Art & science | fluid intake
Recognising and managing acute hyponatraemia Matthew Keane discusses a condition often seen in recreational drug users in which excessive intake of water leads to dangerously low levels of serum sodium Correspondence matthew.keane@bartshealth. nhs.uk Matthew Keane is an emergency department staff nurse at the Royal London Hospital Date of submission November 17 2012 Date of acceptance November 21 2013 Peer review This article has been subject to double-blind review and has been checked using antiplagiarism software Author guidelines en.rcnpublishing.com
Abstract A significant amount of clinicians’ time is spent managing patients with complications arising from the use of sympatheticomimetic drugs such as cocaine and ecstasy, or MDMA. This article examines one of these complications, namely acute hyponatraemia, which can have life-threatening neurological consequences. Although there are few signs or symptoms of this condition, emergency clinicians should be able to recognise when it may have occurred, and should have a basic understanding of the role of sodium in autoregulation of cellular function, the different fluid compartments in the human body and the pathology of cerebral oedema. The article describes the importance of early recognition and swift treatment of acute hyponatraemia, as well as the methods for calculating fluid replacement to optimise chances of full recovery. Keywords Acute hyponatraemia, cerebral oedema, seizures IN 1995, the death of teenager Leah Betts due to hyponatraemia secondary to use of MDMA, or ecstasy, was widely reported in the UK media. At the inquest, Ms Betts was found to have taken MDMA before attending a nightclub, and had later consumed about 7L of fluid in 90 minutes. This indicates that she may have been overcompensating for perceived fluid losses, possibly in response to misguided advice from fellow clubbers. There was some uncertainty about the precise cause of Ms Betts’ death at the time and some initial reports in the media highlighted the importance of rehydration rather than stressing that water intoxication can compound the hyponatraemic effects of the drug (Laurance 1995).
32 February 2014 | Volume 21 | Number 9
The use of recreational drugs such as cocaine, amphetamines and MDMA is common among dancers in nightclubs, who often experience high body temperatures and loss of fluid from sweating, which in turn depletes sodium levels in their blood. In the author’s experience, there remains a misconception that water consumption mitigates, rather than exacerbates, the negative effects of sympatheticomimetic drugs. Such drugs can be sympatheticomimetic in that they mimic the actions of the sympathetic nervous system by stimulating the general adaptation system responsible for the fight-flight response (Marieb 1999). Other common effects include tachycardia, tachypnoea, euphoria and a feeling that the throat is dry, which stimulates the thirst centre (Blows 2001). This stimulation can prompt primary polydipsia, and the production of antidiuretic hormone secretion (ADH), referred to in some literature as vasopressin or argipressin (Despopoulos and Silbernagl 2003). An excess of water relative to the amount of sodium in the blood leads to electrolyte disturbance, the most common form of which is hyponatraemia, which is present in between 20% and 30% of all patients (Thompson and Crowley 2009). It should be noted that hyponatraemia can be caused by conditions other than excessive oral intake of water, including congestive cardiac, kidney or liver failure. Hyponatraemia is diagnosed by measuring the serum sodium level, which normally ranges between 135mmol/L and 145mmol/L. A serum sodium level of below 135mmol/L indicates hyponatraemia, while a level below 125mmol/L indicates severe hyponatraemia and, in 27% of cases, results in death (Hoorn et al 2006, Vaidya et al 2010). Emergency nurses and other healthcare professionals who manage patients with EMERGENCY NURSE
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hyponatraemia should know about its physiology, treatment and the risks involved in correcting electrolyte abnormality too rapidly (Verbalis et al 2007). This article therefore aims to increase nurses’ knowledge of hyponatraemia as a complication of recreational drug use and other conditions, and outlines the importance of sodium in homeostasis.
