CHAPTER Electrolytes in ICU

118 TH Trivedi

INTRODUCTION Patients with chronic usually do not Electrolyte disturbances are common clinical problems have neurological symptoms and manifest with muscle encountered in the intensive care unit (ICU) and are , anorexia, nausea and weakness. associated with increased morbidity and mortality In most of the cases cause of hyponatremia becomes among critically ill patients. Unless suspected they can be apparent by detail clinical evaluation including missed and inappropriate therapy can lead to irreversible medication history. Measurement of osmolality, damage. For management of hyponatremia in ICU urinary , cortisol, thyroid hormone and relevant identifying stimuli for vasopressin secretion, judicious use radiological investigations are needed in selected cases. of hypertonic saline, and close monitoring are essential Low uric acid levels and BUN are found in patients with components. is associated with cellular SIADH, induced hyponatremia, hypopitutarism dehydration and central nervous system dysfunction. and hypervolemia. Concurrent metabolic is seen Water deficit should be corrected with hypotonic fluid, in patients with use, vomiting and hypopitutarism taking into account ongoing water losses. Cardiac while metabolic acidosis is seen in cases of diarrhea and manifestations should be identified and treated before primary adrenalin insufficiency. initiating stepwise diagnostic evaluation of disturbances. Disturbances of phosphorous and Treatment metabolism are also frequently encountered Acute hyponatemia is generally symptomatic and needs in some critically ill patient with trauma, burns, sepsis, rapid correction. Treatment is recommended with and renal failure. Early recognition and 3% NaCl by giving a bolus of 100ml IV over 10 min, prompt correction of these abnormalities are necessary repeated upto maximum 3 doses, or till acute symptoms to avoid catastrophes. A brief description electrolyte subsides. The goal is to provide an urgent correction by disturbance pertaining to ICU patients follows. 4 to 6 mmol/L to prevent brain herniation. For patients with mild to moderate symptoms, 3% NaCl is infused HYPONATREMIA at lower rate of 0.5-2 mL/kg/h. In chronic hyponatremia Hyponatremia may be present on ICU admission or the brain undergoes gradual adaptation and there is less can develop later. In either case it is associated with cerebral edema, and very rapid correction can lead to poor prognosis. A recent study of 151,486 adult patients osmotic demyelination syndrome (ODS). Hence, chronic from 77 intensive care units over a period of 10 years hyponatremia generally needs gradual correction. High demonstrated that severity of dysnatremia is associated risk of ODS is seen with serum sodium < 120meq/L with poor outcome in a graded fashion. Another study reported that both ICU-acquired hyponatremia and Table 1: Causes of Hyponatremia ICU-acquired hypernatremia were associated with increased mortality. It should be noted that patients Pseudohyponatremia Hyperlipidemia with hyponatremia may also have manifestations of (normo-osmolar) Hyperproteinemia concurrent volume depletion and possible underlying Redistributive Hyperglycemia neurologic diseases that predispose to development of Hyponatremia Mannitol therapy hyponatremia due to SIADH or cerebral salt wasting. (hyperosmolar) Hyponatremia-induced cerebral edema occurs with Hypovolemic GI losses sudden fall in the serum sodium concentration, Hyponatremia Third space losses usually within 24 hours. Causes of hyponatremia are Diuretic therapy mentioned in Table 1. Clinically, hyponatremia manifests Cerebral salt wasting with primarily neurologic symptoms. Their severity Mineralocorticoid deficiency depends on rapidity of the change in the serum sodium Euvolemic SIADH concentration in addition to level of sodium. When serum hyponatremia Hypothyroidism sodium falls acutely below 120 meq/L, patients become Glucocorticoid deficiency symptomatic with lethargy, apathy, confusion, Polydipsia and coma. Premenopausal women and young children Hypervolemic Congestive heart failure with acute postoperative hyponatremia have high risk Hyponatremia of liver of brain herniation suggesting a possible hormonally- mediated decrease in the degree of osmotic adaptation. Renal failure CHAPTER 118 559 mL/kg/ infusion at 0.5-1 Manifestations of Nausea, vomiting, diarrhea, intestinal cramps muscle weakness, Paraesthesia, cramps, dizziness ECG changes, risk of Metabolic acidosis This is a common electrolyte disturbance in ICU patients in ICU electrolyte disturbance a common is This (diarrhea, vomiting, nasogastric resulting from GI losses (, diuretic phase of suction), renal losses (beta drugs or trans-cellular shifts renal failure, RTA), stimulants, insulin, aminoglycosides, amphotericin B). Clinical