Hyponatremia in ICU patients

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Information about Hyponatremia in ICU patients
Health & Medicine

Published on April 21, 2014

Author: avaneeshjakkoju

Source: slideshare.net


What we are going to cover…  Why serum sodium falls  How the brain responds to a change in serum Na concentration.  What the goals of therapy should be.

Why serum Sodium level rises and falls… • Serum Sodium is a function of exchangeable Sodium, Potassium and total body water. Total body (Nae+Ke) Serum Sodium = ----------------------------------- Total body water

Serum Sodium levels… • Extra renal losses do not cause fall in serum sodium levels. – For example GI losses such as vomiting and diarrhea leads to loss of Na and K along with free water loss and serum sodium level will be same. – Sweating. What causes hyponatremia in the above situations is replacing the lost fluid with regular water, that makes the Sodium levels to drop.

Why does hyponatremia develop…  Renal loss of Sodium leads to hyponatremia.  To put it simply, if the urine is more concentrated than plasma then there is net loss of Sodium leading to hyponatremia.  ADH (vasopressin) plays a crucial role to this effect.

ADH in normal human beings..  Secreted by hypothalamus Vasopressin is released from posterior pituitary in response to dehydration and/or hyponatremia.

Abnormal secretion of ADH… • Pathologically ADH secretion is released in spite of normal or even low Na concentration in response to stimuli such as – Inadequate circulation – Stress – Hypoxia – Cortisol deficiency – Neurological diseases – Ectopic vasopressin release such as SCC of lung.

Cerebral Salt Wasting…  In acute neurological conditions particularly in SAH, to maintain cerebral perfusion large volumes of isotonic fluids are commonly prescribed.  Volume expansion suppresses aldosterone secretion and enhances natriuretic hormones that increase urine Na excretion leading to hyponatremia.

Hyponatremia in Kidney disease…  Acute kidney injury or advanced chronic kidney disease results in a urine osmolality equal to that of plasma.  Replacing fluid losses with electrolyte free water in kidney diseases leads to hyponatremia due to dilution.

Brain response to changing serum Na concentration…  Na does not readily cross BBB.  If the serum sodium falls rapidly then free water crosses blood brain barrier leading to increase in Intra cranial pressure some times with fatal outcomes.  On the other hand if the serum Sodium concentration increases rapidly, water is drawn from brain.

Slow vs. fast serum Na changes… • Brain cells achieve osmotic equality with plasma by exchanging organic solutes as well as taking on water. • Loss of these organic osmolytes leads to decreased brain swelling. • This is an effective mechanism to prevent cerebral edema in response to hyponatremia, but unfortunately this is a slow process. • It takes 48 hours for the brain to adapt to hyponatremia, any fall in Na faster than this leads to fatal rise in ICP.

Slow vs. fast Na changes… • Rapid correction of chronic hyponatremia starts a cascade of adverse events leading to programmed death of myelin producing oligodendrocytes. • This is because of the delay in repletion of organic osmolytes within the brain cells. • This injury presents clinically as a progressive neurological disease- Osmotic demyelination syndrome (ODS).

Osmotic demyelination syndrome… • Classically associated with demyelination of the central pons- central pontine myelinolysis. • Extra pontine myelinolysis is also equally common. • Clinical symptoms start 2 to 6 days after the correction and include dysarthria, dysphagia, paraparesis or quadriparesis, behavioral disturbances, lethargy, confusion, disorientatio n, obtundation and coma. • Seizures although uncommon are seen. • Severe cases, patients are „locked in‟;

Predisposition to ODS… • ODS is seen not with hyponatremia but with rapid correction; can be prevented by lowering Na with Desmopressin after rapid correction. • Patients who has a very longstanding hyponatremia, with serum Na<105 mEq/L, hypokalemia, alcoholism, malnutrition and liver disease are prone to develop ODS. • On the other hand serum Na<120 mEq/L, with out above risk factors and whose hyponatremia is of very short duration are not prone to develop ODS, they can be treated with rapid Na correction.