Fluid balance Between 50% and 60% of the human body is water, which means that the average adult male is made up of about 42L of fluid (Lamb et al 1991). This fluid is spread around different body compartments, and is broadly divided into extracellular (ECF) and intracellular (ICF) spaces (Beers et al 2006). The division of body water is shown in Figure 1. Antidiuretic hormone is secreted by the posterior pituitary gland and prompts the kidneys to retain fluid in response to low blood pressure (BP). It increases the permeability of the epithelium of the collecting ducts and distal tubules in the nephrons, which are contained in the kidneys (Marieb 1999) (Figure 2). As a result, when there is no ADH the collecting ducts are impermeable to water and urine is dilute, but when there is ADH they are permeable to water and urine is concentrated. Sodium, an essential electrolyte for controlling fluid balance, normally exists as a positively charged ion in solution. These sodium ions control the movement of fluid into the extracellular space, while potassium ions control such movement into the intracellular space, so any disturbance to the concentrations of sodium or potassium ions can affect haemodynamic stability significantly. Diet is the sole provider of sodium, which is excreted almost exclusively by the kidneys (Lamb et al 1991). The mechanism by which fluid is lost or reabsorbed by the body is controlled strictly by the release of ADH (Despopoulos and Silbernagl 2003). Figure 1 Division of body water Extracellular 14L 20% of body weight
Plasma 3L Interstitial fluid 11L
42L Intracellular 28L 40% of body weight
Intracellular fluid 28L
Total body water as a proportion of body weight: 60% in a male, 55% in a female EMERGENCY NURSE
Figure 2 Transport of compounds and ions through the tubule of a kidney Glomerular capsule
NaCl HCO 3
Blood
Distal tubule
Proximal tubule
Some drugs
Glucose and amino acids
H+
Loop of Henle Filtrate: Water (H2O), salt (NaCl), carbonate (HCO3-), hydrogen ion (H+), urea, glucose, amino acids and some drugs
Reabsorption: Active transport Passive transport Secretion Flow direction
NaCl
HCO3-
K+ and H+ some drugs Collecting duct H2O NaCl NaCl
H2O Urea H 2O
NaCl
Urine to bladder
(Adapted from Dirnberger 2009)
Secretion of ADH is central to the reninangiotensin system (RAS), which regulates the overall fluid status of the body by prompting the kidneys to reabsorb fluid when the body is dehydrated or to release fluid when the body is overhydrated (Marieb 1999) (Figure 3, page 34). The RAS also stimulates the thirst receptors and motivates people to drink, while osmoreceptors in the hypothalamus monitor fluid balance constantly (Schrier and Bansal 2008). Catecholemines, such as adrenaline and noradrenaline, also play their part in this system by increasing cardiac output and improving vascular tone to maintain adequate BP. The mechanism for increased fluid intake, which sometimes leads to water intoxication, is known as the syndrome of inappropriate ADH secretion (SIADH) (Decaux et al 2010), defined as excessive oral fluid intake to maintain the total body water and normovolaemia while diluting intravascular sodium levels (Beers et al 2006), for example to less than 135mmol/L. In response to the false stimulus that the body requires rehydration, the pituitary gland secretes ADH, which triggers the thirst response. February 2014 | Volume 21 | Number 9 33
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Art & science | fluid intake Figure 3 Regulation of aldosterone secretion along the renin-angiotensin system Dehydration, sodium deficiency or haemorrhage
Blood volume decreases
Blood pressure decreases
Baroreceptors detect drop in blood pressure and trigger production of antidiuretic hormone (ADH) and other endogenous hormones
ADH and other endogenous hormones stimulate the liver to produce angiotensinogen
ADH and other endogenous hormones stimulate the kidneys to increase production of renin
Renin converts angiotensinogen into angiotensin I
Angiotensin converting enzyme in the lungs turns angiotensin I into angiotensin II
Angiotensin II stimulates vasoconstriction of arterioles
Angiotensin II stimulates the adrenal cortex to increase production of aldosterone
Aldosterone stimulates reabsorption of sodium ions and water in the kidneys, and increased secretion of potassium and hydrogen ions from kidneys into the urine
Blood volume increases
Blood pressure increases
34 February 2014 | Volume 21 | Number 9
Serum osmolality, which refers to the distribution of solutes in fluid, governs whether fluid moves from the extra- to the intracellular space, or in the other direction. It is also a measure of cellular and blood vessel permeability, which is an important factor in fluid shifts.
