of intravascular and cellular osmolality, followed by renal sodium excretion One of the dangers of rapid intravascular osmolar dilution is the risk of developing cerebral oedema. In younger patients with bigger physiological reserve, this may not matter much. However, in older patients, rapid haemodilution is often followed by neurological deterioration. Thank you Competing interests: None declared |
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Hannah L Delaney, SpR Chemical Pathology King's College Hospital, London. SE5 9RS, Caje Moniz, Simon Harris
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Like some of your other correspondents, we enjoyed reading the article by Reynolds et al (1). However, we felt that their text-book presentation of the classification of hyponatraemia does not make for easy learning. As Robert Lord pointed out in his response, keeping it as simple as possible is key to remembering facts at the bedside. In addition, it is important to remember that common things happen commonly, a maxim we all need to reinforce in our teaching. In this respect, we felt the article failed to emphasise this point. In March this year, our department analysed 13,080 inpatient samples for sodium. Of these, the mean sodium was 137 mmol/L, with a standard deviation of 5 mmol/L. 24.4% were less than 135 mmol/L and 0.22% were less than 120 mmol/L. The commonest cause we see for sodium in the range 120- 135 mmol/L is fluid replacement therapy, which receives only a brief mention in Reynold et al’s article. Severe hyponatraemia (<120 mmol/L) is rare. Crook et al (2) have previously found that the commonest causes of severe hyponatraemia in hospital patients are chest infection, diuretics, cardiac failure, post- operative stress, carcinoma and selective serotonin re-uptake inhibitors. In our experience, the commonest cause of hyponatraemia in primary care patients is diuretics, though a few cases of Addison’s have been picked up from a low sodium result. As Reynolds et al (1) stated, hypernatraemia is seen less commonly than hyponatraemia; 3.8% of our sodiums analysed in March were greater than 145 mmol/L. In our experience, hypernatraemic patients are often on ITU and ventilated, with increased insensible losses. We would also like to point out that the Clinical Biochemistry Department is there to offer advice to hospital doctors and GP’s on the possible causes and appropriate laboratory investigation of hypo- and hypernatraemia, if required! 1.Reynolds RM, Padfield PM, Seckl JR. Disorders of sodium balance. BMJ 2006;332:702-705. 2.Crook MA, Velauthar U, Moran L, Griffiths W. Review of investigation and management of severe hyponatraemia in a hospital population. Ann Clin Biochem 1999;36:158-162. Competing interests: None declared |
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Martin M Tisdall, Clinical Research Fellow Neurocritical Care Unit, The National Hospital for Neurology and Neurosurgery, Queen Square, London, Martin Smith
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Reynolds et al.[1] make a useful contribution to the literature on sodium disturbances. However, they make scant mention of cerebral salt wasting syndrome (CSWS). Hyponatraemia occurs in 1-15% of hospital inpatients[2] but is most common in the inpatient neurological population[3], in whom a significant proportion of hyponatraemia is caused by CSWS. This is a poorly understood phenomenon thought to be caused by raised atrial and brain natriuretic peptide levels, and characterised by renal loss of sodium in the presence of intracranial disease, leading to hyponatraemia and hypovolaemia. CSWS is predominantly associated with subarachnoid haemorrhage but has also been described in conjunction with traumatic brain injury, glioma, and tuberculous or carcinomatous meningitis[4]. Reynolds et al. correctly state that plasma and urine osmolalities are rarely helpful in diagnosing the cause of hyponatraemia and that clinical examination is the key to diagnosis. However, in their assessment flowchart for hyponatraemia they erroneously state that, in the context of hypovolaemic hyponatraemia, urine sodium will be <30 mmol/l but may be >30 if intravenous saline has already been administered and associate a urine sodium>30 mmol/l with a euvolaemic state requiring treatment by fluid restriction. CSWS and syndrome of inappropriate antidiuretic hormone secretion are both associated with a high urine sodium[5], often greatly elevated above 30 mmol/l, but the treatment of these two conditions is diametrically opposed. It is not correct to say, as did the authors, that the treatment of asymptomatic hyponatraemia, even if chronic, is fluid restriction. If the diagnosis is CSWS, fluid restriction will worsen the hypovolaemic state and lead to serious complications. The treatment of CSWS is always fluid and sodium resuscitation using 0.9% saline in the first instance. We advocate an expectant and supportive management strategy in asymptomatic hyponatraemic patients, with treatment reserved for those developing symptoms. We have recently published simple algorithms to aid assessment[5] and would strongly counsel against a blanket policy of fluid restriction, even in chronic asymptomatic cases, stressing instead that treatment must always be guided by clinical examination of volaemic status. 1. Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ 2006;332(7543):702-5. 2. Fried LF, Palevsky PM. Hyponatremia and hypernatremia. Med Clin North Am 1997;81(3):585-609. 3. Reeder RF, Harbaugh RE. Administration of intravenous urea and normal saline for the treatment of hyponatremia in neurosurgical patients. J Neurosurg 1989;70(2):201-6. 4. Betjes MG. Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med 2002;13(1):9-14. 5. Tisdall M, Crocker M, Watkiss J, Smith M. Disturbances of sodium in critically ill neurologic patients: a clinical review. J Neuro Anesth 2006;18(1):57-63. Competing interests: None declared |
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Eric J Will, Consultant Nephrologist St James's University Hospital, Beckett Street, Leeds LS9 7TF
