Transcript acid-base problems

Diagnosis and Treatment of
Hyponatremia
Acute: Symptomatic
Chronic: Asymptomatic
Thomas DuBose,M.D.
Professor and Chair, Internal Medicine
Wake Forest University School of
Medicine
Hyponatremia: ICU
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Pseudohyponatremia
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Hyperglycemia, Hyperlipidemia
Post-operative Hyponatremia
SIADH
Cerebral Salt Wasting
Mechanical Ventilation
Cirrhosis
Congestive Heart Failure
SIRS/MODS
Loop diuretics with hypotonic fluid replacement
Certain drug intoxications
Agents that enhance ADH release or action
Major Causes of Hyponatremia
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EIVF Depletion
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SIADH
Hormone mediated
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Adrenal Insufficiency
Hypothyroidism
Pregnancy
Disorders in which ADH levels may be appropriately
suppressed
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True Volume Depletion
CHF or Cirrhosis
Advanced renal failure
Primary polydipsia
Beer drinker’s potomania
Pseudohyponatremia
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High plasma osmolality: hyperglycemia, mannitol, urea
Normal plasma osmolality: hyperlipidemia,
hyperproteinemia, glycine infusion.
Steps in the Evaluation of
Hyponatremia
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Calculate plasma osmolality
Measure plasma osmolality
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Evaluate volume status of patient
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When low; defines true hypo-osmolal state or
clinical hyponatremia
Consider plasma glucose, protein and lipids
Volume depletion
Volume expansion
Euvolemia
Measure urine sodium
Estimating the Serum Osmolality
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2[Na ]p 
BUN
2.8
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GLUCOSE
18
In Spurious Hyponatremia:
Calculated OSMp < Determined OSMp
 Spurious Hyponatremia
(hyperlipemia, hyperproteinemia) is
not a hypoosmolar state.
Causes of Hypoosmolality
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Volume Depletion
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Volume Expansion
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GI, lung or skin losses
Third space sequestration
Adrenal insufficiency
Renal salt wasting
Cerebral salt wasting
CHF, cirrhosis with ascites, nephrotic
syndrome
Euvolemic
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SIADH, water intoxication, reset osmostat,
drugs
Antidiuretic Drugs
Antidiuretic hormones:
Vasopression
Oxytocin
Diuretics:
Thiazides
Furosemide
Ethacrynic acid
CNS-active drugs:
Vincristine
Carbamazepine
Psychotropic drugs
Inhibitors of prostaglandin synthesis:
Chlorpropamide
Salicylates
Acetaminophen
Nonsteroidal anti-inflammatory agents
COX 2 inhibitors
Others:
Clofibrate
Cyclophosphamide
Somatostatin
Ecstasy
Syndrome of Inappropriate ADH
Release (Bartter’s Criteria)
Hyponatremia and true hypoosmolality by
definition
Euvolemia clinical
Urine less than maximally dilute (urinary
osmolality usually > 200 mOsm/kg of H2O)
Normal renal, cardiac, hepatic, adrenal, pituitary,
and thyroid function
No history of antidiuretic drugs
No emotional or physical stress
Urinary sodium > 20 mEq/litera
a Urinary sodium may be <20 mEq/liter if the patient is volume deleted or on
low sodium intake.
Disorders Associated With SIADH
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Carcinomas
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Pulmonary disorders
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Central nervous system disorders
Most Common Causes of SIADH in
Elderly (CDP and NHR)*
Medications
Idiopathic
form
Malignancies
*Aging Clin Exp Res 2003, 15:6-11.
Disorders Associated With SIADH:
Carcinomas
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
Disorders Associated With
SIADH: Pulmonary Disorders
Viral pneumonia
Bacterial pneumonia
Pulmonary abscess
Tuberculosis
Aspergillosis
Positive-pressure breathing
Asthma
Pneumothorax
Cystic fibrosis
Lung cancers
Disorders Associated With SIADH:
Central Nervous Disorders
Encephalitis (viral or
bacterial
Meningitis (viral, bacterial,
tuberculosis, fungal)
Head trauma
Brain abscess
Brain tumors
Guillain-Barré syndrome
Acute intermittent porphyria
Subarachnoid hemorrhage or
subdural hematoma
Cerebellar and cerebral
atrophy
Cavernous sinus thrombosis
Neonatal hypoxia
Hydrocephalus
Shy-Drager syndrome
Rocky Mountain spotted
fever
Delirium tremens
Cerebrovascular accident
(cerebral thrombosis or
hemorrhage)
Acute psychosis
Peripheral neuropathy
Multiple sclerosis
Guiding Principles in the
Treatment of Hyponatremia
1. Neurologic disease can follow both the failure
to promptly treat as well as injudiciously rapid
treatment of hyponatremia.
2. Presence or absence of significant neurologic
signs and symptoms must guide treatment.
3. Acuity or chronicity of the electrolyte
disturbance impacts the rate at which the
correction should be undertaken.
A Prudent Approach to the
Treatment of Hyponatremia - 1
Acute Symptomatic Hyponatremia (duration < 48 hours)
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Risk for complication of cerebral edema
greater than risk of treatment of
complication.
Treat with hypertonic NaCl: 3% NaCl @ 12 mL/kg/hr or 2 mEq/L/hr. until
convulsions subside. Usually means
increasing [Na+] by 10%.