Hyponatraemia The inappropriate movement of fluid can have several causes. Sepsis and hyperosmolar hyperglycaemic states (HHS), for example, can increase vascular permeability and thereby alter serum sodium level (Verbalis et al 2007), while steroid shock due to recent cessation of steroid therapy can cause hyponatraemia, and should be a differential diagnosis (Thompson and Crowley 2009). When all other potential causes of depleted serum sodium levels have been ruled out and the time of onset has been established, a clinical diagnosis of acute hyponatraemia can be made. It should be stressed that the condition is a symptom rather than a disease. There are four types of hyponatraemia, each linked to the loss of sodium from the body (Verbalis et al 2007) (Box 1). In recreational drug users, initial clinical presentation of hyponatraemia can be subtle. Confusion is common, although aggression, headache, muscle spasm and seizure can also be presenting complaints. These signs are often misdiagnosed as a consequence of drug intoxication alone and computed tomography (CT) of the head may be needed to reveal whether there is neurological impairment. Blood results should reveal whether serum sodium levels are low. For these reasons it is essential that practitioners address the underlying causes of hyponatraemia by obtaining clear patient histories, perhaps from those accompanying the patients. Such histories may be inconsistent, however, because most recreational drug users are unlikely to volunteer information that will implicate themselves or others in illegal activities. Management How emergency nurses manage the condition depends on its presenting signs and symptoms, and comorbidities. Although most patients with hyponatraemia are asymptomatic some have serious clinical presentations that require rapid intervention (Schrier and Bansal 2008). Emergency nurses should be able to differentiate acute hyponatraemia from chronic hyponatraemia, which Vaidya et al (2010) define as hyponatraemia that lasts for more than 48 hours. The body can compensate for chronic hyponatraemia, which is often caused by prescribed medications, so that there may be few clinical signs (Schrier and Bansal 2008). EMERGENCY NURSE
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Box 1 Common causes, signs and symptoms, and management of four types of hyponatraemia Type
Causes
Signs and symptoms
Management
Comments
Euvolaemic
Neurological insults, such as head trauma, brain lesions, meningitis or tumours, as well as a low-protein diet and excessive exercise, that deplete serum sodium levels without compromising haemodynamics
Decreased urine output, peripheral oedema
Diuretics and fluid restriction
Can be secondary to hyperglycaemia, particularly in recreational drug users or athletes who have compensated for loss of fluid
Hypovolaemic
Haemorrhage, sepsis, diarrhoeal disease, hyperosmolar hyperglycaemic states and iatrogenic causes, such as diuretic therapy
Tachycardia, hypotension, ketonurea
Isotonic saline to correct the fluid status
Symptomatic of an overall loss of fluid volume
Hypervolaemic
Congestive cardiac failure, nephrotic syndrome, acute or chronic renal failure and generalised oedema
Peripheral Diuretics and or pulmonary oedema fluid restriction
Symptomatic of excess overall fluid volume
Confusion, lethargy and seizures
Secondary to overheating
Inappropriate ADH secretion to aid water Syndrome of retention following inappropriate stimulation inappropriate antidiuretic hormone of the thirst centre of the brain (ADH) secretion
If symptomatic, hypertonic saline. If asymptomatic, fluid restriction
(Henry et al 1998, Fourlanos 2003, Verbalis et al 2007)
If the time of onset of hyponatraemia cannot be established, and the patients concerned are asymptomatic, practitioners should assume that the condition is chronic and treat the patients conservatively by restricting fluids (Schrier and Bansal 2008). This is because, if hypertonic saline is introduced, fluid shifts from the ICF to ECF, in some cases causing the neurones in the brain to shrink and demyelinate. Such overcorrection of hyponatraemia can lead to paralysis and sometimes death (Vaidya et al 2010).
Cerebral oedema The brain is made up of tissue, blood and cerebrospinal fluid, which fills the ventricles, and coats the brain and spinal column. The skull allows the volume of the brain to increase by up to 8% (Schrier and Bansal 2008), which means that an increase in the volume of one of the brain’s three components can result in a decrease in the volumes of one or both of the others until no further compensation is possible and the brain begins to compress (Figure 4). This process produces cerebral oedema, which, if allowed to continue, causes irreparable brain herniation leading to coma and death. Signs and symptoms Clinical signs of cerebral oedema in hypervolaemic hyponatraemia include headaches, confusion and lethargy. Patients with the condition may present with a laboured EMERGENCY NURSE
