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Hyponatremia. Why hyponatremia important ?. Common electrolyte abnormality- inpatient and outpatient Up to 15 % of inpatients 1 Acute- 8.4% in childen 55% in adults Chronic 14-27% 1. Baylis PH. Int J Biochem Cell Biol . 2003;35:1495-1499. Important cause of mortality

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why hyponatremia important
Why hyponatremia important ?
  • Common electrolyte abnormality- inpatient and outpatient
  • Up to 15 % of inpatients 1
  • Acute-
      • 8.4% in childen
      • 55% in adults
    • Chronic
      • 14-27%

1. Baylis PH. Int J Biochem Cell Biol. 2003;35:1495-1499.

slide3

Important cause of mortality

  • Mortality more if hyponatremia develops after hospitalisation
  • Increased duration of hospital stay
  • Increased mortality continues even after discharge
  • Even mild hyponatremia though till now considered benign is associated with osteoporosis and fractures

Adrogué HJ. Am J Nephrol. 2005;25:240-249

Gill ,clin endocrino 2006

Clayton ,QJM 2006

European Jr of Endocrinology,2010

Manisha

definition of hyponatremia
Definition of Hyponatremia
  • Normal serum sodium level

: 135 – 145mEq/L

  • Hyponatremia is defined as a serum sodium level less than 135mEq/L
  • Severe - serum Na < 120mEq/L
clinical manifestations
Clinical Manifestations
  • Hyponatremia not a disease but a manifestation of a variety of disorders.
  • Clinical symptoms
    • hyponatremia itself
    • Disease causing hyponatremia

recognition of hyponatremia incidental.

slide7

Pathogenesis

Acute

Low serum Na

More Na in brain

Water enters brain cells

Cerebral oedema

Chronic

Adaptation

slide8

Symptoms depend on

    • magnitude of the hyponatremia
    • rapidity of its development.

Asymptomatic

GI sym

Headache

Lethargy

Confusion

Obtundation

S [Na] > 125 mmol/L

or

Gradual onset

Stupor

Seizures

Coma

Rhabdomyolysis

Brain stem compressiom

Pulm oedema

Na+ level <120mEq/L

or

Rapid decrease(<48hr)

symptoms signs
Symptoms & signs
  • Gait disturbances
  • Fractures
    • reduction in total hip bone mineral density of 0.037 g/cm2 for every 1 mmol/l drop in plasma sodium concentration.

European Jr Endocrinology 2010

Manisha Sahay

slide10

Etiology -Hyponatremia

?

Hyperlipidemia

Hyperproteinemia

?

?

?

?

Hyperglycemia

Mannitol

CHF

NS

Cirrhosis

CRF

Salt wasting dz

RTA

Diuretics

Cerebral salt wasting

GI loss

3rd space loss

SIADH

GC def

Hypothyroid

Exercise ind

Psychogenic

determine if true hyponatremia
Determine if true Hyponatremia?

IA Pseudohyponatremia/Normal plasma osmolality

(275-295)

  • Hyperlipidemia - ion-specific electrodes avoid this
  • Hyperproteinemia-Multiple myeloma

IB Increased plasma osmolality /Translocational/redistributive

(osmo > 295)

  • Hyperglycemia1.6 mEq/L for every 100 mg/dL [glucose)
  • Mannitol

II. Hypoosmolalhyponatremia (serum osmolality<275mOsm/kg)

2 step check volume status
2 stepcheck volume status

Euvolemic

Hypervolemic

Hypovolemic

hypovolemic low cvp responds to ns
Hypovolemic- Low CVPResponds to NS

Low urine Na(<20 mmol/l)

High urine Na >20 mmol/l

Renal

Salt wasting nephropathy

Mineralocorticoid deficiency-high K

Osmotic diuresis-KB

Cerebral salt wasting

  • Non renal
    • Volume Depletion
      • GI, lung or skin losses -burns
      • Third space sequestration
      • CSW
      • Excess water intake

Step 3

Check renal

or non renal

Urine Na

Manisha Sahay

diuretics
Diuretics

Thiazides

  • Urine excreted- NS
  • Lose more salt than loop
  • Reason for hypoNa
    • Interfere with urine dilution
  • Common in elderly females
  • Occurs within 2-4 weeks
  • Discontinue diuretics