Goals of Therapy…  Serum Na concentration should be increased enough to prevent complications of untreated hyponatremia.  Treatment should be at the optimal rate so as not to cause any iatrogenic brain injury.

Acute hyponatremia…  Brain death from cerebral edema is the most feared complication of acute hyponatremia.  This was observed in patients..  Who were given hypotonic IV fluids after surgery.  Water intoxication associated with psychosis, marathon running or recreational drug use of „ecstasy‟.  Intracranial pathology.

Acute hyponatremia-clinical picture… • Headache, nausea, vomiting, drowsiness and mild confusion can be seen. • These non specific symptoms rapidly progress to seizure, respiratory arrest and permanent or fatal brain injury. • Seizures are uncommon in chronic hyponatremia even with very low Sodium concentration and they usually reflect and underlying seizure pathology.

Acute hyponatremia- how to correct… • Serious neurological symptoms warrant aggressive treatment irrespective of any other factors. • Treatment with hypertonic saline to raise serum sodium concentration 4 to 6 mEq/L is suggested by several studies. • A 4 year, single center study of 63 patients treated for transtentorial herniation caused by a variety of neurosurgical conditions found that, an increase in plasma sodium concentration by 5 mEq/L promptly reversed clinical signs of herniation and reduced ICP by 50% with in 1 hour. • Seizures due to hyponatremia do not respond to anti epileptic drugs.

Severe chronic hyponatremia…  Patients with chronic hyponatremia rarely are symptomatic.  There is little evidence to suggest Sodium level to be brought to „safe‟ (>120 mEq/L or in some cases >130 mEq/L) levels for better outcome.  In spite of lack of evidence correcting well compensated hyponatremia continues to be the standard of care.

Severe Chronic hyponatremia- rationale for treatment… • Typically patients with serum Na<110 mEq/L are admitted to the hospital. • These patients have a very good prognosis and there is no need for aggressive treatment or large increase in Sodium. • As serum sodium levels fall mortality rate rises, but below 120 mEq/L paradoxically mortality rate falls, and at 110 mEq/L mortality rate is same as that of normonatremic patients.

Severe Chronic Hyponatremia- clinical picture… • Although hyponatremia that developed over days rarely ever presents with life threatening symptoms such as seizures and coma, it still causes distressing symptoms. • Even mild chronic hyponatremia which is seemingly “asymptomatic” can cause gait disturbances and disturbed cognition. • It markedly increases the risk of falls and fractures.

Severe Chronic hyponatremia- treatment goals… • Goal of treating chronic hyponatremia should not be aimed at bringing the Sodium level to „normal‟ levels, but bringing it to a level where it provides symptom relief. • Rapid or over correction of Sodium is associated with adverse neurological outcomes that we have reviewed in the beginning. • A correction of 4 to 6 mEq/L/day is considered an ideal Sodium correction rate.

ODS- treatment goals…  It takes about 1 week for the repletion of organic osmolytes in the brain.  Several observational studies have shown, treatment of severe (defined as <120mEq/L) and chronic (>48 h) hyponatremia by >10 to 12 mEq/L/d or >18 mEq/L/2days has been shown to be associated with ODS.  However these values do not represent the treatment guidelines for the correction of hyponatremia, therapeutic goals should be much lower than these values.

A Universal Therapeutic Goal: Rule of Sixes… Six a day makes sense for safety; so give six in six hours for severe Sx and stop.

Rule of Sixes- What does it mean?  For all patients with severe symptoms of hyponatremia therapeutic range of correction should be <6 mEq/L/D.  Give 6 mEq/L on the first day for 6 hours and stop.  Can be resumed on day 2 with a goal of 4 to 6 mEq/L/D.

Rule of Sixes- Why?  An increase of 4 to 6 mEq/L/D is enough to treat most symptoms of hyponatremia.  This level allows enough room for error should correction inadvertently exceed the rate that was intended.  As previously mentioned upper limit of correction 10 to 12 mEq/L/D or 18 mEq/L/2day reported by previous observational studies.