Cheyne-Stokes respiratory pattern and low oxygen saturations on room air. Seizures are common secondary to cerebral oedema (Ayus et al 2000), while ataxia and muscle cramps are common in less severe cases (Vaidya et al 2010). There is usually a decrease in consciousness in patients with severe hyponatraemia, who often tolerate airway adjuncts. Management The most widely used formula for calculating the incremental replacement of serum sodium is the Adrogué-Madias (Adrogué and Madias 2000) formula, in which the sodium deficit in litres is calculated by dividing the patient’s serum sodium Figure 4 Computed tomography scans showing a cerebral oedema
Compressed basilar cistern
Compressed lateral ventricles
Compressed suici
February 2014 | Volume 21 | Number 9 35
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Art & science | fluid intake concentration in mmol/L by the target concentration, namely 130mmol/L, and multiplying the result by the patient’s total body fluid volume, which is equivalent to 60% of body weight in men and 55% in women. For example, if a man weighing 70kg has a serum sodium volume of 120mmol/L, his sodium deficit is calculated by dividing 120 by 130 and multiplying the result by 60% of his weight, or 42kg, to produce 38.8. The man therefore requires 38.8L of saline to replace the salt he has lost. In such cases sodium should be replaced by continuous intravenous infusion of 3% saline, a hypertonic solution, in some cases following an initial bolus of 100ml (Hew-Butler et al 2005). To gauge the correct rate of infusion for optimal recovery, levels of urea and electrolytes in the blood, and sodium and potassium in the urine, must be monitored. Oral sodium intake with highly salted food should be encouraged and urea tablets can also be used to increase serum sodium levels (Vaidya et al 2010). Intravenous infusion of hypertonic saline raises serum sodium in the short term and encourages ICF and solutes, including sodium, back into the ECF. Administration of ADH-receptor antagonists (Decaux et al 2010), such as tolvaptan, inhibits the effects of ADH by blocking the V1 and V2 receptors in the renal tubules, and thereby increases excretion of excess electrolyte-free fluid and helps restore the natural electrolyte balance. This process is particularly useful in patients with SIADH secondary to drug use and hypervolaemic hyponatraemia. Primary nursing considerations include maintaining a strict fluid balance, regular urine osmolarity screening, and continued hypertonic fluid resuscitation over several days while the patients concerned occupy acute medical, high dependency or intensive care beds. They also include the use of a urethral catheter and urometer to measure fluid
balance, whereby the risks of urinary tract infections secondary to a catheter are mitigated by the short length of time such monitoring is required. The need for catheterisation can be reviewed when patients’ conditions have improved. Nurse managers should ensure that stocks of hypertonic saline are readily available in their clinical areas. Neurological observations and the Glasgow Coma Scale should be used regularly to monitor for variance of consciousness. Overall, patient management should involve the treatment of symptoms, close monitoring for signs of deterioration and escalation of treatment when appropriate. If CT scans indicate compression of the ventricles, a primary compensatory mechanism to raised intracranial pressure (Marieb 1999), cerebral oedema is confirmed.
Conclusion Acute hyponatraemia is a rare complication of sympatheticomimetic drug use but can have life‑threatening consequences, including cerebral herniation and death secondary to cerebral oedema. Care must be taken in the management of patients with the condition because overly aggressive sodium replacement therapy can cause diuresis and a net drop in the serum sodium secondary to hypovolaemic hyponatraemia. Evidence suggests that, in asymptomatic, haemodynamically stable patients, conservative management is preferable. In symptomatic patients with significant neurological deficits, electrolyte replacement should be calculated and titrated to therapeutic response with closely monitored electrolyte input and output. If sympatheticomimetic drug use grows, therefore, emergency department staff will have to deal robustly with the complications that arise.
Online archive For related information, visit our online archive and search using the keywords Conflict of interest None declared
References Adrogué HJ, Madias NE (2000) Hyponatremia. New England Journal of Medicine. 342, 21, 1581-1589.
Despopoulos A, Silbernagl S (2003) Color Atlas of Physiology. Fifth edition. Thieme Publications, New York NY.
Ayus J, Varon J, Arieff A (2000) Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Annals of Internal Medicine. 132, 9, 711-714.
Dirnberger J (2009) Physiology: Osmoregulation and Excretion. tinyurl.com/na3umjy (Last accessed: January 21 2012.)
Beers M, Porter R, Jones T et al (2006) The Merck Manual of Diagnosis and Therapy. Merck Research Laboratories, Whitehouse Station NJ.
Fourlanos S (2003) Managing drug-induced hyponatraemia in adults. Australian Prescriber. 26, 5, 114-117.
Blows WT (2001) The Biological Basis of Nursing: Clinical Observations. Routledge, Oxford.
