Nephrology: Hypo and Hypernatremia (Exam 2)

What are approaches for treatment fo chronically hyponatremic patients with moderate or no symptoms?

1) fluid restriction 2) loop diuretics + sodium chloride 3) Vasopressin receptor antagonists 4) isotonic saline

How might symptoms vary in hyponatremia?

1)Absent symptoms - usually with Serum [Na+] > 120 mmol/L 2)Mild to moderate symptoms - non-specific, neurological 3)Severe symptoms - seizures, coma, respiratory arrest

What are the guidelines for duration of sodium imbalance?

1)Acute or hyperacute (< 24 hours) 2)Subacute (>24, <48 hours) 3)Chronic (> 48 hours or unknown)

What is the treatment for acute asymptomatic treatment of hyponatremia?

1)Acute, asymptomatic: Can give hypertonic saline bolus (50 - 100 mL) and observe for increase in serum sodium; repeat as needed

What is the treatment for acute symptomatic hyponatremia?

1)Emergent therapy (acute, symptomatic): Can give hypertonic saline (3% Saline) 100 mL bolus and can repeat every 10 - 15 minutes as needed. You must continue to monitor neurological status and chemistry closely

What are the different severities of hyponatremia?

1)Mild hyponatremia: 130 - 135 meq/L 2)Moderate hyponatremia: 121 - 129 meq/L 3)Severe hyponatremia: <120 meq/L

What are possible complications of rapid correction of hyponatremia?

1)Osmotic demyelination 2)Herniation 3)Seizures

What is te treatment for severe chronic hyponatremia with symptoms?

1)Severe chronic with symptoms: Can give hypertonic saline 50 mL +/- desmopressin (1-2 mcg) - why? Will favor water reabsorption: stems sodium rise and helps place a brake on the system, effect is not long lasting, gives you more of a steady improvement in sodium instead of a rapid peak

How might hydrochlorothiazide affect sodium levels? How does this compare to loop diuretics?

Can lead to hyponatremia especially at higher doses 1)Thiazides act in the cortex of the distal tube and therefore do not interfere with the medullary function 2)May promote water permeability and reabsorption in the inner medullary collecting duct 3)Excretion of sodium and potassium in the urine 4)Can activate ADH through intravascular volume depletion Loop diuretics - less likely to induce hyponatremia, because they interfere with the medullary gradient and therefore reduce responsiveness to ADH

}Our patient is a 35 year old gentleman, with a history of depression and obsessive compulsive disorder (OCD), who presents to the emergency department for evaluation of a mild headache and generalized fatigue over the past 24 hours. He is accompanied by his spouse, who states that his OCD has been "acting up" this month and that his psychiatrist recently increased his sertraline (Zoloft) dose. She describes her husband has been trying to "loose weight and cleanse his system" with "lots of water and vegetable shakes" for the past two weeks. Labs are attached, what additional tests should be ordered and what is the differential diagnosis?

Chloride low Sodium level is low (hyponatremic) Low potassium Normal kidney function Additional studies: serum osmolality, glucose levels Differential: SIADH (urine osmolality elevated), sodium wasting, primary polydipsia (last 2 would cause dilute urine osmolality)

How is orthostatic hypotension defined?

Decrease in SBP by > 20 and DBP by > 10 with upright position and increased heart rate > 100 bpm

When should a patient with hyponatremia be admitted?

General rule, if the hyponatremia is acute and/or if there are any symptoms - admit If it is chronic and the patient is asymptomatic, can usually manage as an outpatient

Define hyper and hyponatremia

Hyponatremia: serum sodium is too low Hypernatremia: serum sodium is too high (normal range of 135 - 145 mmol/L)

What is the approach of initial treatment for exercise associated hyponatremia?

Infusion of 100 mL 3% Saline solution, via IV bolus over 10 minutes, then reassess Use D5W if overcorrection occurs

You are the night float intern at St. John's Riverside Hospital. Your colleague from the day shift requested that you follow up a pending chemistry on her patient, John Doe. Mr. Doe is a 72 year old gentleman with a history of hypertension, diabetes mellitus an coronary artery disease, who presented with progressive shortness of breath and worsening ankle edema. In the emergency department, he was noted to have bilateral pleural effusions. An EKG revealed NSR and LVH, without acute ST changes. He had 2 negative troponin tests, collected 8 hours apart. An echocardiogram revealed cardiomegaly, LVH and an left ventricular EF of 35%. He received 40 mg of furosemide intravenously 3 hours prior to the collection of the chemistry, with some clinical improvement. What is the most likely diagnosis?

Left sided heart failure decompensation

What is the function of ADH?

Promoted H2O reabsorption; reduces urine volume, increases concentration. stimulated by low blood volume

Be familiar with sodium and water handling in the nephron

Proximal convoluted tubule is where the majority of sodium is reabsorbed H2O reabsorption picks up after loop of henle into collecting duct This allows gradient that allows reabsorption

Label the approach to hyponatremia

Spent alot of time on this, be able to label well Thiazide diuretics most common cause of idosyncratic drug reaction

You are an intern in a local emergency department. You are asked to see a 78 year old gentleman with a history of advanced dementia, who was brought to the emergency department for evaluation of worsening weakness and lethargy. Initial evaluation reveals a blood pressure of 90/60, HR: 88 R: 16 and oral temp of 99 F. He is 60 kg. Upon physical exam, he is noted to have dry oral mucosa and scattered rhonchi in the right base. His CXR appeared as follows:

Suspect pneumonia

What is the goal of emergent treatment of hyponatremia?

The goal is to increase the serum sodium quickly, by 4- 6 meq/L over 2-3 hours. You do not want to exceed correction of > 8 meq/L in 24 hours Want to correct enough to avoid brain herniation

Be familiar with the following

Water moves out when interstitial space is hyperosmotic numbers may change relatively speaking due to loop and thiazide diuretics (loop increases uptake later on in tubule although it inhibits in LOH)

What must sodium be corrected for?

glucose

When is hyponatremia of clinical significance?

only when it reflects corresponding hypoosmolality of the plasma The presence of significant hypoosmolality always indicates excess water relative to solute in the extracellular fluid compartment Hyponatremia and hypoomolality are usually synonymous, except in cases of pseudohyponatremia (high lipids or protein) and/or high concentrations of effective solutes other than Na+ Posm (mOsmol/kg H20) = 2 x serum [Na+](mEq/L) + glucose (mg/dL)/18 + BUN (mg/dL)/2.8

What patients with hyponatremia need emergent therapy?

those with severe symptoms (seizure, LOC) acute hyponatremia with ANY symptoms hyperacute hyponatremia from water intoxication symptomatic patients who are post-op hyponatremia associated with intracranial pathology