Clinical Review: Practical Approach to Hyponatraemia and Hypernatraemia in Critically Ill Patients
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Overgaard-Steensen and Ring Critical Care 2013, 17:206 http://ccforum.com/content/17/1/206 REVIEW Clinical review: Practical approach to hyponatraemia and hypernatraemia in critically ill patients Christian Overgaard-Steensen1,2,* and Troels Ring3 Abstract Disturbances in sodium concentration are common in the critically ill patient and associated with increased mortality. The key principle in treatment and prevention is that plasma [Na+] (P-[Na+]) is determined by external water and cation balances. P-[Na+] determines plasma tonicity. An important exception is hyperglycaemia, where P-[Na+] may be reduced despite plasma hypertonicity. The patient is fi rst treated to secure airway, breathing and circulation to diminish secondary organ damage. Symptoms are critical when handling a patient with hyponatraemia. Severe symptoms are treated with 2 ml/kg 3% NaCl bolus infusions irrespective of the supposed duration of hyponatraemia. The goal is to reduce cerebral symptoms. The bolus therapy ensures an immediate and controllable rise in P-[Na+]. A maximum of three boluses are given (increases P-[Na+] about 6 mmol/l). In all patients with hyponatraemia, correction above 10 mmol/l/day must be avoided to reduce the risk of osmotic demyelination. Practical measures for handling a rapid rise in P-[Na+] are discussed. The risk of overcorrection is associated with the mechanisms that cause hyponatraemia. Traditional classifi cations according to volume status are notoriously diffi cult to handle in clinical practice. Moreover, multiple combined mechanisms are common. More than one mechanism must therefore be considered for safe and lasting correction. Hypernatraemia is less common than hyponatraemia, but implies that the patient is more ill and has a worse prognosis. A practical approach includes treatment of the underlying diseases and restoration of the distorted water and salt balances. Multiple combined mechanisms are common and must be searched for. Importantly, hypernatraemia is not only a matter of water defi cit, and treatment of the critically ill patient with an accumulated fl uid balance of 20 litres and corresponding weight gain should not comprise more water, but measures to invoke a negative cation balance. Reduction of hypernatraemia/hypertonicity is critical, but should not exceed 12 mmol/l/day in order to reduce the risk of rebounding brain oedema. Introduction with losartan/thiazid and is receiving nonsteroidal anti- Hyponatraemia and hypernatraemia are frequent in infl ammatory drugs (NSAIDs). He is spontaneously patients admitted to the ICU and may even be acquired breathing with a patent airway. Mean arterial pressure is during their stay [1-8]. Th ese patients have a higher 100 mmHg, heart rate = 120 beats/minute. Arterial blood + overall mortality, and even slight changes in plasma [Na ] gas analysis is as follows: pH = 7.57, pCO2 = 3.4 kPa/ + (P-[Na ]) are associated with an increased risk of death 26 mmHg, pO2 = 7.9 kPa/59 mmHg, Hgb = 7.3, lactate = [3,9]. 1.6 mmol/l, BE = 1.3, plasma [Glucose] (P-[Glc]) = 7.6 mmol/l, P-[Na+] = 90 mmol/l and P-[K+] = 3.5 mmol/l. Case story Cerebral CT scanning shows no bleeding. Infusion of A 58-year-old male is admitted somnolent (Glasgow 0.9% NaCl is instituted and he is transferred to the ICU. Coma Scale = 11) to the emergency department. He has a After 6 hours (P-[Na+] = 95 mmol/l), the patient is more newly discovered tonsil cancer, consumes too much awake, but delirious. To achieve P-[Na+] = 120 mmol/l, alcohol, has arterial hypertension that is being treated the 0.9% NaCl infusions are increased. After 12 hours (P- [Na+] = 105 mmol/l), the patient is awake but confused, and phenobarbital and haloperidol are given. Respiratory *Correspondence: [email protected] 1Department of Neuroanaesthesiology, Rigshospitalet, Blegdamsvej 9, DK-2100 insuffi ciency necessitates intubation after 24 hours + Copenhagen Ø, Denmark (P-Na = 115 mmol/l). Th e patient is seen by an Full list of author information is available at the end of the article oncologist and diagnosed quite informally with syndrome of inappropriate antidiuretic hormone (SIADH). P-[Na+] © 2010 BioMed Central Ltd © 2013 BioMed Central Ltd rises progressively. On day 6, quadriplegia and coma Overgaard-Steensen and Ring Critical Care 2013, 17:206 Page 2 of 14 http://ccforum.com/content/17/1/206 (Glasgow Coma Scale = 3 without sedation) are observed Equations 1 and 2 assume that plasma tonicity is (P-[Na+] = 144 mmol/l). A neurologist proposes a diag- determined by P-[Na+]. Th is is true in hypernatraemia nosis of osmotic demyelinisation (OD). Over the next and, by far, in the most common hyponatraemic condi- 2 days, P-[Na+] increases to 151 mmol/l and he dies from tions. Translocational hyponatraemia is an exception. In intractable cardiac arrest. this condition osmotically active substances confi ned to Th is case story illustrates common and important the extracellular/plasma compartment cause a shift