Henry JA, Fallon JK, Kicman AT et al (1998) Low-dose MDMA (‘ecstasy’) induces vasopressin secretion. The Lancet. 351, 9118, 1784,
Decaux G, Andres C, Gankam Kengne F et al (2010) Treatment of euvolemic hyponatremia in the intensive care unit by urea. Critical Care. 14, 5, 184. doi: 10.1186/cc9292
Hew-Butler T, Almond C, Ayus J C et al (2005) Consensus statement of the 1st international exercise associated hyponatremia consensus development conference, Cape Town, South
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Africa. Clinical Journal of Sports Medicine. 15, 4, 208-213 Hoorn E, Lindemans J, Zietse R (2006) Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management. Nephrology Dialysis Transplant. 21, 1, 70-76. Lamb J, Ingram C, Johnston I et al (1991) Essentials of Physiology. Third edition. Blackwell Scientific Publications, London. Laurance J (1995) Leah Betts died of drinking water to counter drug’s effect. The Times. November 22. Marieb EN (1999) Essentials of Human Anatomy and Physiology. Sixth edition. Addison-Wesley, New York NY.
Schrier R, Bansal S (2008) Diagnosis and management of hyponatremia in acute illness. Current Opinions in Critical Care. 14, 6, 627-634. Thompson CJ, Crowley RK (2009) Hyponatraemia. Journal of the Royal College of Physicians Edinburgh. 39, 154-157. Vaidya C, Ho W, Freda B (2010) Management of hyponatremia: providing treatment and avoiding harm. Cleveland Clinic Journal of Medicine. 77, 10, 715-726. doi: 10.3949/ccjm.77a.08051 Verbalis J, Goldsmith S, Greenberg A (2007) Hyponatremia treatment guidelines 2007: expert panel recommendations. American Journal of Medicine. 120, 11, Supplement, 1-21.
EMERGENCY NURSE
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Recognising and managing acute hyponatraemia Matthew Keane discusses a condition often seen in recreational drug users in which excessive intake of water leads to dangerously low levels of serum sodium Correspondence matthew.keane@bartshealth. nhs.uk Matthew Keane is an emergency department staff nurse at the Royal London Hospital Date of submission November 17 2012 Date of acceptance November 21 2013 Peer review This article has been subject to double-blind review and has been checked using antiplagiarism software Author guidelines en.rcnpublishing.com
Abstract A significant amount of clinicians’ time is spent managing patients with complications arising from the use of sympatheticomimetic drugs such as cocaine and ecstasy, or MDMA. This article examines one of these complications, namely acute hyponatraemia, which can have life-threatening neurological consequences. Although there are few signs or symptoms of this condition, emergency clinicians should be able to recognise when it may have occurred, and should have a basic understanding of the role of sodium in autoregulation of cellular function, the different fluid compartments in the human body and the pathology of cerebral oedema. The article describes the importance of early recognition and swift treatment of acute hyponatraemia, as well as the methods for calculating fluid replacement to optimise chances of full recovery. Keywords Acute hyponatraemia, cerebral oedema, seizures IN 1995, the death of teenager Leah Betts due to hyponatraemia secondary to use of MDMA, or ecstasy, was widely reported in the UK media. At the inquest, Ms Betts was found to have taken MDMA before attending a nightclub, and had later consumed about 7L of fluid in 90 minutes. This indicates that she may have been overcompensating for perceived fluid losses, possibly in response to misguided advice from fellow clubbers. There was some uncertainty about the precise cause of Ms Betts’ death at the time and some initial reports in the media highlighted the importance of rehydration rather than stressing that water intoxication can compound the hyponatraemic effects of the drug (Laurance 1995).
32 February 2014 | Volume 21 | Number 9
The use of recreational drugs such as cocaine, amphetamines and MDMA is common among dancers in nightclubs, who often experience high body temperatures and loss of fluid from sweating, which in turn depletes sodium levels in their blood. In the author’s experience, there remains a misconception that water consumption mitigates, rather than exacerbates, the negative effects of sympatheticomimetic drugs. Such drugs can be sympatheticomimetic in that they mimic the actions of the sympathetic nervous system by stimulating the general adaptation system responsible for the fight-flight response (Marieb 1999). Other common effects include tachycardia, tachypnoea, euphoria and a feeling that the throat is dry, which stimulates the thirst centre (Blows 2001). This stimulation can prompt primary polydipsia, and the production of antidiuretic hormone secretion (ADH), referred to in some literature as vasopressin or argipressin (Despopoulos and Silbernagl 2003). An excess of water relative to the amount of sodium in the blood leads to electrolyte disturbance, the most common form of which is hyponatraemia, which is present in between 20% and 30% of all patients (Thompson and Crowley 2009). It should be noted that hyponatraemia can be caused by conditions other than excessive oral intake of water, including congestive cardiac, kidney or liver failure. Hyponatraemia is diagnosed by measuring the serum sodium level, which normally ranges between 135mmol/L and 145mmol/L. A serum sodium level of below 135mmol/L indicates hyponatraemia, while a level below 125mmol/L indicates severe hyponatraemia and, in 27% of cases, results in death (Hoorn et al 2006, Vaidya et al 2010). Emergency nurses and other healthcare professionals who manage patients with EMERGENCY NURSE
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hyponatraemia should know about its physiology, treatment and the risks involved in correcting electrolyte abnormality too rapidly (Verbalis et al 2007). This article therefore aims to increase nurses’ knowledge of hyponatraemia as a complication of recreational drug use and other conditions, and outlines the importance of sodium in homeostasis.