How to treat: General Measures…  Unless urine is maximally dilute, patients should be fluid restricted.  No unintended sources of electrolyte-free water such as tube feedings and IV meds administered in D5W.  If it is unavoidable, give 300 ml of 3% saline (150 mEq of Na) for every liter of free water.

How to treat: Avoiding hyponatremia in patients with Intracranial disease…  High risk for cerebral edema and resultant tentorial herniation.  Fluid restriction will be ineffective in presence of concentrated urine and not suggested as it can compromise cerebral circulation.  Most reliable way is to give sodium rich fluids based on this proposed sliding scale.

How to treat: Sliding Scale protocol to avoid Hypo-natremia in Neurosurgical patients with serum Sodium < 140 mEq/L… Serum Sodium Infusion Rate <130 mEq/L Increase by 20 ml/h to maximum of 80 ml/h 130 – 135 mEq/L Increase by 10 ml/h to maximum of 80 ml/h 136 – 140 mEq/L No change in infusion rate >140 mEq/L Hold infusion and resume when in therapeutic range. 3 gm of NaCl orally or NG tube Q6hr RTC and 3% IV NaCl given at an initial rate of 20 ml/hr and adjusting infusion rates Q6hrs based on serum sodium.

How to treat: Urgent intervention…  Acute (<24 h) symptomatic hyponatremia, Severe neurological sx (seizures and/or coma) regardless of duration of hyponatremia and patients with coexistent intracranial pathology…  Should be treated urgently with hypertonic saline.  100 ml bolus of 3% saline with two additional doses administered every 15 min till the patient improves.

How to avoid over correction in Chronic hyponatremia… • In many patients SIADH and/or concentrated urine resolves after initial management such as fluid repletion in hypovolemia, hormone replacement in adrenal insufficiency or discontinuation of thiazide diuretics etc. • In such circumstances, body starts to lose free water instead of making concentrated urine and Sodium level may start to rise more than anticipated. • Once the urine becomes maximally dilute the resulting water diuresis can increase serum Na level by >2mEq/L/h

How to avoid over correction in Chronic hyponatremia: Desmopressin.. • If urine sodium concentration is increasing too rapidly, urine water losses can be matched with D5W. OR • We can give desmopressin 2 to 4 mcg parenterally to halt water diuresis.

How to avoid over correction in Chronic hyponatremia: D5W or Desmopressin?  If serum sodium level has already increased by >10 to 12 mEq/L over 24 hours  Or by >8 mEq/L in high risk patients*  Bring the sodium level down again.  Bring to 8 mEq/L more than previous day.  Do this by giving infusions of 3ml/kg D5W over 1 hour or 2 to 4 mcg of Desmopressin parenterally.

Correction of chronic hyponatremia: Desmopressin and 3% saline… • Rather than giving desmopressin to stop water diuresis after it has begun we can start giving desmopressin along with 3% saline to achieve a more controlled rate of correction. • Hypertonic saline is titrated to achieve the desired rate of correction, with an initial bolus if clinically indicated. • Combination therapy is continued until the serum Na concentration has been increased to >128 mEq/L.

Correction of chronic hyponatremia: When to avoid combination treatment? • We avoid desmopressin combination treatment when there is little likelihood of a reversible cause of water retention such as SIADH due to small cell lung cancer or brain tumor. • In hypotensive patients with hyponatremia who require large amounts of isotonic fluid for volume resuscitation we would still give desmopressin but avoid 3% saline, as each liter of NS increases serum Na by 1mEq.

Correction of chronic hyponatremia: Patients who are hypokalemic… • In patients who are hypokalemic, Potassium replacement will increase serum Na level too as it is a function of exchangeable K as well as Na. • In such patients dose of hypertonic saline must be reduced. • A recent report described a case of ODS following overcorrection primarily attributable to replacement of a large K deficit. • In such patients KCl infusion along with desmopressin achieved a controlled rate of correction of both Na and K levels.