Loop Diuretics

  • Urine excreted 1/2 NS
  • Lose > water than thiazides
  • Reason for hypoNa:
    • Impair generation of medullary hypertonicity
cerebral salt wasting
Cerebral Salt Wasting
  • Causes: Head injury, surgery, tumors, Infections
  • Signs/symptoms:
    • Polyuria, Dehydration/hypovolemia/Hypotension
    • High urine Na > 20 mmol/L
  • Pathogenesis:
    •  renal Na loss d/tplasma ANP, BNP 
    • Volume depletion could be protective for ICP
  • Treatment:
    • Volume replacement - large volumes of NS
    • Oral Na supplementation for a period of time

Berendes Lancet 1997, Isotani Stroke 1994, Wijdicks Stroke 1991

Mather J Neuro Nsurg Psych 1981; Wijdicks Ann Neuro 1985

treatment hypovolemic hyponatremia
TreatmentHypovolemichyponatremia
  • Isotonic saline

 Restoration of euvolemia removes the hemodynamic stimulus for AVP release

 Excretion of the excess free water

slide17

Hypervolemic

Euvolemic

Hypovolemic

hypervolemic high cvp increased total body water that exceeds the increase in total body na
Hypervolemic -High CVPIncreased total body water that exceeds the increase in total body Na+

Low urine Na <20 mmol/l

High urine Na >20 mmol/l

Advanced renal failure

  • CHF
  • Cirrhosis with ascites
  • Nephrotic syndrome

Step 3

Check urine

Na

Manisha Sahayin

treatment hypervolemic hyponatremia
TreatmentHypervolemic hyponatremia

Restriction of Na+ and water intake

  • Promotion of water loss in excess of Na+
  • Vasopressin antagonists approved for use
  • Correction of underlying disorder
slide20

Hypervolemic

Euvolemic

Hypovolemic

euvolemic normal cvp
Euvolemic – Normal CVP

Normal sodium stores (N ECF) & total body excess of free water.

  • SIADH/Reset osmostat
  • Primary polydipsia
  • Hypothyroidism
  • Glucocorticoid deficiency
  • Exercise induced
  • Beer potomania
  • Post op

Step 3

All have high urine Na

U osm <100 in PP, BP

siadh bartter s criteria 60 of all euvolemic hyponatremia
SIADH (Bartter’s Criteria)60% of all euvolemic hyponatremia

Step 4

Check urine osmolality

K/Cr/ Cr/Urea/uric acid

T3/T4/TSH

Cortisol

CT as needed

  • F

Essential criteria

  • Hyponatremia
    • pl osm<275
  • Euvolemia clinical
    • u osmolality > 200 mOsm/kg
  • N renal, cardiac, hepatic, adrenal, pituitary, thyroid
  • No H/o antidiuretic drugs
  • No emotional or physical stress
  • Urinary sodium > 20 mEq/l
  • Cr N, N ABG, K+ handling

Supplemental features

  • uric acid<4
  • BUN<10
  • failure to correct hypoNa after NS infusion
  • correction of hypoNa after fluid restriction
  •  S ADH

U SP gravity can be used if u osm not possible, U osm 100= u sp gr 1.005

a

disorders associated with siadh
Disorders associated with SIADH

CNS-ADH secr

Encephalitis /Meningitis , trauma

Brain abscess/Brain tumors

GBS/Acute intermittent porphyria

Subarachnoid/subdural hematoma

Cerebellar and cerebral atrophy

Cavernous sinus thrombosis

Neonatal hypoxia

Hydrocephalus

Delirium tremens

CVA, Acute psychosis

Peripheral neuropathy

Multiple sclerosis

Pulmonary

Pulmonary abscess

Tuberculosis

Aspergillosis

Positive-pressure breathing

Asthma

Pneumothorax

Cystic fibrosis

Lung cancers

Cancers

Small cell carcinoma of the lung

Carcinoma of the duodenum

Carcinoma of the pancreas

Thymoma

Lymphoma

Ewing’s sarcoma

Mesothelioma

Carcinoma of the bladder

Prostatic carcinoma

Olfactory neuroblastoma

PULMONARY

CANCERS

CNS

drugs
DRUGS

Antidiuretic hormones:

