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SIADH VS CSW VS DI

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)

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SIADH VS CSW VS DI

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  1. SIADH VS CSW VS DI 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. SIADH • ANTIDIURETIC HORMONE ( ADH ) CAUSES RENAL WATER REABSORPTION AND EXPANDS THE EXTRACELLULAR FLUID VOLUME • ADH IS INAPPROPRIATELY SECRETED VIA THE PITUITARY GLAND IN SIADH

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

  5. SIADH • 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. SIADH • 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. SIGN AND SYMPTOMS OF SIADH • 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)

  8. SIADH

  9. MANAGEMENT OF SIADH • 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. TREATMENT 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

  11. HYPONATREMIA

  12. CEREBRAL SALT WAISTING • POORLY UNDERSTOOD MECHANISM • LOSS OF NA+ THROUGH URINE SECRETION • NATRIURESIS • INCREASE IN TOTAL SYSTEMIC VOLUME

  13. CAUSES OF CEREBRAL SALT WAISTING • SUB-ARACHNOID HEMORRHAGE • INCREASE INTRA CRANIAL PRESSURE • TUBERCULOSIS MENINGITIS • INTRA CRANIAL SURGERY

  14. SIADH VS CSW • SIMILAR PRESENTATION ALTOUGH DIFFERENT MECHANISM • DIFFERENTIAITON LIES IN THE VOLUME STATUS OF THE PATIENT • VARIATIONS IN SERUM OSMOLARITY • PATIENT DIAGNOSIS

  15. SIGNS AND SIMPTOMS • 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. TREATMENTS

  17. SIADH VS CSW

  18. NURSES’S ROLE • 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. DIABETES INSIPIDUS (DI) • 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. SYMPTOMS OF DIABETES INSIPIDUS • 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

  21. ETIOLOGY OF DI • 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

  22. DI

  23. 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

  24. TREATMENT OF 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

  25. NURSING MANAGEMENT IN DI • 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

  26. SIADH VS DI

  27. SIADH VS DI

  28. MEDIC ALERT FOR DI

  29. REMEMBER • 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. WHAT IS PONTINE MYELINOLYSIS • 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. POTASSIUM • 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.

  32. POTASSIUM

  33. SODIUM • 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

  34. CALCIUM AND MAGNESIUM • 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. CALCIUM • 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. MAGNESIUM • 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. MAGNESIUM • 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. PHOSPHORUS • 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

  39. http://www.youtube.com/watch?v=SE5IbNdTJfg

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