Fluid balance Between 50% and 60% of the human body is water, which means that the average adult male is made up of about 42L of fluid (Lamb et al 1991). This fluid is spread around different body compartments, and is broadly divided into extracellular (ECF) and intracellular (ICF) spaces (Beers et al 2006). The division of body water is shown in Figure 1. Antidiuretic hormone is secreted by the posterior pituitary gland and prompts the kidneys to retain fluid in response to low blood pressure (BP). It increases the permeability of the epithelium of the collecting ducts and distal tubules in the nephrons, which are contained in the kidneys (Marieb 1999) (Figure 2). As a result, when there is no ADH the collecting ducts are impermeable to water and urine is dilute, but when there is ADH they are permeable to water and urine is concentrated. Sodium, an essential electrolyte for controlling fluid balance, normally exists as a positively charged ion in solution. These sodium ions control the movement of fluid into the extracellular space, while potassium ions control such movement into the intracellular space, so any disturbance to the concentrations of sodium or potassium ions can affect haemodynamic stability significantly. Diet is the sole provider of sodium, which is excreted almost exclusively by the kidneys (Lamb et al 1991). The mechanism by which fluid is lost or reabsorbed by the body is controlled strictly by the release of ADH (Despopoulos and Silbernagl 2003). Figure 1 Division of body water Extracellular 14L 20% of body weight
Plasma 3L Interstitial fluid 11L
42L Intracellular 28L 40% of body weight
Intracellular fluid 28L
Total body water as a proportion of body weight: 60% in a male, 55% in a female EMERGENCY NURSE
Figure 2 Transport of compounds and ions through the tubule of a kidney Glomerular capsule
NaCl HCO 3
Blood
Distal tubule
Proximal tubule
Some drugs
Glucose and amino acids
H+
Loop of Henle Filtrate: Water (H2O), salt (NaCl), carbonate (HCO3-), hydrogen ion (H+), urea, glucose, amino acids and some drugs
Reabsorption: Active transport Passive transport Secretion Flow direction
NaCl
HCO3-
K+ and H+ some drugs Collecting duct H2O NaCl NaCl
H2O Urea H 2O
NaCl
Urine to bladder
(Adapted from Dirnberger 2009)
Secretion of ADH is central to the reninangiotensin system (RAS), which regulates the overall fluid status of the body by prompting the kidneys to reabsorb fluid when the body is dehydrated or to release fluid when the body is overhydrated (Marieb 1999) (Figure 3, page 34). The RAS also stimulates the thirst receptors and motivates people to drink, while osmoreceptors in the hypothalamus monitor fluid balance constantly (Schrier and Bansal 2008). Catecholemines, such as adrenaline and noradrenaline, also play their part in this system by increasing cardiac output and improving vascular tone to maintain adequate BP. The mechanism for increased fluid intake, which sometimes leads to water intoxication, is known as the syndrome of inappropriate ADH secretion (SIADH) (Decaux et al 2010), defined as excessive oral fluid intake to maintain the total body water and normovolaemia while diluting intravascular sodium levels (Beers et al 2006), for example to less than 135mmol/L. In response to the false stimulus that the body requires rehydration, the pituitary gland secretes ADH, which triggers the thirst response. February 2014 | Volume 21 | Number 9 33
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Art & science | fluid intake Figure 3 Regulation of aldosterone secretion along the renin-angiotensin system Dehydration, sodium deficiency or haemorrhage
Blood volume decreases
Blood pressure decreases
Baroreceptors detect drop in blood pressure and trigger production of antidiuretic hormone (ADH) and other endogenous hormones
ADH and other endogenous hormones stimulate the liver to produce angiotensinogen
ADH and other endogenous hormones stimulate the kidneys to increase production of renin
Renin converts angiotensinogen into angiotensin I
Angiotensin converting enzyme in the lungs turns angiotensin I into angiotensin II
Angiotensin II stimulates vasoconstriction of arterioles
Angiotensin II stimulates the adrenal cortex to increase production of aldosterone
Aldosterone stimulates reabsorption of sodium ions and water in the kidneys, and increased secretion of potassium and hydrogen ions from kidneys into the urine
Blood volume increases
Blood pressure increases
34 February 2014 | Volume 21 | Number 9
Serum osmolality, which refers to the distribution of solutes in fluid, governs whether fluid moves from the extra- to the intracellular space, or in the other direction. It is also a measure of cellular and blood vessel permeability, which is an important factor in fluid shifts.