of problems in managing the hyponatraemic patient. First, water from the intracellular compartment. In this the initial 0.9 % NaCl approach is inadequate to ensure a situation, the resulting hyponatraemia is hypertonic. Th e rapid and controllable response [10]. Second, no most frequent clinical condition is hyperglycaemia (P- measures to avoid overcorrection are taken, and he gets [Na+] is reduced approximately 0.4 mmol/l per mmol/l hypernatraemia despite being in the ICU [8]. Th ird, increase in P-[Glc] (or a reduction of 2.4 meq/l per hyponatraemia often has multiple causes [11]. Fourth, 100 mg/dl increase)) [17], but the condition can also be nothing is done to identify the mechanisms of hypo- caused by mannitol. Pseudohyponatraemia is an unusual natraemia [12]. measurement fl aw in patients with hyperlipaemia/hyper- Th is review takes a practical approach to the critically proteinaemia whose plasma tonicity is normal. In the rest ill patient with dysnatraemia. of this article, ‘hyponatraemia’ refers to hyponatraemia where plasma tonicity is decreased. Plasma [Na+] is determined by water and electrolytes Regulation of P-[Na+] Knowledge about what determines P-[Na+] is crucial for P-[Na+] is tightly regulated between 135 and 145 mmol/l understanding the mechanisms behind dysnatraemia and primarily by water intake (thirst) and renal water how to correct/prevent these disorders. Within a popu- excretion [15]. Of lesser quantitative importance, P-[Na+] lation of heterogeneous patients, Edelman and colleagues is regulated by the kidney’s regulation of cation excretion [13] demonstrated that P-[Na+] is determined by ex- via the renin-angiotensin-aldosterone system. Th irst is change able cations (eNa+ and eK+) and total body water stimulated when P-[Na+] increases a few percent [18]. It (TBW) according to Equation 1: is also stimulated by a decrease in the eff ective circulating volume, which is the part of the extracellular volume eNa+ + eK+ P-[Na+] = α × —————— + β E q u a tion 1 (ECV) that eff ectively perfuses the tissue [19]. Arginine TBW vasopressin (vasopressin, or antidiuretic hormone (ADH)) where α and β are the coeffi cients from the linear reduces renal water excretion. Vasopressin binds to the regression. V2-receptor in the collecting duct. Th is promotes Equation 1 is not readily useful at the bedside; however, traffi cking of aquaporin 2 to the apical membrane and it was recently demonstrated that it is valid in the passive water reabsorption to the hypertonic medullary individual and that changes in P-[Na+] can be determined interstitium [20]. Vasopressin secretion is stimulated by the external balances of water and cations (Na+ + K+) when P-[Na+] increases [18]. Vasopressin release can also [14]. Th e simplifi ed version (Equation 2) where α = 1 and be stimulated non-osmotically by a reduced eff ective β = 0 provides a good estimate of the P-[Na+] changes circulating volume, stress, pain, nausea, vomiting, various and is useful for planning fl uid and electrolyte treatment drugs and exercise. in the individual patient [14-16]: Irrespective of vasopressin, the kidney’s ability to + + + excrete water is infl uenced by solute intake (protein/urea + [Na ]1 × TBW + Δ(Na + K ) [Na ]2 = ———————————————— E q u a tion 2 and cations) since the urine volume is the solute TBW + ΔTBW excretion divided by the urine osmolality: + where [Na ]1 is the initial plasma concentration and + solute excretion urea + electrolytes [Na ]2 is the concentration that results from the change urinevolume = —————————— = ——————————— in the external balances of water (ΔTBW) and cations urine osmolality urine osmolality (Δ(Na+ + K+)). A low solute intake reduces urine solute excretion and Equation 2 is fundamental in understanding changes in thereby urine volume despite maximally diluted urine. In P-[Na+]. It is, therefore, also fundamental in practical contrast, a high protein/urea intake or generation will patient treatment. It is important, however, to keep in increase the urine volume. However, urea does not mind that the impending output side of the water and directly determine P-[Na+] (according to Equation 2). cation balances can only be guessed. Frequent measure- Th is is so because in the whole body perspective, urea ment of output (especially diuresis) and P-[Na+] is eventually crosses cell membranes and therefore is an necessary and input of fl uids must be adjusted ineff ective osmolyte that does not contribute to water dynamically. fl ux between cells and extracellular volume [15]. Overgaard-Steensen and Ring Critical Care 2013, 17:206 Page 3 of 14 http://ccforum.com/content/17/1/206 Altogether, the renal eff ects infl uencing P-[Na+] are induction/worsening of hypovolemia can be hazardous gathered in excretion of electrolyte-free water [21]: [30]. Cerebral disease, hepatic encephalopathy and sedation U[Na+] + U[K+] cH O = urine × ( 1 – ————————— ) can cause severe symptoms similar to those of hypo- 2 e volume + P-[Na ] natraemia [31], but a slight P-[Na+] increase will not where U[Na+] and U[K+] are urine Na+ and K+ con cen- worsen these conditions [32,33].