Renal replacement therapy… • Hyponatremia is commonly seen in oliguric kidney failure. • Conventional hemodialysis has shown to increase serum Na concentration very rapidly. • Luckily ODS after dialysis is rare and uremia has been shown to be protective. • However large increases in the serum Na concentration during dialysis should be avoided if possible.

Hyponatremia in edematous conditions…  Hyponatremia is associated with poor outcomes in heart failure and liver disease.  Hypertonic saline is usually not advisable in volume overloaded patients, but it can be given combined with high doses of loop diuretics.  Alternatively “aquaretics” can be used to treat hyponatremia in volume overloaded patients.

Samsca (tolvaptan) • Tolvaptan is an oral vasopressin V2 receptor antagonist. • Increases free water clearance and increases serum Sodim concentrations. • Indicated for the treatment of clinically significant hypervolemic and euvolemic hyponatremia that is symptomatic and has resisted correction with fluid restriction. • Most commonly used in heart failure and SIADH.

Samsca (tolvaptan) Dosing… • Initial dose of 15 mg P.O. qD • Can be increased to 30 mg P.O qD after atleast 24 hours of beginning of the treatment. • Can be increased to a maximum of 60 mg P.O. qD titrating at 24 hours intervals to desired Sodium concentration. • Avoid fluid restriction for first 24 hours. • Can be used for a maximum duration of 30 days.

Samsca (tolvaptan) Contraindications… • As of April 2013, the U.S. Food and Drug Administration (FDA) determined that tolvaptan can not be used in patients with underlying liver disease including cirrhosis. • A double blinded, placebo controlled trial showed an increase in serum ALT and total bilirubin in 3 patients (n=1445) with ADPKD. • Other contraindications include acute hyponatremia with sever symptoms, anuria, patients who have altered mental status who cannot respond to thirst and anuria.

Samsca (tolvaptan) Adverse reactions… • GI: Nausea (21%), Xerostomia (7% to 13%), GI bleeding (10%, in cirrhosis patients), Constipation (7%), anorexia (4%), hepatotoxicity (<4%) • Renal: Polyuria (4% to 11%) • Endocrine and metabolic: hyperglycemia (6%), hypernatremia (<2%) • Musculoskeltal: Weakness (9%) • Misc: Thirst (12% to 16%), Fever (4%)

Thank you References: Stern RH, Hix JK, Silver SM; Management of hyponatremia in the ICU. Chest. 2013 Aug; 144 (2): 672-9 Sterns RH, Silver SM. Cerebral salt wasting versus SIADH: what difference? J Am Soc Nephrol. 2008;19(2):194-196. Lin SH, Chau T, Wu CC, Yang SS. Osmotic demyelination syndrome after correction of chronic hyponatremia with normal saline. Am J Med Sci. 2002;323(5):259-262. Laureno R. Central pontine myelinolysis following rapid correction of hyponatremia. Ann Neurol. 1983;13(3):232-242. Arieff AI, Llach F, Massry SG. Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore). 1976;55(2):121-129 Woo CH, Rao VA, Sheridan W, Flint AC. Performance characteristics of a sliding-scale hypertonic saline infusion protocol for the treatment of acute neurologic hyponatremia. Neurocrit Care. 2009;11(2):228-234 Gowrishankar M, Chen CB, Mallie JP, Halperin ML. What is the impact of potassium excretion on the intracellular fluid volume: importance of urine anions. Kidney Int. 1996;50(5):1490-1495. Wendland EM, Kaplan AA. A proposed approach to the dialysis prescription in severely hyponatremic patients with end-stage renal disease. Semin Dial. 2012;25(1):82-85. Cluitmans FH, Meinders AE. Management of severe hyponatremia: rapid or slow correction? Am J Med. 1990;88(2):161-166

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