siadh vs csw vs di
DESCRIPTION
SIADH VS CSW VS DI. WHAT IS THE DIFFERENCE Carol Monette MNH NEURO ICU. THE PATHOPHYSIOLOGY OF THE SYNDROME OF INAPPROPRIATE ANTIDURETIC HORMONE SECRETION ( SIADH ) THE PATHOPHYSIOLOGY OF CEREBRAL SALT WAISTING (CSW ) THE PATHOPHYSIOLOGY OF INSIPID DIABETIS (DI) - PowerPoint PPT PresentationTRANSCRIPT
WHAT IS THE DIFFERENCECarol Monette
MNH NEURO ICU
SIADH VS CSW VS DI
THE PATHOPHYSIOLOGY OF THE SYNDROME OF 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 TREATMENTSNURSES ROLE
ANTIDIURETIC HORMONE ( ADH ) CAUSES RENAL WATER REABSORPTION AND EXPANDS THE EXTRACELLULAR FLUID VOLUME
ADH IS INAPPROPRIATELY SECRETED VIA THE PITUITARY GLAND IN SIADH
SIADH
WHAT IS A SYNDROME
LIST OF A MULTIPLE FINDINGS THAT DEFINE A SINGLE DISEASE PROCESS
SYNDROME
FLUID RETENTION ( CAUSES EXCESS FREE WATER RETENTION)
SERUM HYPO OSMOLARITY (DUE TO RETAIN FREE WATER)
DILUTIONAL HYPONATREMIA (NA+) (THIS MEANS FREE WATER EXCESS)
HYPOCHLOREMIA (CL)CONCENTRATED URINENORMAL RENAL FUNCTION
SIADH
TUMORS CAN MAKE A LOT OF THINGS AND IT IS A SIMPLE MOLECULE EASY TOMAKE BY MISTAKE
TUMORS CAN MAKE INAPPROPRIATE ADHCAUSES BY : SMALL CELL LUNG – PANCREATIC
– LYMPHOMAS – LEUKEMIAS – THYMUS – PROSTATE – COLO RECTAL (MALIGNANT TUMORS)
DRUGS CAN CAUSE EXCESS ADH SECRETIONNEUROLOGIC INJURY CAN ALSO CAUSE
EXCESS ADH ( HEAD INJURY, CVA, BRAIN TUMORS, INFECTION, LUPUS, GUILLAN-BARRE)
SIADH
HYPONATREMIA ( NA) 130 meq /lMUSCLE CRAMPS AND WEAKNESSFATIGUEANOREXIAVOMITTING & ABDOMINAL CRAMPSHYPONATREMIA ( 120 meq/l)TWITCHING & SEIZURESLETHARGYCONFUSIONCEREBRAL EDEMA BODY WEIGHT (FLUID SHIFTS FROM
EXTRACELLULAR SPACE INTO THE INSIDE CELLS)
SIGN AND SYMPTOMS OF SIADH
SIADH
TREAT UNDERLYING CAUSEFLUID RESTRICTION < 1000 ml/dayREPLACEMENT OF NA WITH NS OR 3% SALINESTRICT INTAKE / OUTPUTDAILY WEIGHTSFREQUENT ORAL HYGIENEICE CHIPSOBSERVE FOR NEUROLOGICAL PROBLEMS (SZ)MONITOR BOWEL FUNCTION (FLUID
RESTRICTION = CONSTIPATION)
MANAGEMENT OF SIADH
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
TREATMENT OF SIADH
HYPONATREMIA
POORLY UNDERSTOOD MECHANISMLOSS OF NA+ THROUGH URINE
SECRETIONNATRIURESISINCREASE IN TOTAL SYSTEMIC VOLUME
CEREBRAL SALT WAISTING
SUB-ARACHNOID HEMORRHAGE
INCREASE INTRA CRANIAL PRESSURE
TUBERCULOSIS MENINGITIS
INTRA CRANIAL SURGERY
CAUSES OF CEREBRAL SALT WAISTING
SIMILAR PRESENTATION ALTOUGH DIFFERENT MECHANISM
DIFFERENTIAITON LIES IN THE VOLUME STATUS OF THE PATIENT
VARIATIONS IN SERUM OSMOLARITY
PATIENT DIAGNOSIS
SIADH VS CSW
SIADH : BP – SEIZURE ACTIVITY – DRY MUCOUS MENBRANES – DROUSINESS – SOB
CSW : CVP - BP – INCREASED SKIN TURGOR – HYPOVOLEMIA – POLYURIA ( LARGE PRODUCTION OF URINE) - POLYDIPSIA (EXCESSIVE THIRST)
SIGNS AND SIMPTOMS
SIADH CSWFLUID RESTRICTION SALT REPLACEMENT (NA
TABLETS)FUROSEMIDE (LASIX) -DIURESIS
HYPERTONICS (3% SALINE)
TREATMENTS
CLINICAL MARKERS
CSW SIADH
EXTRACELLULAR VOLUME (PRIMARY DISTINCTION)
LOWPATIENT IS VOLUME DEPLETED
EXPANDEDPATIENT IS EUVOLEMIC (NORMAL BODY FLUID CONTENT)
HEMATOCRITE (HCT) BUN - CREATININE URIC ACID NORMAL TO POTASSIUM (K) NORMAL TO NORMAL
SIADH VS CSW
ASSESMENT SKILLSLAB VALUES DAILY OR Q 12HRS IF PT ON 3%
INFUSIONACKNOWLEDGING SIGNS ANS SYMPTOMS:
ASSES PRESENCE OF EDEMA – LOOK AT TISSUE TURGOR – DRY MUCOUS MENBRANES – NECK VEIN DISTENSION – POSTURAL HYPOTENSION – DECREASE CVP
PATIENT AT RISKCOMPLICATIONS
NURSES’S ROLE
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
DIABETES INSIPIDUS (DI)
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
SYMPTOMS OF DIABETES INSIPIDUS
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
ETIOLOGY OF DI
DI
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
DI
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
TREATMENT OF DI
URINARY OUTPUT Q 1-2 HOURSURINARY SPECIFIC GRAVITY Q 1-2 HOURSSTRICT INTAKE/ OUTPUT BALANCEF/U SERUN OSMOLARITY AND
ELECTROLYTES DAILYOBSERVE FOR SIGNS & SYMPTOMS OF
DEHYDRATION AND HYPOVOLEMIADAILY WEIGHTS
NURSING MANAGEMENT IN DI
SIADH VS DI
SIADH VS DI
MEDIC ALERT FOR DI
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)
REMEMBER
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 THREATENINGIT OCCURS AS A CONSEQUENCE OF RAPID RISE
IN SODIUM TONICITY
WHAT IS PONTINE MYELINOLYSIS
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.
POTASSIUM
POTASSIUMHYPERKALEMIA HYPOKALEMIA
NORMAL RANGE : 135-145 meq/lNA > 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
SODIUM
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
CALCIUM AND MAGNESIUM
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
CALCIUM
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)
MAGNESIUM
HYPERMAGNESEMIA: MAG > 3 meq/lSIGNS AND SYMPTOMS : hypotension,
progressing PR intervals and finally to heart block, sedation, hyporeflexia, muscle paralysis, respiratory weakness, nausea, vomiting and skin warmth
HEART BLOCK
MAGNESIUM
NORMAL RANGE : 1.8 -2.6 meq/lPHOSPHORUS 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
PHOSPHORUS
http://www.youtube.com/watch?v=SE5IbNdTJfg