Hyponatraemia The inappropriate movement of fluid can have several causes. Sepsis and hyperosmolar hyperglycaemic states (HHS), for example, can increase vascular permeability and thereby alter serum sodium level (Verbalis et al 2007), while steroid shock due to recent cessation of steroid therapy can cause hyponatraemia, and should be a differential diagnosis (Thompson and Crowley 2009). When all other potential causes of depleted serum sodium levels have been ruled out and the time of onset has been established, a clinical diagnosis of acute hyponatraemia can be made. It should be stressed that the condition is a symptom rather than a disease. There are four types of hyponatraemia, each linked to the loss of sodium from the body (Verbalis et al 2007) (Box 1). In recreational drug users, initial clinical presentation of hyponatraemia can be subtle. Confusion is common, although aggression, headache, muscle spasm and seizure can also be presenting complaints. These signs are often misdiagnosed as a consequence of drug intoxication alone and computed tomography (CT) of the head may be needed to reveal whether there is neurological impairment. Blood results should reveal whether serum sodium levels are low. For these reasons it is essential that practitioners address the underlying causes of hyponatraemia by obtaining clear patient histories, perhaps from those accompanying the patients. Such histories may be inconsistent, however, because most recreational drug users are unlikely to volunteer information that will implicate themselves or others in illegal activities. Management How emergency nurses manage the condition depends on its presenting signs and symptoms, and comorbidities. Although most patients with hyponatraemia are asymptomatic some have serious clinical presentations that require rapid intervention (Schrier and Bansal 2008). Emergency nurses should be able to differentiate acute hyponatraemia from chronic hyponatraemia, which Vaidya et al (2010) define as hyponatraemia that lasts for more than 48 hours. The body can compensate for chronic hyponatraemia, which is often caused by prescribed medications, so that there may be few clinical signs (Schrier and Bansal 2008). EMERGENCY NURSE
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Box 1 Common causes, signs and symptoms, and management of four types of hyponatraemia Type
Causes
Signs and symptoms
Management
Comments
Euvolaemic
Neurological insults, such as head trauma, brain lesions, meningitis or tumours, as well as a low-protein diet and excessive exercise, that deplete serum sodium levels without compromising haemodynamics
Decreased urine output, peripheral oedema
Diuretics and fluid restriction
Can be secondary to hyperglycaemia, particularly in recreational drug users or athletes who have compensated for loss of fluid
Hypovolaemic
Haemorrhage, sepsis, diarrhoeal disease, hyperosmolar hyperglycaemic states and iatrogenic causes, such as diuretic therapy
Tachycardia, hypotension, ketonurea
Isotonic saline to correct the fluid status
Symptomatic of an overall loss of fluid volume
Hypervolaemic
Congestive cardiac failure, nephrotic syndrome, acute or chronic renal failure and generalised oedema
Peripheral Diuretics and or pulmonary oedema fluid restriction
Symptomatic of excess overall fluid volume
Confusion, lethargy and seizures
Secondary to overheating
Inappropriate ADH secretion to aid water Syndrome of retention following inappropriate stimulation inappropriate antidiuretic hormone of the thirst centre of the brain (ADH) secretion
If symptomatic, hypertonic saline. If asymptomatic, fluid restriction
(Henry et al 1998, Fourlanos 2003, Verbalis et al 2007)
If the time of onset of hyponatraemia cannot be established, and the patients concerned are asymptomatic, practitioners should assume that the condition is chronic and treat the patients conservatively by restricting fluids (Schrier and Bansal 2008). This is because, if hypertonic saline is introduced, fluid shifts from the ICF to ECF, in some cases causing the neurones in the brain to shrink and demyelinate. Such overcorrection of hyponatraemia can lead to paralysis and sometimes death (Vaidya et al 2010).