Vasopressin,oxytocin

Diuretics:

Thiazides,furosemide,

CNS-active drugs:

Vincristine,carbamazepine,

Psychotropic drugs

Inhibitors of prostaglandin

Chlorpropamide, Salicylates,

Acetaminophen, NSAIDS,COX 2 I

Others:

Clofibrate,Cyclophosphamide,

Somatostatin

Manisha Sahay

primary polydipsia
Primary Polydipsia
  • Psychiatric disorder,  thirst with antipsychotics
  • ±Hypothalamic lesions
  • No hyponatremia unless intake >10-15 L/d, or acute 3-4 L water load
  • Urine osm below 100
  • Rx: Restrict free water ;classically rapid correction
reset osmostat
Reset osmostat
  • Can excrete water load (10 to 15 mL/kg given orally or intravenously). -excrete more than 80 percent within 4 hours
  • Mild hyponatremia
  • No treatment needed

Manisha Sahay

beer protomania low dietary solute intake
Beer protomaniaLow Dietary Solute Intake
  • Elderly, malnourished (“tea and toast” diets) -poor in solutes (Na/K)
  • Beer drinkers (high water intake, low protein)
  • Pathogenesis
    • Minimum urine osmolarity- 60 mosm/l
    • At least 600-900 msom/kg/d solute load needed to excrete water >4 l
    • Beer protomania- daily solute excretion < 250 mosmol /kg, hence maximum urine output can be <4 L day ,if more water ingested -hyponatremia
    • Urine appears dilute (osm of< 100)
  • Rx: NS, increased dietary solute
exercise associated hyponatremia eah
Exercise associated hyponatremia (EAH)

Clinical features

  • May be severe: cerebral edema, non cardiac PE

Pathogenesis

  • H2O excess; impaired renal H2O excretion
  • Nonosmolar AVP release esp if water in >out

Treatment

  • Limit water to 400-800 ml/h; drink only when thirsty
  • No role of NS, 3% Nacl if severe

JCEM 2008;93:2072-78

slide30

Investigations

History & volume status

Serum Osmolality

Urine Osmolality/sp gr

Urine Na

S Cr/urea/K

T3/T4/TSH

CXR

CT Scan

Manisha Sahay

slide31

Hyponatremia

Step1 S osmolality

N 275-295

Hyperlipidemia

Hyperproteinemia

Low<275

True

High>295

Hyperglycemia

Mannitol

Step 2 Volume

High

Hypovolemic

Euvolemia

Step3 Urine Na

Step 3 Urine Na

Step 4 U Osm/TSH/GC

< 20 mmol/l

CHF

NS

Cirrhosis

>20 mmol/l

CRF

Renal

Salt wasting dz

RTA

Diuretics

Cerebral salt wasting

Extra renal

GI loss

3rd space loss

SIADH

GC def

Hypothyroid

Exercise ind

Psychogenic

slide33

Hyponatremia

Asymptomatic

Symptomatic

Chronic

Acute <48 hrs

Chronic>48 hrs

Some immediate correction

Hypertonic saline

+ Furosemide

Change to water restriction

Frequent serum & urine electrolytes

Do not exceed 12 meq/l/d

No immediate

Correction needed

Emergency Hypertonic saline+ furosemide

Long term management

Treat etiology

Water restriction

Demeclocycline

Urea

V2 receptor antagonist

Thurman et al,Therapy in nephrology and

Hypertension,Saunders 2003

therapeutic strategy euvolemic hyponatremia
Therapeutic Strategy Euvolemic hyponatremia
  • Treatment varies with
    • Presence or Absence of Symptoms
    • Duration
    • Magnitude of Hyponatremia
    • Risk for neurological dz- young, females, elderly,menstruation
slide36
Rate of correction of hyponatremia
    • Acute
    • severe (S Na+ <115mmol/L)
    • symptomatic
    • Hypertonic (3% NaCl)
    • 0.5 mmol/l/hr or 12 mmol/l/day
    • Stop
      • if convulsions subside
      • if S Na 120 mEq/L

