oncological emergency (siadh) february 19, 2003...oncological emergency (siadh) february 19, 2003...
TRANSCRIPT
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Oncological emergency
(SIADH)
February 19, 2003
Harmesh R. Naik, MD.
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Oncologic emergency
SIADH
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SIADH: Actual case-1
70 year old female
Lethargy, weakness
On Lasix
CT head: negative
Sodium: low
Chest x-ray: Lung mass
E. Coli UTI
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SIADH: Actual case-1
CT Chest (11-17-03):
1.5 cm left lung mass
5.5 x 3 cm mediastinal mass
Biopsy: Small cell lung cancer
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SIADH: Actual case-1
Sodium, serum: 117
Urine sodium: 52
Serum osmolality: 238 mmol
Urine osmolality: 361 mmol
U. Osm>S. Osm
Urine is inappropriately
concentrated compared to
serum
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SIADH: Actual case-1
CT Chest (11-17-03):
1.5 cm left lung mass
5.5 x 3 cm mediastinal mass
CT Chest (1-14-03 post 3 cycles
of chemotherapy):
1 cm left lung mass
2 cm mediastinal mass
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SIADH: Actual case-1
Pre-treatment Post-treatment
Small cell ,lung cancer-lung mass
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SIADH: Actual case-1
Pre-treatment Post-treatment
Small cell lung cancer-mediastinal adenopathy
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SIADH: Actual case-1
Pre-treatment Post-treatment
Small cell lung cancer-liver metastases
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SIADH: Actual case-1
11-16-2002: Na 117
11-19-02: Na 126
11-20-02: Na 125
11-22-02: Na 119
11-25-02: Na 122
12-09-02: Na 133
12-16-02: Na 146
1-27-03: Na 140 (post 3 cycles)
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SIADH: Actual case-1
115
120
125
130
135
140
145
150
Na level
CHEMOTHERAPY
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SIADH
Syndrome of
inappropriate secretion
of anti-diuretic hormone
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SIADH
First described in two lung
cancer patients in 1957
Hypothesis: Abnormal
production of ADH or ADH like
substance
In 1968 ADH was extracted from
cancers confirming the
hypothesis
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SIADH
Observed in 1-2% of cancer
patients
3-15% of small cell lung cancer
patients have the syndrome
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SUBCLINICAL SIADH
Ectopic production of ADH is
more common (without SIADH)
in up to 40% of lung cancer
patients
Majority of small cell cancers
stain positive for ADH (Arginine
Vasopressin )
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ADH (anti-diuretic hormone,
Arginine Vasopressin )
Released by posterior pituitary in response to increase in plasma osmolalaity or decrease in plasma volume
It increases water resorption from renal collecting tubules and concentrates the urine
Volume repletion inhibits ADH secretion
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SIADH: Mechanism
Inappropriate secretion of anti-
diuretic hormone of central
origin
OR
Ectopic production of anti-
diuretic hormone (or ADH type
substance)
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SIADH: Pathophysiology
Unregulated ADH production results in ADH binds to receptors in renal
collectiong ducts and ascending loop of henle
Increased sodium delivery to distal nephron
Water retention by kidney
Increase in renal perfusion
Decreased resorption of sodium in proximal tubule
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SIADH: Pathophysiology
End result
Increased total body water
Increase in plasma volume
Inability to excrete maximally
dilute urine in presence of low
serum osmolality
ADH secretion continues
despite low plasma osmolality
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SIADH: Patterns of ADH
concentration
Erratic ADH release
In 37% case
ADH release is independent of
osmotic control
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SIADH: Patterns of ADH
concentration
Reset Osmostat
In 33% case
Abnormally low threshold for
ADH release
At very low sodium level,
patients can produce maximally
dilute urine
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SIADH: Patterns of ADH
concentration
ADH leak pattern
In 16% case
Sustained ADH production
below the threshold
Normal ADH release in
response to osmotic challenge
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SIADH: Patterns of ADH
concentration
Normal ADH level
14% patients Failure to dilute
urine despite normal ADH levels
Mechanism not understood
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SIADH: Patterns of ADH concentration
0
2
4
6
8
10
12
14
16
100 120 200 250 280 290 300 320
plasma osmolality
pla
sma
AD
H
Normal
Erratic ADH Reset osmostat
ADH leak
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Ectopic ANP induced
hyponatremia
Atrial natriuretic peptide is
released by atria
Excess ANP may produce
syndrome similar to SIADH
Small cell cancer may have
excess levels of ANP producing
hyponatremia (with normal ADH
levels)
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SIADH: Symptoms
Asymptomatic
Neurological changes: memory loss, apathy, loss of thinking, lethargy, confusion, focal findings (Na level 120-125 meq)
Fatigue, anorexia, myalgia
Seizures and coma and death if Na is <115 (medical emergency).