Alternative: furosemide and hypertonic
NaCl
Full correction is dangerous. Correct by
10% or to 120-122 mEq/L slowly.
Then initiate water restriction.
A Prudent Approach to the
Treatment of Hyponatremia - 2
Symptomatic Hyponatremia (Chronic or
Unknown Duration)
1. Increase serum sodium by 10%, that is, approximately 10
mEq/L and then water restrict. Usually 1 -2 mL/kg/hr
of hypertonic saline.
2. Do not exceed a correction rate of 1.5 mEq/L/hr at any
given time.
3. Do not increase serum sodium by more than
15 mEq/day.
4. Long-term
• H2O restriction
• Demeclocycline 300 - 600 mg bid
• V2 receptor antagonist? Aquaretics
Therapeutic Strategy Based On
Volume Status of Patient
 Presence of Absence of Symptoms
 Duration of Hypoosmolality
 Presence of absence of risk factors for
development of neurological
complication
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Osmotic demyelination is rare in
patients with initial Na+ > 120mEq/L
A Prudent Approach to the
Treatment of Hyponatremia - 3
Asymptomatic Hyponatremia
1. Almost always chronic.
2. Treat with water restriction regardless
of how low the serum sodium.
Calculating Sodium Requirement
in Hyponatremia
In correcting hyponatremia the approximate expansion of total
body water must be determined first by calculating the volume of
water which was required to dilute the serum sodium
concentration to its observed value. For example, in a 70 kg patient
with a serum Na+ concentration of 120 mEq/L rather than 140
mEq/L, this calculation is made as follows:
Body water in normal state = (70 kg) (0.60) = 42 L
Body water in abnormal state = (x) (120) = (42)(140) = 49L
Excess body water = 7 L
The amount of Na+ in milliequivalents required for correction
can then be calculated; again it is necessary to assume Na+ is
distributed throughout the total body water.
(140-patient’s - Na+) (calculated total body water) = total Na+
requirement.
How to predict the effect of therapy on
the patient’s serum sodium
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[Na
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[Na
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Bot
[Na ] Pa tien t
TBW  1
The Bottle:
0.9% = 154 mEq/L
Ringer’s = 130 mEq/L
0.45% = 77 mEq/L
3% = 513 mEq/L
Diagnosis and Treatment
of Hypernatremia
Steps in Evaluation of Hypernatremia
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Establish history of water intake, and
integrity of thirst mechanism
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Severe hypernatremia is unusual unless
thirst mechanism is defective or water
is not available to the patient.
Determine patient’s volume status
 Measure urine sodium concentration
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Causes of Hypernatremia
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Volume Depletion
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Volume Expansion
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Urine Na+ < 20: sweating, diarrhea, burns
Urine Na+ > 20: Renal losses: Hyperglycemia,
mannitol, urea (osmotic diuresis), or intrinsic
renal disease
Urine Na+ > 20: Salt loading, Cushing’s
syndrome, NaHCO3, hypertonic dialysis
Eulovemic
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Urine Na+ < 20: Fever, heat exhaustion,
hypermetabolic state
Urine Na+ variable or > 20: Central DI,
Nephrogenic DI
Diuretic Drugs
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Alcohol
Diphenylhydantoin
Lithium
Demeclocycline
Acetohexamde
Tolazamide
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Glyburide
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Propoxyphene
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Amphotericin
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Methoxyflurane
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Norepinephrine
Patient Groups at Increased
Risk for Hypernatremia
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Post craniotomy (sellar tumors)
Elderly, nursing home residents
Hypertonic infusions
Tube feedings
Osmotic diuretics
Lactulose
Mechanical ventilation
Diabetes mellitus with poor glycemic control
Polyuric disorders
Diabetes Insipidus
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Central DI
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Failure to synthesize or secrete ADH
 Unable
to concentrate urine with water
deprivation (caution !)
– 3% decrease in BW or increase in Posm
to 295 normally results in increase in
Uosm > 700
– Submaximal response: give ADH
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Central DI Uosm will increase by 100% or
more
Therapeutic Regimens for the
Treatment of Diabetes Insipidus
Drug
Complete central
dDAVP
diabetes insipidus
Partial central
Vasopressin
diabetes insipidus
tannate
Aqueous
vasopressin
Chlorpropamide
Clofibrate
Carbamazepine
Nephrogenic
Thiazide
diabetes insipidus
diuretics
(NDI)
NSAIDS
Dose
10-20 mg intranasally
q 12-24 hr
2-5 U IM q 24-48 hr
5-10 U SQ q 4-6 hr
250-500 mg/day
500 mg tid-qid
400-600 mg/day
Conventional doses
Conventional doses
Amiloride (for
5 mg qd
lithium-related
NDI)
Nephrogenic Diabetes Insipidus
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Does not respond to AVP
Causes:
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Congenital NDI - AVPR2 or AQP2 mutation
Hypokalemia
Hypercalcemia
Drugs: Lithium, demeclocycline, glyburide,
colchicine, amphotericin B
Treatment:
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Thiazides
Reduce solute intake (low Na+ diet)
NSAIDS
Treatment of Symptomatic
Hypernatremia
1. Drop Na+S by 2 mEq/L/hr.
2. Replace 50% of water deficit over 12-24
hrs.
3. Replace rest over next 24 hrs.
4. Perform serial neurological exams.
5. Decrease rate of correction when patient
improved.
6. Measure Na+ in serum and urine q 12 hrs.