Transcript SIADH VS CSW

WHAT IS THE DIFFERENCE
Carol Monette
MNH NEURO ICU
 THE PATHOPHYSIOLOGY OF THE SYNDROME OF
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INAPPROPRIATE ANTIDURETIC HORMONE
SECRETION ( SIADH )
THE PATHOPHYSIOLOGY OF CEREBRAL SALT
WAISTING (CSW )
THE PATHOPHYSIOLOGY OF INSIPID DIABETIS (DI)
DIFFERENTIATING BETWEEN SIADH & CSW & DI
SIGNS AND SYMPTOMS IN SIADH & CSW & DI
CURRENT TREATMENTS
NURSES ROLE
 ANTIDIURETIC HORMONE ( ADH ) CAUSES
RENAL WATER REABSORPTION AND EXPANDS
THE EXTRACELLULAR FLUID VOLUME
 ADH IS INAPPROPRIATELY SECRETED VIA THE
PITUITARY GLAND IN SIADH
 WHAT IS A SYNDROME
 LIST OF A MULTIPLE FINDINGS THAT DEFINE A
SINGLE DISEASE PROCESS
 FLUID RETENTION ( CAUSES EXCESS FREE WATER
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RETENTION)
SERUM HYPO OSMOLARITY (DUE TO RETAIN
FREE WATER)
DILUTIONAL HYPONATREMIA (NA+) (THIS
MEANS FREE WATER EXCESS)
HYPOCHLOREMIA (CL)
CONCENTRATED URINE
NORMAL RENAL FUNCTION
 TUMORS CAN MAKE A LOT OF THINGS AND IT IS
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A SIMPLE MOLECULE EASY TOMAKE BY MISTAKE
TUMORS CAN MAKE INAPPROPRIATE ADH
CAUSES BY : SMALL CELL LUNG – PANCREATIC –
LYMPHOMAS – LEUKEMIAS – THYMUS –
PROSTATE – COLO RECTAL (MALIGNANT
TUMORS)
DRUGS CAN CAUSE EXCESS ADH SECRETION
NEUROLOGIC INJURY CAN ALSO CAUSE EXCESS
ADH ( HEAD INJURY, CVA, BRAIN TUMORS,
INFECTION, LUPUS, GUILLAN-BARRE)
 HYPONATREMIA ( NA) 130 meq /l
 MUSCLE CRAMPS AND WEAKNESS
 FATIGUE
 ANOREXIA
 VOMITTING & ABDOMINAL CRAMPS
 HYPONATREMIA ( 120 meq/l)
 TWITCHING & SEIZURES
 LETHARGY
 CONFUSION
 CEREBRAL EDEMA
  BODY WEIGHT (FLUID SHIFTS FROM
EXTRACELLULAR SPACE INTO THE INSIDE CELLS)
 TREAT UNDERLYING CAUSE
 FLUID RESTRICTION < 1000 ml/day
 REPLACEMENT OF NA WITH NS OR 3% SALINE
 STRICT INTAKE / OUTPUT
 DAILY WEIGHTS
 FREQUENT ORAL HYGIENE
 ICE CHIPS
 OBSERVE FOR NEUROLOGICAL PROBLEMS (SZ)
 MONITOR BOWEL FUNCTION (FLUID
RESTRICTION = CONSTIPATION)
 MEDICATIONS : LITHIUM 900 – 1200 mg (to inhibit
the renal response to ADH)
DEMECLOCYCLINE 300 mg qid (to
suppress ADH activity)
THESE DRUGS BLOCK THE EFFECT OF ADH ON RENAL
TUBES, ALLOWING MORE FREE WATERDIURESIS AND
MORE DILUTE URINE
LASIX FOR DIURESIS
 POORLY UNDERSTOOD MECHANISM
 LOSS OF NA+ THROUGH URINE SECRETION
 NATRIURESIS
 INCREASE IN TOTAL SYSTEMIC VOLUME
 SUB-ARACHNOID HEMORRHAGE
 INCREASE INTRA CRANIAL PRESSURE
 TUBERCULOSIS MENINGITIS
 INTRA CRANIAL SURGERY
 SIMILAR PRESENTATION ALTOUGH DIFFERENT
MECHANISM
 DIFFERENTIAITON LIES IN THE VOLUME STATUS
OF THE PATIENT
 VARIATIONS IN SERUM OSMOLARITY
 PATIENT DIAGNOSIS
 SIADH :  BP – SEIZURE ACTIVITY – DRY MUCOUS
MENBRANES – DROUSINESS – SOB
 CSW :  CVP -  BP – INCREASED SKIN TURGOR –
HYPOVOLEMIA – POLYURIA ( LARGE
PRODUCTION OF URINE) - POLYDIPSIA