Kumar S, Berl T. The Lancet 1998; 352: 220-8

Adrogue HJ, Madias NE. NEJM 2000; 342: 1581-9

fluids for correction
Fluids for correction

Ringer’s = 130 mEq/L

0.45%NS = 77 mEq/L

  • 3% NaCl- 513 meq/L

0.9% NaCl- 154 meq/L

total correction in 12 hrs 6 mmol
Total correction in 12 hrs = 6 mmol
  • Volume of infusate needed =

B Wt X 0.6 X Desired increment in Na (120-114)

Infusate Na X 1.5

  • 50 kg
  • 50X 0.6x6 = 0.23 litre or 230 ml

513X1.5

230 ml in 12 hours

19 ml/hr

chronic symptomatic 48 hrs
Chronic symptomatic>48 hrs
  • 3% NaCL
    • < 0.5 to 1.0mmol/L per h
    • (<10 to 12mmol/L over first 24h)
  • Water restriction

Chronic asymptomatic > 48 hours

  • No immediate correction
  • Water restriction

Manisha Sahay

long term management euvolemic hyponatremia
Long term management Euvolemic hyponatremia
  • Water restriction
    • Free water restriction ,¾ maintenance (1 L/d)
  • Clozapine -schizophrenic patients with compulsive water drinking
  • Pharmacological agents (Long-term)
    • Demeclocycline 300 - 600 mgbd
    • Urea 15-60 gm/d
    • Lithium
    • V2 receptor antagonist- Aquaretics
avp receptor antagonists
AVP Receptor antagonists

Mechanism of action

Bind to the V2 receptors in renal collecting tubules/ducts

Vasopressin antagonist

Uses

  • Euvolemic/ hypervolemic hypo Na+; Contraindicated in hypovolemia
  • Chronic hyponatremia

not in acute hyponatremia or in patients with sNa < 115 mmol/L

as slow aquaresis

Adverse effects:

Thirst ; dry mouth

SALT NEJM 2006

vasopressin receptor antagonists
Vasopressin Receptor Antagonists

*SALT I and SALT II Trials.

slide45
CI
  • Concomitant use of vaptan and potent CYP3A4 inhibitors such as ketoconazole, itraconazole, clarithromycin, ritonavir, or indinavir is contraindicated

Manisha Sahay

central pontine myelinolysis osmotic demyelination
Central Pontine MyelinolysisOsmotic demyelination
  • Pathogenesis
    • rapid correction / overcorrection of ch hyponatremia.
    • hypoxic encephalopathy / complication of therapy
  • Prevention
    • Adequate oxygenation
    • Gradual increase in serum sodium level to 120-125 mEq/L.
  • Symptoms
    • Dysarthria, dysphagia, seizures, altered mental status, quadriparesis, hypotension ,locked in syndrome, extrapontine
    • Begin 1-3 days after correction of S Na
    • Irreversible , devastating
    • MRI diagnostic < 24 h
  • Risk factors- Hypokalemia, females,alcoholism, liver transplant
  • Treatment- Relowering S Na - hypotonic fluids, Desmopressin

dsMsh S

summarising
Summarising……

Manisha Sahay

slide48

Hyponatremia

S osmolality

N 275-295

Hyperlipidemia

Hyperproteinemia

Low<275

True

High>295

Hyperglycemia

Mannitol

Volume

High

Hypovolemic

Euvolemia

Urine Na

Urine Na

Urine Osm, S Cr,Ur,TSH

< 20 mmol/l

Extrarenal

CHF

NS

Cirrhosis

>20 mmol/l

Renal

CRF

Renal

Salt wasting dz

Diuretics

Cerebral salt wasting

Extra renal

GI loss

3rd space loss

SIADH

GC def

Hypothyroid

Exercise ind

Psychogenic

slide49

Hyponatremia

Asymptomatic

Symptomatic

Acute <48 hrs

Emergency

No immediate

Correction needed

Long term management

Hypertonic saline

Go slow

take home message
Take home message
  • Hyponatremia –a common, life theatening problem
  • Step wise evaluation important
  • Inappropriate treatment – Worse than disease

Practising is the best way of learning!!!

Manisha Sahay