Approach to the patient with electrolyte disorders Hyponatremia-Hypernatremia Zehra Eren, M.D.

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Transcript of Approach to the patient with electrolyte disorders Hyponatremia-Hypernatremia Zehra Eren, M.D.

Approach to the patient with electrolyte disorders

Hyponatremia-Hypernatremia

Zehra Eren, M.D.

LEARNING OBJECTIVES

• recall body water and fluid distribution• recall serum osmolality• recall etiology of hyponatremia and hypernatremia

• describe sing and symptoms of hyponatremia and hypernatremia

• describe laboratory findings of hyponatremia and hypernatremia

• explane treatment of hyponatremia and hypernatremia

Solute Composition of Body Water

•Predominant solutes in ECF: Sodium (Na+)Chloride (Cl−)Bicarbonate (HCO3−)

•Predominant solutes in ICF: Potassium (K+)Protein−Phosphate−

Osmolality

•Posm=2×plasma Na+ +

Glucose/18 + BUN/2.8

Osmolality

• Normal ECF osmolality: 280-290mOsm/kgH2O

• ECF and ICF are in osmotic equilibrium, at steady state

• Vasopressin (antidiuretic hormone (ADH)-osmotic stumuli-nonosmotic stumuli: HF, Cirrhosis, vomiting,

postoperative pain, pregnancy

Hyponatremia 

•Serum Na <135 mEq/L

European Society of Intensive Care Medicine (ESICM)European Society of Endocrinology(ESE) European Renal Association – European Dialysis and Transplant Association (ERA–EDTA)

Hyponatremia 

•Serum Na <135 mEq/L

Hyponatremia is a disorder of water balance

Dısorders of water and sodium balance

•Hyponatremia (too much water)

•Hypernatremia (too little water)

•Hypovolemia (too little sodium, the main

extracellular solute)

•Edema (too much sodium with associated

water retention)

Hyponatremia •almost always due to the oral or intravenous

intake of water that cannot be completely excreted

• impaired water excretion that is most often due to an inability to suppress the release of antidiuretic hormone (ADH) or to advanced renal failure

Diagnosis

• Volume status and serum osmolality are

essential to determine etiology

• Hyponatremia usually reflects excess water

retention relative to sodium rather than sodium

deficiency, the sodium concentration is not a

measure of total body sodium

• Hypotonic fluids commonly cause

hyponatremia in hospitalized patients

Differences between SIADH and

cerebral salt wasting

Sherlock M, O’Sullivan E, et all. The incidence and pathophysiology of hyponatraemia after

subarachnoid haemorrhage. Clinical Endocrinology; 2006, 64: 250–254

6.3. Which parameters to be used for

differentiating

causes of hypotonic hyponatraemia?

Clinical practice guideline on diagnosis and treatment of hyponatraemia; Nephrol Dial Transplant (2014) 0: 1–39

Symptoms and Sing of Hyponatremia

• symptoms depends on severity and acuity hyponatremia

• the symptoms reflect neurologic dysfunction induced by cerebral edema and possible adaptive responses of brain cels to osmotic swelling

• Nausea, malaise, headache, lethargy, seizures, coma, respiratory arrest

• the physical examination should help categorize the patient's volume status into hypovolemia, euvolemia, or hypervolemia.

Classification of symptoms of hyponatraemia

Clinical practice guideline on diagnosis and treatment of hyponatraemia; Nephrol Dial Transplant (2014) 0: 1–39

Adaptation of the brain to hypotonicity

Adrogue HJ & Madias NE. Hyponatremia. NEJM; 2000 342 1581–1589

Complications of hyponatraemia

Hyponatraemia with severe symptoms

7.2. Hyponatraemia with moderately severe symptoms

7.3. Acute hyponatraemia without severe or moderately severe symptoms

7.4. Chronic hyponatraemia without severe or moderately severe symptoms

7.4. Chronic hyponatraemia without severe or moderately severe symptoms

7.4. Chronic hyponatraemia without severe or moderately severe symptoms

Na+ deficit ≈ body weight X 0.6 X

(desired plasma Na+ concentration –

plasma Na+ concentration)

1mg/dl/ h10-12mg/dl /24h

Hypernatremia 

•Serum Na>145 mEq/L

Symptoms and Sings of Hypernatremia

• Dehydrated patient → orthostatic hypotension

and oliguria

• Rise in plasma Na and osmolality

→water movement out of the brain

→rupture of the cerebral veins

→focal intracerebral and subarachnoidal hemorrages

→possible irreversible neurologic damage

• Lethargy, weaknees, irritability, twitching, seuzures,

coma

• Osmotic demyelination (uncommon)

Laboratory Findings

•Urine osmolality > 400 mosm/kg → renal water-conserving ability is functioning (hypotonic fluid losses from excessive sweating, the respiratory tract, or bowel movements and lactulose)

•Urine osmolality < 250 mosm/kg → characteristic of DI

-Central DI: inadequate ADH release -Nephrogenic DI: renal insensitivity to ADH(lithium, demeclocycline, relief of urinary obstruction, interstitial nephritis,

hypercalcemia, and hypokalemia)

•Water deficit ≈ body weight X 0.6 X

(plasma Na concentration/

desired plasma Na concentration) - 1

Case 1• A 72-year-old woman from a nursing home presents to the

emergency department with a change in her mental state over the past few hours. She has a medical history of coronary artery disease and hypertension.

• Her medications include hydrochlorothiazide: 25 mg a day, and aspirin, 80 mg a day.

• On physical examination, she has decreased skin turgor, orthostatic hypotension, and disorientation to time, place, and person without focal neurologic deficits.

• Initial laboratory tests show a serum sodium level of 110 mmol/L;blood urea nitrogen 65 mg/dL; creatinine 3.6mg/dL and plasma osmolality, 278 mOsm/kg of water.

• Her serum sodium level 2 months before admission was 135 mmol/L, and her urine output was 400 mL a day.

Case2

• A 82-year-old women with Dementia, HTN and DM is admitted for work-up of hyponatremia. Her sodium has been 118 for the last 4 days.

• She is taking Paxil for depression and she is not on any diuretics.

Case 3

• A 85 year-old male presents to the emergency room with pneumonia. He has been febrile for several days and has had a cough productive of yellow sputum.

• On physical exam he is a well-developed, thin male in moderate respiratory distress. Blood pressure (supine) 120/86, pulse 74, blood pressure 115/85, pulse 70, respirations 24. Temperature was 39oC. Body weight 60 kg. Cardiopulmonary exam demonstrated decreased breath sounds at the base of the right lung.

• Sodium 120 mmol/L, Potassium 3.9, BUN 10 mg/dl , Creatinine 0.8 mg/dl, U Osmolality 500 mosm/kg,  Glucose 90 70-110 mg/dl

 • Urine Sodium 60 mmol/L,Potassium 30 mmol/L,

Case4

• A 60 year-old male with alcoholic cirrhosis presents to your office because of worsening edema.

• On physical exam the patient is a well-developed, poorly nourished, jaundiced male in mild distress due to his anasarca. Blood pressure (supine) 110/75, pulse 100, (standing) 90/60, pulse 120, respirations 23 and he was afebrile. Body weight 80 kg. Cardiopulmonary exam was unremarkable. The abdomen was remarkable for tense ascites and a shrunken liver. Lower extremities had 3+ pitting edema.

• Sodium 127 mmol/L, Potassium  3.63mmol/L, BUN 35 mg/dl, Creatinine 1.8 mg/dl, Glucose 105 mg/dl 

• Urine Sodium 6 mmol/LOsmolality 600 mosm/kg