(EXCESSIVE THIRST)
SIADH
CSW
FLUID RESTRICTION
SALT REPLACEMENT (NA TABLETS)
FUROSEMIDE (LASIX) -DIURESIS
HYPERTONICS (3% SALINE)
CLINICAL MARKERS
CSW
SIADH
EXTRACELLULAR
VOLUME (PRIMARY
DISTINCTION)
LOW
PATIENT IS VOLUME
DEPLETED
EXPANDED
PATIENT IS EUVOLEMIC
(NORMAL BODY FLUID
CONTENT)
HEMATOCRITE (HCT)
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BUN - CREATININE
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URIC ACID
NORMAL TO 
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POTASSIUM (K)
NORMAL TO 
NORMAL
 ASSESMENT SKILLS
 LAB VALUES DAILY OR Q 12HRS IF PT ON 3%
INFUSION
 ACKNOWLEDGING SIGNS ANS SYMPTOMS: ASSES
PRESENCE OF EDEMA – LOOK AT TISSUE TURGOR –
DRY MUCOUS MENBRANES – NECK VEIN
DISTENSION – POSTURAL HYPOTENSION –
DECREASE CVP
 PATIENT AT RISK
 COMPLICATIONS
 THIS IS A CONDITION OF DECREASED SECRETION
OF ADH.
 THE AFFECTED PATIENTS VOID LARGE AMOUNTS
OF DILUTED URINE
 THEY ARE AT HIGH RISK FOR FLUID AND
ELECTROLYTE IMBALANCE
 THEY ARE AT RISK FOR DEHYDRATION
 POLYURIA (URINE VOLUME WILL RANGE FROM 4-
10 LITERS DAILY) THE HOURLY OUTPUT WILL
EXCEED 200 ml/ hour
 LOW URINE SPECIFIC GRAVITY (1.001 – 1.005)
 POLYDIPSIA (EXTREME THIRST)
 HIGH SERUM OSMOLALITY
 IT IS A CESSATION OF THE PITUITARY GLAND’S
SECRETION OF ADH THAT COULD BE CAUSE BY:
INJURY TO THE HYPOTHALAMUS – THE
SUPRAORTIC HYPOPHYSIAL TRACT – POSTERIOR
LOBE OF THE PITUITARY GLAND
 THE MOST COMMON CAUSE IS HEAD TRAUMA,
PITUITARY TUMORS, BRAIN DEATH
 IF THE PATIENT HAS A TRANSIENT DI = THE
NORMAL SECRETION OF ADH SHOULD
REESTABLISHED WITHIN FEW DAYS TO FEW
WEEKS
 A CONDITION OF PERMANENT DI WILL DEVELOP
ONLY 80% OR MORE IF THE PITUITARY STALK IS
DESTROYED. THIS SITUATION WILL REQUIRE LIFE
LONG TREATEMENT WITH REPLACEMENT
HORMONAL THERAPY
 REPLACEMENT OF FLUIDS IF THE PATIENT IS
UNABLE TO TAKE INADEQUATE AMOUNT OF
FLUID ORALLY
 FOR URINE OUTPUT MORE THEN 200 ml/hr FOR 2
CONSECUTIVE HOUR WITH S.G. < 1.005 :
- ADMINISTRATION OF ADH
(VASOPRESSIN) 5-10 units s/c q 3-6 hours
- DDAVP (DESMOPRESSIN) 1-4 mcg IV
 URINARY OUTPUT Q 1-2 HOURS
 URINARY SPECIFIC GRAVITY Q 1-2 HOURS
 STRICT INTAKE/ OUTPUT BALANCE
 F/U SERUN OSMOLARITY AND ELECTROLYTES
DAILY
 OBSERVE FOR SIGNS & SYMPTOMS OF
DEHYDRATION AND HYPOVOLEMIA
 DAILY WEIGHTS
 ADH / VASOPRESSIN CAUSES KIDNEYS TO RETAIN
FREE WATER
 FLUID RESTRICTION IN A PATIENT WITH CSW
PLACES PATIENT AT HIGH RISK FOR VASOSPASM
AND CEREBRAL ISCHEMIA
 IT IS IMPORTANT NOT TO CORRECT
HYPONATREMIA AGGRESSIVELY BECAUSE OF THE
RISK OF PONTINE MYELINOLYSIS
 CORRECTION SHOULD OCCUR IN 3-6 DAYS (NA
should not be corrected faster than 8-10mmol/l / day)
 SEVERE DAMMAGE OF THE MYELIN SHEATH OF
THE NERVE CELLS IN THE BRAIN STEM PONS
 IT IS CHARACTERIZED BY ACUTE PARALYSIS,
DYSPHAGIA AND DYSARTHRIA THEN ACUTE BRAIN
