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WHAT IS THE DIFFERENCE Carol Monette MNH NEURO ICU.

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Presentation on theme: "WHAT IS THE DIFFERENCE Carol Monette MNH NEURO ICU."— Presentation transcript:

1 WHAT IS THE DIFFERENCE Carol Monette MNH NEURO ICU

2 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 TREATMENTS NURSES ROLE

3 ANTIDIURETIC HORMONE ( ADH ) CAUSES RENAL WATER REABSORPTION AND EXPANDS THE EXTRACELLULAR FLUID VOLUME ADH IS INAPPROPRIATELY SECRETED VIA THE PITUITARY GLAND IN SIADH

4 WHAT IS A SYNDROME LIST OF A MULTIPLE FINDINGS THAT DEFINE A SINGLE DISEASE PROCESS

5 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 URINE NORMAL RENAL FUNCTION

6 TUMORS CAN MAKE A LOT OF THINGS AND IT IS 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)

7 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) 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)

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9 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)

10 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

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12 POORLY UNDERSTOOD MECHANISM LOSS OF NA+ THROUGH URINE SECRETION NATRIURESIS INCREASE IN TOTAL SYSTEMIC VOLUME

13 SUB-ARACHNOID HEMORRHAGE INCREASE INTRA CRANIAL PRESSURE TUBERCULOSIS MENINGITIS INTRA CRANIAL SURGERY

14 SIMILAR PRESENTATION ALTOUGH DIFFERENT MECHANISM DIFFERENTIAITON LIES IN THE VOLUME STATUS OF THE PATIENT VARIATIONS IN SERUM OSMOLARITY PATIENT DIAGNOSIS

15 SIADH :  BP – SEIZURE ACTIVITY – DRY MUCOUS MENBRANES – DROUSINESS – SOB CSW :  CVP -  BP – INCREASED SKIN TURGOR – HYPOVOLEMIA – POLYURIA ( LARGE PRODUCTION OF URINE) - POLYDIPSIA (EXCESSIVE THIRST)

16 SIADHCSW FLUID RESTRICTIONSALT REPLACEMENT (NA TABLETS) FUROSEMIDE (LASIX) -DIURESISHYPERTONICS (3% SALINE)

17 CLINICAL MARKERSCSWSIADH EXTRACELLULAR VOLUME (PRIMARY DISTINCTION) LOW PATIENT IS VOLUME DEPLETED EXPANDED PATIENT IS EUVOLEMIC (NORMAL BODY FLUID CONTENT) HEMATOCRITE (HCT)  BUN - CREATININE  URIC ACIDNORMAL TO   POTASSIUM (K)NORMAL TO  NORMAL

18 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

19 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

20 POLYURIA (URINE VOLUME WILL RANGE FROM LITERS DAILY) THE HOURLY OUTPUT WILL EXCEED 200 ml/ hour LOW URINE SPECIFIC GRAVITY (1.001 – 1.005) POLYDIPSIA (EXTREME THIRST) HIGH SERUM OSMOLALITY

21 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

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23 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

24 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. < : - ADMINISTRATION OF ADH (VASOPRESSIN) 5-10 units s/c q 3-6 hours - DDAVP (DESMOPRESSIN) 1-4 mcg IV 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. < : - ADMINISTRATION OF ADH (VASOPRESSIN) 5-10 units s/c q 3-6 hours - DDAVP (DESMOPRESSIN) 1-4 mcg IV

25 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

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29 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)

30 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

31 NORMAL: 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.

32 HYPERKALEMIAHYPOKALEMIA

33 NORMAL RANGE : 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

34 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

35 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

36 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)

37 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

38 NORMAL RANGE : 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

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