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FLUID AND ELECTROLYTES DISASTERS

FLUID AND ELECTROLYTES DISASTERS. JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006. COMPOSITION OF BODY FLUID COMPARTMENTS. COMPOSITION OF ECF AND ICF ECF ICF Na 141 10 K 4.1 120-150 Cl 113 3 HCO 3 26 10 PHOSPHATE 2.0 140 (ORGANIC).

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FLUID AND ELECTROLYTES DISASTERS

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  1. FLUID AND ELECTROLYTES DISASTERS JOSE-MARIE EL-AMM NEPHROLOGY DIVISION WSU/DMC/HUH AUGUST, 2006

  2. COMPOSITION OF BODY FLUID COMPARTMENTS COMPOSITION OF ECF AND ICF ECF ICF Na14110 K 4.1120-150 Cl 113 3 HCO3 26 10 PHOSPHATE2.0140(ORGANIC)

  3. TOTAL BODY WATER= 0.6 X TOTAL BODY WEIGHT (0.5 IN THE ELDERLY OR OBESE, 0.7 IN INFANTS AND VERY YOUNG CHILDREN) ¼ IVV ¾ ISV 2/3 ICF 1/3 ECF

  4. (Principal Cells)

  5. CLINICAL APPROACH TO HYPONATREMIA • IS HYPONATREMIA REALLY HYPOTONICITY? • Translocational vs. isotonic • WHAT IS THE VOLUME STATUS? • What are the physiological signals to the kidney and the brain • WHAT IS THE URINE SODIUM AND OSMOLALITY? • Is ADH present and is it physiologically appropriate

  6. CASE STUDY 1 A 30 year old woman is admitted for an increase in edema and worsening jaundice. She is a known alcoholic and has had several admissions for jaundice and ascites. She stopped taking her diuretic approximately 10 days ago. Physical examination: blood pressure 128/80, heart rate 76 supine. No orthostatic change in BP noted. She has icteric sclera, ascites, sacral and pedal edema. Her liver span is 10 cm. Labs: 125 89 5 bilirubin= 12mg/dL 80 albumin= 2.5 g/Dl 3.2 28 0.8 UNa = 1mEq/L Uosm= 300mOsm/kg H2O What is her Posm? What is her cell size?

  7. CASE STUDY 1 • What is her effective arterial volume? • mild volume depletion(4%) • history • change in body weight • no orthostatic changes BP or pulse • moderate volume depletion(5% to 10%) • HR  15/min on standing • systolic BP  15mm Hg on standing • severe volume depletion(10%) • supine hypotension • supine tachycardia

  8. CASE STUDY 1 • Is her total body water high, low or normal? • Is her total body sodium high, low or normal?

  9. EDEMA=INCREASED TOTAL BODY SODIUM AND WATER BUT DOES NOT! NOT! NOT! TELL YOU THE PROPORTIONS (SODIUM CONCENTRATION) ORTHOSTATIC HYPOTENSION=DECREASED TOTAL BODY SODIUM AND WATER BUT DOES NOT! NOT! NOT! TELL YOU THE PROPORTIONS (SODIUM CONCENTRATION)

  10. BODY COMPARTMENT VOLUMES • 70 kg person  0.6 =42 liters total body water • 25 liters intracellular (ICF)-3/5 TBW 28 liters intracellular (ICF)-2/3 TBW • 17 liters extracellular (ECF)-2/5 TBW 14 liters extracellular (ECF)-13 TBW • 3.5 liters intravascular (IVV)-1/5 ECF 3.5 liters intravascular (IVV)-1/4 ECF • 13.5 liters interstitial (ISV)-4/5 ECF 10.5 liters interstitial (ISV)-3/4 ECF

  11. PRINCIPAL SENSORS IN VOLUME REGULATION EFFECTIVE CIRC VOL/ /  SYMPATHETIC TONE VENOUS RETURN / VENOUS CONSTRICTION/RELAXATION /  CARDIAC CONTRACTILITY /  CARDIAC OUTPUT ARTERIAL CONSTRICTION or RELAXATION /  BP /  A II /  RENIN SECRETION BARORECEPTOR STIMULATION/  /  TUBULAR Na+ REABSORPTION /  ALDO

  12. CASE STUDY 1 • Can you tell if ADH is being secreted? How? • Why is her ADH status the way it is? • What turns ADH off? • What turns it on?