manifestations of hypo and hperkalemia are 2. The most dreaded complications enumerated in Table Treatment Treatment occurring in is rare, hours) hypernatremia Acute (<48 iatrogenic. The or is insipidus patients with diabetes D5-5 with therapy fluid is patients such in regimen initial at a rate of 3 to intravenously, water, percent dextrose in monitoring of serum sodium 6 mL/kg per hour with close until the serum sodium is lowered and blood glucose by below 145 meq/L, followed 24 hours. is restored over hour till normonatremia hypernatremia Chronic (>48 hours) even is more common, present with acute changes in mentation. who in those in such patients is D5 infusion, The initial regimen in kg weight x patient’s (1.35 at a rate of intravenously, ml/hour) by the serum sodium a maximum of to lower 10 meq/L in a 24-hour period (0.4 meq/L/hour). It is likely by less sodium the serum lower will that this regimen ongoing than 10 meq/L in 24 hours, as many patients have nasogastric losses (osmotic diuresis, diarrhea, free water can Potassium suction) slowing the rate of correction. be added to of A potential hypokalemia. concomitant the intravenous fluid intravenous rapid administration of dextrose-containing in patients with fluids is the development of hyperglycemia, more so in can lead to an patients with diabetes. Hyperglycemia electrolyte-free osmotic diuresis, which creates water losses further limiting in serum sodium. the reduction solution e.g. 2.5% dextrose in water- concentration Lower hypernatremia can be used in such patients. Hypervolemic in that develops is usually an iatrogenic complication patients Renal replacement therapy with renal failure. is the only effective lower to be adjusted should solution hemodialysis of treatment them.in Composition sodium concentration in such patients. hypernatremia hypernatremia brain traumatic complicate can The injury. with begin hypernatremia of acute manifestations clinical irritability, and to can progress and lethargy, weakness, is >160meq/L. serum sodium and coma if convulsions most thirst initially, intense however may have Patients same. cannot communicate ICU patients Manifestations of Hypokalemia Anorexia, nausea, vomiting, paralytic ileus Muscle cramps, weakness, paraesthesia, paralysis Postural hypotension, ECG changes, cardiac dysrhymias Metabolic alkalosis GI manifestations Neuromuscular Manifestations Manifestations Cardiovascular Acid Base Disorders Associated Table 2: Clinical of Hypokalemia and Hyperkalemia manifestations Table HYPERNATREMIA Predisposing factors for hypernatremia in ICU include the administration of sodium bicarbonate solutions for loss, use of renal water correction; selective acidosis nasogastric through losses fluid gastrointestinal diuretics; drainage losses through fever, water suction, and selective with Acute diabetes insipidus tubes, and open wounds. or if there are comorbidities such as alcoholism, liver liver as alcoholism, such comorbidities there are or if are present. hypokalemia or severe malnutrition, disease, with symptomatic is hyponatremia if chronic However, therapy aggressive severe, is features or neurological and Initial hyponatremia as for acute is indicated to raise the serum is needed of 3% NaCl administration baseline. 4-6 mmol above sodium by the [Na+] following change in plasma Estimated administration of 1 L of an can be by calculated equations proposed by Madias and intravenous fluidregimen Adrogue: [Na+] =Infusate [Na+] – plasma [Na+]/ Change in plasma + 1 Total body water to underestimate the achieved There is a tendency Also ongoing losses this formula. plasma [Na+] using to be laboratory accounted for and close clinical and have hyponatremia, In hypovolemic monitoring is needed. the initial intravenous fluid ofor symptomatic the patient is chloride, unless sodium choice should be 0.9% acutely developed to have hyponatremia is documented hyponatremia does asymptomatic Euvolemic (< 48 hours). not require urgent therapy. Identification andof removal reversible causes should be done diuretics Loop SIADH. restriction in patients with chronic followed by fluid concurrently used are beneficial in patients with SIADH to serum electrolyte ratio (>1). a high urine who have hyponatremia in addition for chronic are useful Vaptans to fluid restriction and sodium chloride administration. are associated Many cases of hypervolemic hyponatremia with significant dysfunction of the orheart, kidney. liver, and sodium water Treatment includes restriction of intake, diuretics and treatment administration of loop of hyponatremia in patients with Treatment of severe cause. may require extracorporeal heart failure decompensated ultrafiltration, which requirements, and correct diuretic congestion, lower has been can be in cirrhotic patients used hyponatremias. Vaptans shown improve