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