Sodium Disorders of sodium concentration reflect abnormalities in water homeostasis Serum sodium concentration does not provide any information about sodium content i.e. volume status It is only the ratio of sodium to extracellular fluid in which it is contained

Hyponatremia Hx: duration of hyponatremia, presence of symptoms,( change in mental status, lethargy, seizure, coma ) potential causes PE: asses volume status, skin turgor, BP/orthostasis, pulmonary edema, peripheral edema

Lab Evaluation

Dilutional Hyponatremia

Low volume

Dilutional Hyponatremia

SIADH Inappropriate ADH response in a patient with hyponatremia. Urine is less than maximally dilute in the presence of relative euvolemia Tx: free water restriction, loop diuretics, high protein and salt intake. Occasionally demeclocycline

Symptomatic Hyponatremia CNS symptoms often respond to modest increases in sodium (<5%) Initial rate 1-2 mmol/L until symptoms resolve Then 8 mmol total in first 24 hrs. Then 10 mmol in next 24 hrs.

Severity of Symptoms Moderately severe: nausea without vomiting, confusion, headache, Severe: nausea with vomiting, cardio- respiratory distress, abnormal and deep somnolence, seizures, coma Glasgow < 8

Severe Symptoms – 1st hour 150 ml of 3% saline over 20 min Check serum sodium after 20 min while starting second 150 ml bolus of 3% Repeat up to 2 more times until a rise of 5 mmol/l is acheived

Severe Symptoms – f/u care f/u care if improvement in symptoms after 5 mmol/L increase is achieved Stop hypertonic saline Start a diagnosis specific treatment Limit rise in sodium to no more than 10 mmol/L in first 24 hrs, and no more than 8 mmol/L in subsequent days till reach 130 Check Na every 6 and 12 hrs and then daily

Severs symtoms – f/u care f/u care if no improvement in symptoms after 5 mmol/L rise in first hour of treatment Continue 3% saline IV aiming for an increase in 1 mmol/h rise in sodium Stop IV if symptoms improve, a rise in sodium of 10 mmol/L occurs, or sodium reaches 130 check sodium q4hrs during hypertonic drip

Rate of 3%– Adrogue-Madias To achieve 1 mmol/L per hr increase Change Na = infusate Na – serum Na/TBW + 1 Include any potassium if in the infusate, i.e. infusate Na + infusate K TBW = .6 X body weight in men = .5 X body weight in women

Correction Example Chg in Na/L of fluid=IV Na – Pna/TBW+1 3%saline = 513 mmol/L Vol IV = desired change/expected chg 1L Rate infusion = Vol/time

Correction Example 70 kg man obtunded Na = 110 Goal inc Na by 4 mmol/L 513 – 110 / 42+1 = 9.37 with 1L of 3% Vol of 3% = 4/9.37 = 400cc Rate = 400cc / 2hrs = 200 cc/hr of 3%

Moderate Symptoms 150 cc of 3% saline over 20 min Aim for a 5 mmol/L increase in Na over 24 hours Limit rise in sodium to no more than 10 mmol/L in first 24 hrs, and no more than 8 mmol/L in subsequent days till reach 130 Check Na after 1, 6 and 12 hrs and then daily

Acute hyponatraemia w/o symptoms Cause specific treatment A single dose of 150 ml of 3% saline over 20 min, only if the acute decease in serrum sodium exceeds 10 mmol/L

Chronic Hyponatremia w/o symptoms Mild hyponatremia 130 – 135 no treatment soley to increase sodium Moderate (125 – 129) and severe (< 125) avoid an increase of more than 10 mmol/L in first 24 hrs and no more than 8 mmol/L each subsequent 24 hrs till reach 130 Check sodium every 6 hrs till sodium has stabalized

Expanded extracellular volume No treatment with sole aim of increasing sodium in mild and moderate cases Fluid restriction to prevent further fluid overload

SIADH In moderate and profound cases – fluid restriction is first line tx 2 choices for second line therapy a) Combination of low dose loop diuretic and oral salt tablets b) increase solute load with 0.25 – 0.5 g/d of urea

