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Renal > Hypernatremia > Flashcards

Hypernatremia Flashcards

1
Q

Definition?

A

An electrolyte imbalance consisting of a rise in serum sodium concentration. Hypernatraemia is defined as a serum sodium concentration of >145 mmol/L

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2
Q

RF?

A
  • Dehydration
  • Infancy
  • Old age
  • Renal concentrating defect
  • GI disorders
  • Insensible water losses
  • DI
  • Drugs
  • Large salt intake
  • Traumatic brain injury
  • Primary hypodipsia
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3
Q

DDX?

A

spurious

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4
Q

Epidemiology?

A

Age: Infants/older pts
Sex:
Ethnicity:
P:

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5
Q

Aetiology?

A

Hypovolaemic
euvolaemic
hypervolaemic

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6
Q

hypovolaemic?

A
  • Description:high serum Na+levels with decreased extracellular volume as a result of hypotonic fluid loss
  • Extrarenal cause(manifests witholiguriadue todehydration)
    • Gastrointestinal loss(e.g.diarrhea, vomiting, drainage from nasogastric tubes,fistula)
    • Dermalfluid loss (e.g.,burns,excessive sweating)
    • Third-spacing(peritonitis,ascites)
  • Renal cause(leads todehydrationdue topolyuria)
    • Diuretics
    • Osmotic diuresis(e.g.,hyperglycemia,mannitol,uremia,high-proteintube feeding,osmotic diuretics)
    • Recovery (polyuric) phase ofacute tubular necrosis
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7
Q

euvolaemic?

A

• Description: high serum Na+levels with normal or minimal changes in extracellular volume as a result of pure water deficit
• Extrarenal causes(manifests witholiguriadue to decreased water intake)
• Lack of access to water
○ Altered mental status (e.g.,dementia, drug-induced)
○ Immobilization
○ Physically restrained patients
○ Quadriparesis
• Impaired thirst mechanism: primary hypodipsia
• Mechanical ventilation
• Renal cause(causes increased thirst due topolyuria)
• Diabetes insipidus
○ Central: complete or partial lack ofADHsecretion
○ Nephrogenic: complete or partial resistance to the action ofADH

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8
Q

Hypervolaemic?

A
  • Description: high serum Na+levels with increased extracellular volume as a result of intake of hypertonic water or retention of sodium in excess of water
  • Extrarenal causes(initially manifests withpolyuriadue to fluid overload, followed bydehydrationdue topolyuria)
    • Iatrogenic: excessive infusion of NaCl,sodium bicarbonatesolutions, or hypertonic saline;hemodialysis
    • Seawater consumption
  • Renal causes(causeshypertensionandhypokalemiawith normalurineoutput and no fluid overload)
    • Primary hyperaldosteronism
    • Cushing syndrome
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9
Q

CP?-acute?

A 
Symptoms are primarily neurological and depend on the severity of hypernatremia.
• Mild symptoms:signs ofdehydration
	• Decreased salivation
	• Drymucous membranesandskin
• Moderate symptoms
	• Confusion
	• Irritability, restlessness
	• Lethargy
	• Muscle weakness
	• Hyperreflexia
• Severe symptoms: typically occur only withsevere hypernatremia (serum concentration> 160 mEq/L)[2]
	• Focal neurological deficits
	• Seizures
	• Altered consciousness
	• Stupor
	• Coma
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10
Q

CP-chronic?

A
  • Often asymptomatic or nonspecific, mild symptoms
  • Commonly:signs ofdehydration(especially inhypovolemic hypernatremia)
  • Rarely: irritability,anorexia, nausea, weakness, and/or altered mental status
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11
Q

CP GI Loss?

A

diarrhoea
n and v
NG tube
enteric fistula

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12
Q

CP Skin?

A

febrile
burns
increased sweating

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13
Q

CP dehydration

A

vulnerable
immobile
ENT
Incorrect fluids

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14
Q

CP Impaired thirst

A

elderly
dementia
no change in recent fluid intake

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15
Q

excessive salt intake

A

iatrogenic

ingestion

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16
Q

Patho?