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It was interesting to see that none of your correspondents have commented on the shift in the use of the word 'Balance' in the recent article on Sodium abnormalities [1]. The authors apply the balance word to shifts in the concentration of plasma Sodium rather than relating it conventionally to total body Sodium, for which they harness 'Volaemia' of various degrees. Generations of medical students and trainees have confounded conventional sodium balance and sodium concentration, to the detriment of bedside clinical physiology and safe clinical management. The problem seems to develop from the occurrence of Hyponatraemia in Addison's Disease, where sodium wasting is also present. The fact that the Hyponatraemia may come from the secretion of vasopressin, responding to a hypovolaemic rather than an osmotic stimulus, is not widely enough considered. The Hyponatraemia is then easily attributed to sodium losses rather than dilution by retained water. The common disorders of Sodium Concentration (Balance?) are largely the result of disordered Water Balance, however that may have developed. Sodium (conventional) balance is manifest through blood pressure, weight and signs of the congested state, at whatever concentration of plasma Sodium that is determined by current water balance. The authors structure this usefully in Table form. If Balance is used for shifts in concentration, what term shall we use for the variation of total body Sodium, when concentration is not at all the issue? Nephrotic Syndrome comes to mind. Most nephrosis occurs with elevated total body sodium (positive conventional balance), normal plasma Sodium and little or no evidence of central volume disturbance, so that reliance on a derivative of volaemia to express Sodium status would be unhelpful. Was it the intention of the authors to reform the clinical vocabulary in this way? If so, they may create as much confusion as they aimed to dispel, with clinical physiology redefined without proper notice and some flaws. 1. Rebecca M Reynolds, Paul L Padfield, and Jonathan R Seckl Disorders of sodium balance BMJ 2006; 332: 702-705 Competing interests: None declared |
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Gerardo O. Mogni, staff physician nephrology division Hospital Posadas. B1685ABU El Palomar, Provincia de Buenos Aires, Argentina
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Being in agreement with your review about the importance of proper diagnosis and treatment of "dysnatremias" and far from criticizing a good job, I´d just like to suggest calling them what they are, that is disorders of "plasma sodium concentration" and not of "sodium balance". Everyone in the nephrology field knows that, but for general practitioners and students I think it would be better to use the proper name, mentioning that "the disorders of sodium concentration mostly reflect disorders in water balance". In that way it is easier to understand the pathophysiology and treatment. I know that I´m saying an obvious thing, but sometimes it is good to remember what we were taught. Sincerely yours.
Competing interests: None declared |
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Richard G Fiddian-Green, FRCS, FACS None
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"Dysnatremias" are "disorders of "plasma sodium concentration" and not of "sodium balance" and "disorders of sodium concentration mostly reflect disorders in water balance", writes Gerardo O. Mogni in his rapid response to this article (1). If the intercompartmental movement of sodium is accompanied by an osmotic equivalent of water then dysnatremias and disorders of water balance may both be disorders of pH balance which in turn may be a reflection of energy balance or Daniel Atkinson enrgy charge. An intracellular acidosis, which is commonly a reflection of anerobiosis, has as its dominant intracellular pH regulator the Na(+)/H(+) antiport which increases intracellular [Na+]..and its osmotic equivalent of water. This might be inhibited when the interstitial pH falls to abnormally low levels or perhaps more accurately when the interstitial pH falls below the intracellular pH. If so this is likely to be a largely passive process certainly in the short term (2) but clearly one that has an active component, one possibly (3) activated by the generation of cAMP (4). The generation of cAMP from ATP is increasingly unlikely to occur as the pH falls in accordances with the Daniel Atkinson energy charge hypothesis (5). The inference is that plasma [Na+], and the movement of its osmotic equvalent of water, is influenced by the energy charge, the pH, and the pH gradient between intraceullar and interstitial fluid. To determine the quantitative significance of these possibilities it would seem necessary to perturb normal balances by clamping plasma pH at different levels, possibly by means of the pH-stat technique (2), and inducing changes in the energy charge and Na(+)/H(+) antiport activity possibly with EGF. The notion that, "disorders of sodium concentration mostly reflect disorders in water balance" might be a gross oversimplification especially in pathologic circumstances in which an energy deficit is likely to be present. 2. Fiddian-Green RG, Silen W.Mechanisms of disposal of acid and alkali in rabbit duodenum. Am J Physiol. 1975 Dec;229(6):1641-8. 3. Nylander-Koski O, Mustonen H, Puolakkainen P, Kiviluoto T, Kivilaakso E. Epidermal Growth Factor Enhances Intracellular pH Regulation via Calcium Signaling in Acid-Exposed Primary Cultured Rabbit Gastric Epithelial Cells. Dig Dis Sci. 2006 Jul 11; 4. Chaturvedi D, Edwin F, Sun H, Patel TB. Analysis of EGF receptor interactions with the alpha subunit of the stimulatory GTP binding protein of adenylyl cyclase, Gs. Methods Mol Biol. 2006;327:49-59. 5. Hardie DG, Hawley SA. AMP-activated protein kinase: the energy charge hypothesis revisited. Bioessays. 2001 Dec;23(12):1112-9. 6. Noakes TD, Speedy DB. Case proven: exercise associated hyponatraemia is due to overdrinking. So why did it take 20 years before the original evidence was accepted? Br J Sports Med. 2006 Jul;40(7):567-72. unreversed ATP hydrolysis is neutralized in part by the Competing interests: None declared |
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