Cerebral oedema The brain is made up of tissue, blood and cerebrospinal fluid, which fills the ventricles, and coats the brain and spinal column. The skull allows the volume of the brain to increase by up to 8% (Schrier and Bansal 2008), which means that an increase in the volume of one of the brain’s three components can result in a decrease in the volumes of one or both of the others until no further compensation is possible and the brain begins to compress (Figure 4). This process produces cerebral oedema, which, if allowed to continue, causes irreparable brain herniation leading to coma and death. Signs and symptoms Clinical signs of cerebral oedema in hypervolaemic hyponatraemia include headaches, confusion and lethargy. Patients with the condition may present with a laboured EMERGENCY NURSE
Cheyne-Stokes respiratory pattern and low oxygen saturations on room air. Seizures are common secondary to cerebral oedema (Ayus et al 2000), while ataxia and muscle cramps are common in less severe cases (Vaidya et al 2010). There is usually a decrease in consciousness in patients with severe hyponatraemia, who often tolerate airway adjuncts. Management The most widely used formula for calculating the incremental replacement of serum sodium is the Adrogué-Madias (Adrogué and Madias 2000) formula, in which the sodium deficit in litres is calculated by dividing the patient’s serum sodium Figure 4 Computed tomography scans showing a cerebral oedema
Compressed basilar cistern
Compressed lateral ventricles
Compressed suici
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Art & science | fluid intake concentration in mmol/L by the target concentration, namely 130mmol/L, and multiplying the result by the patient’s total body fluid volume, which is equivalent to 60% of body weight in men and 55% in women. For example, if a man weighing 70kg has a serum sodium volume of 120mmol/L, his sodium deficit is calculated by dividing 120 by 130 and multiplying the result by 60% of his weight, or 42kg, to produce 38.8. The man therefore requires 38.8L of saline to replace the salt he has lost. In such cases sodium should be replaced by continuous intravenous infusion of 3% saline, a hypertonic solution, in some cases following an initial bolus of 100ml (Hew-Butler et al 2005). To gauge the correct rate of infusion for optimal recovery, levels of urea and electrolytes in the blood, and sodium and potassium in the urine, must be monitored. Oral sodium intake with highly salted food should be encouraged and urea tablets can also be used to increase serum sodium levels (Vaidya et al 2010). Intravenous infusion of hypertonic saline raises serum sodium in the short term and encourages ICF and solutes, including sodium, back into the ECF. Administration of ADH-receptor antagonists (Decaux et al 2010), such as tolvaptan, inhibits the effects of ADH by blocking the V1 and V2 receptors in the renal tubules, and thereby increases excretion of excess electrolyte-free fluid and helps restore the natural electrolyte balance. This process is particularly useful in patients with SIADH secondary to drug use and hypervolaemic hyponatraemia. Primary nursing considerations include maintaining a strict fluid balance, regular urine osmolarity screening, and continued hypertonic fluid resuscitation over several days while the patients concerned occupy acute medical, high dependency or intensive care beds. They also include the use of a urethral catheter and urometer to measure fluid
balance, whereby the risks of urinary tract infections secondary to a catheter are mitigated by the short length of time such monitoring is required. The need for catheterisation can be reviewed when patients’ conditions have improved. Nurse managers should ensure that stocks of hypertonic saline are readily available in their clinical areas. Neurological observations and the Glasgow Coma Scale should be used regularly to monitor for variance of consciousness. Overall, patient management should involve the treatment of symptoms, close monitoring for signs of deterioration and escalation of treatment when appropriate. If CT scans indicate compression of the ventricles, a primary compensatory mechanism to raised intracranial pressure (Marieb 1999), cerebral oedema is confirmed.
Conclusion Acute hyponatraemia is a rare complication of sympatheticomimetic drug use but can have life‑threatening consequences, including cerebral herniation and death secondary to cerebral oedema. Care must be taken in the management of patients with the condition because overly aggressive sodium replacement therapy can cause diuresis and a net drop in the serum sodium secondary to hypovolaemic hyponatraemia. Evidence suggests that, in asymptomatic, haemodynamically stable patients, conservative management is preferable. In symptomatic patients with significant neurological deficits, electrolyte replacement should be calculated and titrated to therapeutic response with closely monitored electrolyte input and output. If sympatheticomimetic drug use grows, therefore, emergency department staff will have to deal robustly with the complications that arise.
Online archive For related information, visit our online archive and search using the keywords Conflict of interest None declared
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