for to management of fluid overload with hyponatremia if restriction and diuretics do not help. water 560 of hypokalemia are cardiac , especially in is most effective therapy. Exchange resins are advocated patients with hypertension and IHD, heart failure and in long term management in chronic cases. neuromuscular paralysis. ECG changes seen in patients with hypokalemia include ST-segment depression, MAGNESIUM IMBALANCE T-wave flattening followed by inversion, and the presence It is second most abundant intracellular cation but only of U waves. In presence of life threatening symptoms like 1% of body’s Mg is present in ECF. Hypomagnesemia respiratory muscle paralysis or changes in ECG, therapy is common finding in hospitalised patients (10-20%) should precede investigations. In cases where cause is not especially in emergency department and ICU patients obvious clinically, urinary potassium excretion should be (as high as 50%). It may result from impaired intake measured. If it is appropriately low (urine K+ < 20 mEq/ (alcoholism, starvation, malabsorption, TPN), increased day then trans-cellular shift or extrarenal K+ loss should losses (diuretics, DKA, hyperaldosteronism, magnesium be suspected. If urinary K+ excretion is high, trans-tubular losing kidney disease). Drugs like aminoglycosides, potassium gradient (TTKG), acid-base status, and the amphotericin, beta agonists, diuretics and PPIs predispose presence or absence of hypertension help in identifying to hypomagnesemia. Severe hypomagnesemia can result in cause of hypokalemia. ECG changes, arrhythmias including , seizures, coma, and death. Neuromuscular manifestations CRITICAL CARE Treatment are muscle weakness, tremors and hyperreflexia. Parentral therapy is reserved for patients with severe Hypomagnesemia can also lead to refractory hypokalemia symptoms and ECG changes. Infusion of > 10–20 mEq/ and . Severe hypomagnesemia(serum Mg < hr of potassium requires a central venous catheter, as 1mg/dl) is treated with IV infusion of 1.5 meq/Kg MgSO4 infusion via peripheral line causes phlebitis. Total amount over 12-24 hours with monitoring of serum Mg level and of daily K+ replacement should be less than 240–300 renal function. is rare but can be seen mEq with close monitoring. Parenteral K+ replacement in ICU patients following administration of IV MgSO4 for should be given in dextrose-free vehicle. Hypocalcemia eclampsia, Mg containing laxatives and in patients with and hypomagnesemia should be suspected and corrected renal failure. It manifests with lethargy, hyporeflexia, if hypokalemia persists despite adequate potassium hypotension, confusion and coma and respiratory supplementation. Milder hypokalemia should be paralysis. Treatment of hypermagnesemia includes corrected with oral therapy. stopping Mg supplementation, IV Calcium infusion in severe cases, hydration, loop diuretics and dialysis for HYPERKALEMIA patients with life threatening manifestations. It is seen in 1-2% of hospitalized patients. Increased intake, impaired renal excretion, hypoaldosteronism, transcellular CALCIUM IMBALANCE shifts (acidosis, drugs, periodic paralysis, exercise) and Hypocalcemia is a frequent electrolyte abnormality cellular injury are important causes. Pseudohyperkalemia encountered in the ICU. Prevalence of hypocalcemia due to hemolysis of sample, leukocytosis, thrombocytosis measured as ionized calcium is estimated to be about and laboratory error should be suspected in absence 15–20%. Hypocalcemia is also associated with increased of obvious cause, symptoms and ECG changes. ECG mortality in ICU patients. Spuriously low concentration changes include tall T waves, low p wave, prolongation of calcium can be seen following the administration of of PR interval and widening of QRS complex. Table 2 gadolinium based contrast, as gadolinium interferes enumerates clinical manifestations. Initial step after with calorimetric calcium assays. Common causes exclusion of pseudohyperkalemia is to identify the cause of hypocalcemia in ICU patients are trauma, renal of trans-cellular potassium shift, and discontinuation failure, sepsis, pancreatitis, massive transfusion, post of medications responsible for hyperkalemia. The next , associated hypomagnesemia and step is to assess urinary potassium excretion. If there deficiency. The symptoms and signs of is relatively low urinary K+ excretion, calculation of severe acute hypocalcemia include , seizures, TTKG should follow. A low TTKG may warrant further cardiovascular manifestations such as prolonged QT tests to differentiate between aldosterone deficiency interval and ventricular arrhythmias. and resistance to aldosterone. If ECG abnormality of should be preferred over for urgent hyperkalemia is present, emergency management should situations, since it contains three times more elemental