EDEMA = BRAIN HERNIATION = COMA
 IT IS LIFE THREATENING
 IT OCCURS AS A CONSEQUENCE OF RAPID RISE IN
SODIUM TONICITY
 NORMAL: 3.5-5.0 meq/l
 IF K < 3.5 signs and symptoms would be : EKG
changes or cardiac arrhythmias ( low or flat T wave,
depressed ST segment, prolonged QT interval, U
wave)
 IF K > 5-7 (mild hyperkalemia) and IF K > 7 (severe)
the signs and symptoms would be : Also EKG changes (
tall peaked T waves, widening of QRS complex or
shortening of QT interval, V fib leading to cardiac
arrest), muscle weakness, paresthesia(sensation of
tingling) and respiratory paralysis.
HYPERKALEMIA
HYPOKALEMIA
 NORMAL RANGE : 135-145 meq/l
 NA > 145 the signs and symptoms are: dehydration (
poor skin turgor, dry skin and mucous membranes,
sunken eyeballs), stupor, thirst and oliguria (low urine
output)
 NA < 135 or severe hyponatremia < 125 will have
symptoms such as : confusion, lethargy, seizures,
hypotension, tachycardia, cold, clammy skin and coma
 WHEN CALCIUM AND MAGNESIUM FALL, THEY
USUALLY FALL TOGETHER SINCE BOTH ARE
BOUND TO ALBUMIN
 CALCIUM IS INVOLVED IN BLOOD COAGULATION,
SKELETAL AND CARDIAC MUCLE CONTRACTILITY
AND SEVERAL CELLULAR FUNCTION
 CA & MAG ARE IMPORTANT IN NEUROMUSCULAR
CONDUCTION AND ACTIVATION
 DEFICIENCY OF MAG HAS BEEN ASSOCIATED WITH
FAILURE TO WEAN PATIENTS FROM VENTILATOR
 HYPERCALCEMIA: CA > 5.5 meq/l signs and
symptoms are : Deep bone pain, muscle hypo tonicity,
flank pain from renal calculi, nausea and vomiting,
dehydration, progression from stupor to coma.
 HYPOCALCEMIA : CA < 4.5 meq/l signs are : tingling
of fingertips, tetany( involuntary contractions),
abdominal cramps, muscle cramps, carpopedal
cramps(hands or feet), seizure, prolonged QT interval
 HYPOMAGNESEMIA is a deficiency usually related to
gastro intestinal or kidney problems. Also common
with long term diuretic therapy: MAG < 1.3
 SIGNS AND SYMPTOMS: Neuromuscular (twitching,
tremors, muscle weakness, paresthesia, hyperflexia),
depression, delirium, agitation, confusion,
cardiac(PVC’s, V fib, tachycardia, TORSADE DE
POINTES)
 HYPERMAGNESEMIA: MAG > 3 meq/l
 SIGNS AND SYMPTOMS : hypotension, progressing
PR intervals and finally to heart block, sedation,
hyporeflexia, muscle paralysis, respiratory weakness,
nausea, vomiting and skin warmth
HEART BLOCK
 NORMAL RANGE : 1.8 -2.6 meq/l
 PHOSPHORUS IS ESSENTIAL FOR INTRACELLULAR
STORAGE AND CONVERSION OF ENERGY
 HYPERPHOSPHATEMIA : PO4 > 2.6 meq/l signs and
symptoms are not usually present. Elevated PO4 levels
are often associated with renal failure
 HYPOPHOSPHATEMIA : PO4 < 1.8 meq/l signs are not
present in patients with acute deficits. Some signs are
bone pain, dizziness, anorexia, muscle weakness also
associated with hyperparathyroidism
 http://www.youtube.com/watch?v=SE5IbNdTJfg