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SIADH: Symptoms
Factors determining the
symptoms:
Level of sodium
Rapidity of sodium decline
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SIADH
Diagnosis is suspected because
of low sodium level
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Hyponatremia
Hyponatremia
Hypervolemic Euvolemic Hypovolemic
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SIADH: Differential diagnosis of
hyponatremia (Hypervolemic)
Excess sodium and water
Excess ECF volume (edema)
Liver disease-cirrhosis
Congestive heart failure
Nephrotic syndrome
Renal failure
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SIADH: Differential diagnosis of
hyponatremia (Hypovolemic)
Deficit of sodium and water-volume depletion
Renal losses
Diuretic excess
Salt losing nephritis
Osmotic diuresis (mannitol, glucose, urea)
Extra-renal losses
Vomiting, diarrhea, pancreatitis
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SIADH: Differential diagnosis
of hyponatremia (Euvolemic)
Hypothyroidism
Adrenal insufficiency
SIADH
Drugs
Pain
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SIADH: Physical exam
Determine volume status (fluid
overload, euvolemic or volume
depletion)
Neurological findings sometimes
focal
Signs of primary cancer
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SIADH
Establish the diagnosis
Lab work is the key to diagnosis
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SIADH: Diagnostic tests
Serum and urine electrolytes
and osmolality
Less than maximally dilute urine
with low p. osmolality (water
intoxication)
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SIADH: Diagnostic criteria
Euvolemic status
Normal renal, thyroid, pituitary
and adrenal function
Serum hyponatremia (< 135
meq)
Urine sodium >20 mmol/L
High urine Osm (>500 mosm)
Low plasma Osm (<280 mosm)
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SIADH: Laboratory features
Low sodium and low uric acid are almost only abnormalities in electrolytes
Suspect additional complications for any additional electrolyte abnormalities (eg. Hypokalemia—ACTH production, Hypercalcemia—bone mets or ectopic PTH like)
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SIADH: Etiologic work up
Determine the etiology of SIADH
Chest x-ray
Many times cancer diagnosis is
obvious
Sometimes cancer is diagnosis
of exclusion
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SIADH: Causes
Malignancy
CNS disease (CNS metastases,
infections, trauma, bleeding)
Pulmonary diseases (cancer,
TB, abscess, pneumonia)
Drugs (Cytoxan, Morphine,
Vincristine, diuretics,
Amitriptyline etc.)
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SIADH: Common cancers
Small cell lung cancer (60%)
Carcinoid tumors
Pancreatic, esophageal, colon cancers
Prostate cancer
Bladder cancer
Adrenal carcinoma
Hodgkin’s disease, AML
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SIADH and Cancer prognosis
Not an indicator of poor
outcome
Not an indicator of disease
burden
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SIADH: Acute therapy goals
Slow correction at 0.5-1 meq/l/hr
Increase sodium to no more than 20-25 meq/48 hours from the baseline
Target sodium level 125-130 meq/L
Na needed =(desired serum Na-measured Na) x kg body weight x 0.6
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SIADH: Acute therapy
Induced diuresis (N. Saline with
Lasix)-replace electrolytes
3% Hypertonic saline-for coma
or seizures
Central pontine Myelinolysis if
correction is >2meq/l/hr
Acute therapy for CNS or other
cancer
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Central pontine Myelinolysis
Symmetrical focal myelin
destruction in basal central pons
Follows 1-3 days of
hyponatremia followed by rapid
correction over 20 meq/L
Flaccid or Spastic quadriparesis
Meticulous maintenance of
electrolytes may reverse it
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SIADH: Chronic therapy
Treat the underlying tumor
Fluid restriction (<0.5-1 L/day)
Demeclocycline PO 300-600-1200 mg/day
Induces renal resistance to ADH and allows free water excretion (reversible nephrogenic diabetes insipidus)
Lithium salts-less reliable
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SIADH and Status of cancer
Hyponatremia correlates with
the activity of cancer
May serve as a marker
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SCLC and SIADH-case-2
(lung, adenopathy, liver mets)
110
115
120
125
130
135
140
145
m 1 m 6 m 7 m-8-1 m-8-2 m-8-3 m 9
Na+ level
Diagnosis
Chemotherapy
completed Local chest
recurrence
Radiation Recurrent
Liver mets
Hospice