A
  • Either losing more water than sodium or gaining more sodium than wate-increased sodium conc-draws water out
  • Chronic-osmotically active particles are generated to stop water from moving out
  • Acute-no adaptation-water leaves-shrivel
  • Dehydration-thirst is increased
  • Central DI-no signal from hypothalamus to release ADH and increase absorption in the DCT/CD-can drink more water
  • Nephrogenic DI-receptors in CD don’t respond to ADH release-drink more water
  • Damage to thirst water-no response
  • Sodium gain
  • IV fluids
  • Increased diet
  • Precipitated by worsening kidney function
17
Q

Investigations-first line

A
  • History and exam
  • Electrolyte panel-high sodium, urea, creatinine,hypokalaemia
  • Urine osmolality
    • High UOsm(> 600 mOsmol/kg) supports an extarenal mechanism.
    • Low UOsm(< 600 mOsmol/kg) supports an intrarenal mechanism.
  • Serum osmolality-hyperosmolality
  • Urine electrolytes
    • UNa< 20 mEq/Lsupportshypovolemia.
    • UNa> 100 mEq/Lsupports sodium overload
  • Urine flow rate-to help calculate electrolyte-free water excretion
18
Q

Investigations second line

A
  • Desmopressin challenge test-DI
  • AVP level-low
  • MRI or CT brain-pituitary adenoma
  • Find underlying cause
19
Q

What is free water deficit?

A

ideal serum Na

20
Q

Electrolytes free water ?

A

Vx (1- Urinary sodium and potassium/ plasma sodium)

21
Q

Management fluids?

A
  • Give water orally if possible. If not, give glucose 5%ivslowly (1L/6h) guided by urine output and plasma Na+. Use 0.9% salineivif hypovolaemic, since this causes less marked fluid shifts and is hypotonic in a hypertonic patient.
    • Avoid hypertonic solutions.
    • Some physicians recommend an initial rate of approximately 3-6 mL/kg/hour (acute hypernatraemia) or 1.35 mL/kg/hour (chronic hypernatraemia)
    • Serum sodium correction rate: in patients with severe symptoms (e.g., neurological symptoms), the serum sodium concentration should be lowered by 2 mmol/L/hour in the first 2-3 hours, followed by a correction rate of 0.5 mmol/L/hour thereafter.
22
Q

Management next?

A
  • Treatment of the underlying cause (e.g., giving insulin, treating renal failure/obstructive uropathy, treating nausea/diarrhoea/fever) should be a priority.
  • Causative medications (e.g., mannitol, loop diuretics, activated charcoal/sorbitol) should be ceased.
  • Monitoring
    • Frequent measurement of the serum sodium concentration (e.g., every 1-2 hours for acute hypernatraemia or every 4-6 hours for chronic hypernatraemia until stable, then every 12-24 hours) is necessary to make sure that levels are returning to the correct range at the desired rate.
    • Urine sodium concentration, urine osmolality, and urine output.
    • Serum electrolytes should also be monitored to assess for electrolyte imbalances (e.g., hypokalaemia)
    • serum glucose to assess for treatment-related hyperglycemia (if dextrose-containing solutions are used).
23
Q

Management second line?

A

• Desmopressin- Central DI

Thiazide-Nephrogenic DI

24
Q

Managment Third line?

A

RRT

25
Q

Prognosis?

A
  • MR 32-70%
  • Hospital-acquired is worse
  • Severity worse than duration
26
Q

Complications?

A 
• Treatment-related brain oedema
• Treatment releated hyperglycaemia
• Myelinolysis
• Rhabdomyolysis
• Cardiac toxicity
Metabolic effects
27
Q

Complications?

A 
• Treatment-related brain oedema
• Treatment related hyperglycaemia
• Myelinolysis
• Rhabdomyolysis
• Cardiac toxicity
Metabolic effects

Renal (14 decks)

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