be started before further investigations. Intravenous calcium. Hypomagnesemia should be suspected and calcium gluconate is the first therapy to antagonize the corrected if hypocalcemia is not getting corrected by depolarizing effect of hyperkalemia. Administration of repeated calcium administration. If metabolic acidosis is Insulin with 50% glucose follows. It takes 30 minutes present concomitantly, hypocalcemia should be corrected to produce effect that lasts for 4-6 hours. Nebulization first as the treatment of acidosis with bicarbonates further with beta stimulants lower potassium levels for at least 2 decreases level of ionized calcium, precipitating tetany hours. Sodium bicarbonate should be avoided in patients or cardiac arrest. Hypercalcemia is seen in ICU patients with volume overload. Infusion of with , prolonged immobilization, 44 meq over 5-15 minutes lowers serum potassium for malignancies, use of thiazide diuretics and milk alkali approximately 2 hours. In case of emergency and in syndrome. Clinical manifestations are vomiting, presence of renal failure or , hemodialysis constipation, hypertension, renal dysfunction and CNS CHAPTER 118 561 Am J 2010; 8:72-81. 2014;18:760-71. Funk GC, Lindner G, Druml W, et al. Incidence and Funk GC, Lindner G, Druml W, ICU admission. prognosis of dysnatremias present on Care Med 2010; 36:304-311. 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CONCLUSION REFERENCES Various types of electrolyte imbalances are found in imbalances are of electrolyte types Various critically ill patients along of cases there disturbances. In majority symptoms are no with fluid andand even if acidpresent are non-specific. Thus base high index of depending needed to identify these disorders is suspicion in these patients. Their conditions on predisposing of and appropriate treatment are prompt recognition be fatal if left these can of some as importance utmost of disturbances for most is simple untreated. Treatment but patients fluid status, is and close monitoring to be considered conditions have renal function, pre-existing too rapid correction of complications required to avoid with long term sequel. 1. 2. 3. with with acute is by Treatment hyperphophatemia. restricting with of glucose infusion hydration, supplementation, or calcium Aluminium cases. severe in and dialysis insulin to used commonly are binders containing is a non calcium/aluminium Sevelamer retard absorption. lipid profile. effect on binder with additional containing 4. A, Korzelius C, Schrier SR, Greenberg JG, Goldsmith Verbalis 5. 6. 7. 8. PHOSPHOROUS IMBALANCE PHOSPHOROUS is a frequent disorder in critically ill disorder in is a frequent Hypophosphatemia sepsis, DKA, malnutrition, patients with Gram-negative therapy alcoholism, diuretic surgery (20- and cardiac decreased may result from Hypophosphatemia 25%). renal loss, absorption, increased intestinal phosphate phosphate to intracellular of shift trans-cellular and containing solution of glucose space. Rapid infusion patients to chronically malnourished can precipitate by causing trans-cellular shift know hypophosphatemia It may manifest with leukocyte, as re-feeding syndrome. platelet dysfunction. Clinical features erythrocyte, and convulsions ataxia, confusion, weakness, are muscular cardiac arrhythmias. and coma; respiratory failure and dependence are frequent Hypotension and ventilator due to hypophoaphatemia. problems encountered in ICU (< 1.0 mg/dL) hypophosphatemia Symptomatic or severe or potassium sodium be treated with intravenous should infusion of 2–5 mg/kg phosphate with initial intravenous in 0.45% saline given of inorganic phosphate dissolved Monitoring needed. and repeated as 6–12 hours over IV phosphate for hypocalcemia is required during Milder on CRRT need higher dose. infusion. Patients hypophosphatemia is treated with oral supplementations such as potassium phosphate. increased from can result phosphate excretion, or phosphate intake, decreased extracellular shift of intracellular phosphate to space. mortality in ICU for It is an independent risk factor and lysis tumor acidosis, patients. Rhabdoomyolysis, to due hyperphosphatemia can cause acute hemolysis are cellular shifts. Renal failure and hyperphosphatemia due to decreased of causes common loss. Most patients are asymptomatic but occasionally symptoms of hypocalcemia, such as muscle have cramps, tetany, and perioral numbness or tingling. Bone rash are other symptoms. and joint pain, pruritus, and patients in develop can seizures and Carpopedal disturbances including coma. Management is with saline with is Management coma. including disturbances by Biphosphonates, diuretics. loop followed hydration, in chronic role have plicamycin and steroids calcitonin, with in patients Dialysis is required cases. and severe or fluid overload. renal failure