Reduced circulating volume 0.9 % saline infusion at 0.5 – 1.0 ml/kg per H In case of hemodynamic instability the need for rapid fluid resuscitation overrides the risk of an overly rapid increase in serum sodium concentration

Overcorrection Prompt intervention for sodium rise > 10 mmol/L for the first day and 8 mmol/L for following days Start an infusion of 10 ml/kg of free water over 1 hour Consider IV desmporessin 2 micrograms, not more frequently than every 8 hours

Correction There is no substitute for frequent monitoring of the sodium response

Hypernatremia All forms of hypernatremia are associated with hyperosmolarity Volume status cannot be inferred from the presence of hypernatremia

Symptoms CNS invovlement – lethargy, irritability, weakness, confusion – usually occur with sodium greater than 160

Etiology

Low ECF Volume

Correction of Hypernatremia Rate of correction .5 mmol/L/hr Severe Vol depletion or hemodynamic instability merits tx with .9NS Lesser degrees of volume depletion can be treated with ½ or ¼ normal saline Once volume is corrected can use D5W

Correction Example 70 kg female Na 170 stable vitals Goal 12 mmol/L over 24 hrs with D5W 70kg X .4 = 28L of body water Chg Na 1L D5W = 170-0/28+1 = 5.86 mmol/L Vol of D5W = 12/5.86 = 2.04L Rate = 2.04L/24hrs = 80 cc/hr No accounting for ongoing losses

Potassium Hypo and hyper kalemia results from alterations in intake, cellular shifts or alterations in elimination

Hyperkalemia Etiology Transcellular Shift Exercise, hyperchloremic metabolic acidosis, Insulin deficiency, hypertonicity, alpha adrenergic stimulation, tissue breakdown/ischemia (rhabdo, brain, gi)

etiology Decreased renal excretion – CRF, Hypoaldo (meds i.e. ACE/ARB, NSAIDs, heparin. Type 4 RTA

Etiology Pseudohyperkalemia ischemic/traumatic blood draw,increased wbc/plts (100,000 400,000)

Hyperkalemia Sx: neuromuscular weakness and cardiac conduction problems Level of K at which problems occur is very variable between patients

Etiology Increased Total Body K increased intake (rare as sole cause) decreased renal excretion Spurious – Thrombocytosis, Leukocytosis, ischemic blood draw

Diagnosis Normal to High 24 hr urinary K >40 meq/d relative increase in K intake Low 24 hr urinary K < 20 – 40 meq/d Decreased renal K excretion GFR < 20 ml/min endogenous K load drugs that impair K excertion

Diagnosis Low 24 hr urine K – GFR > 20 ml/min decrease mineralcorticoid production/action Action – pseudohypoaldo type 1 or 2 Acquired ARB, aldactone, amiloride, sickle cell, obstruction Production - Hypoaldo, ACE, Heparin,

Diagnosis Decreased distal nephron sodium delivery Heart failure, cirrhosis, volume depletion

hypokalemia Mild is asymptomatic (3.0 – 3.5) Sever muscle weakness,pain can cause rhabdo prominent U waves diminished or inverted T waves ST depression leads to v-fib

Hypokalemia - Etiology Shift Alkalemia, insulin, refeeding, thyrotoxicosis, Hypokalemic perodic paralysis, Barium Decreased Total Body K Decreased intake Increased Loss GI or Renal Spurious – Extreme leukocytosis

Diagnosis Low 24 hr K loss < 20 mEq/d Extrarenal metabolic acidosis – GI loss Diarrhea normal pH – decreased intake metabolic alkalosis – GI Loss Vomiting

Diagnosis High 24 hr urine K >20 mEq/d Metabolic alkalosis low Urine Cl vomiting/diuretics High Urine Cl – Hpertension Nl Aldo – Cushing/Liddle/Appatent Mineralcorticoid excess High Aldo – 1 hyperaldo/GRA - normal/low BP – Bartter/Gitelman

Etiology Met Acidosis Proximal or distal RTA Variable pH Magnesium depletion Anionic drugs