  13. CONTROL OF ADH ALL ADH NONE POSM 280 300 50 1200 UOSM

  14. CASE STUDY 1 A 30 year old woman is admitted for an increase in edema and worsening jaundice. She is a known alcoholic and has had several admissions for jaundice and ascites. She stopped taking her diuretic approximately 10 days ago. Physical examination: blood pressure 128/80, heart rate 76 supine. No orthostatic change in BP noted. She has icteric sclera, ascites, sacral and pedal edema. Her liver span is 10 cm. Labs: 125 89 5 bilirubin= 12mg/dL 80 albumin= 2.5 g/dL 3.2 28 0.8 UNa = 1mEq/L Uosm= 300mOsm/kg H2O

  15. CASE STUDY 1 • Which IV fluids would you select?

  16. CASE STUDY 1 • What diuretic(s) would you use? • What would be the most likely or severe complications using diuretics in her case?

  17. (Principal Cells)

  18. CASE STUDY 1 CLARISSA’S TEAM HAVE BEEN WORKING ON HER FOR THE LAST WEEK. WITH ‘JUDICIOUS’ USE OF DIURETICS AND FLUID RESTRICTION, THEY HAVE DROPPED HER WEIGHT BY 12 LBS AND INCREASED HER SODIUM BY 5 MEQ/L. THE ON-CALL CHECK-OUT TO YOU IS “DON’T WORRY ABOUT HER.” AT 2 AM YOU ARE CALLED BY THE NURSE BECAUSE CLARISSA’S BP IS 80/60 AND HER HR IS 110/MIN. WHAT DO YOU DO?

  19. CASE STUDY 1 • DON’T WORRY ABOUT IT. • START AN IV OF NS AT 150CC/HR • BOLUS HER WITH NS IN 100CC INCREMENTS UNTIL HER BP INCREASES • GIVE 25 GRAMS OF ALBUMIN IVPB • START DOPAMINE

  20. CASE STUDY 2 A patient with severe congestive heart failure and massive edema is admitted to the hospital complaining of progressive dyspnea. Laboratory values 125 94 40 4.1 25 2 What is his Posm? What is his cell size?

  21. CASE STUDY 2 1-Spironolactone is administered but no diuresis occurs despite 2 days of treatment. Why? 2-A thiazide diuretic is then added to spironolactone with equally discouraging results. Why? 3-What single diuretic might result in successful diuresis? Why?

  22. (Principal Cells)

  23. CASE STUDY 2 • A loop diuretic is given with better results but still not impressive diuresis • What diuretic might you add to the loop diuretic to increase the loop diuretic potency?

  24. CASE STUDY 3 A 60 year old man was evaluated for persistent cough and a 25 pound weight loss over a 3 month period. He smoked a pack a day for 40 years. P.E.: BP sitting 110/70, no signs of dehydration and no evidence of edema. A pleural effusion is present on the right. PPD was positive. Weight 65 kg.

  25. CASE STUDY 4 115 88 4 105 3.7 24 0.6 Posm245 mOsm/kg H2O Uosm340 mOsm/kg H2O UNa39 mEq/L

  26. In order to get rid of a water load, one needs to produce very dilute urine. What are the requirements for such urinary dilution? 1)Extrarenal requirements adequate GFR adequate solute delivery 2)Intrarenal requirements intact vasa recta and loop function absence of ADH

  27. CAUSES OF SIADH • Carcinomas (lung, pancreas, duodenum) • Pulmonary disease(pneumonia, Tb, abscess, etc.) • CNS disorders (meningitis, encephalitis, SDH, SAH, CVA, trauma, etc)

  28. CASE STUDY 4 A 40 year old man is brought to the ER by EMS after a witnessed seizure. His family states that he has been complaining of a severe headache and has had progressive mental deterioration over the last week or 10 days. They say he takes no medications and has no significant medical history. Physical exam is completely negative except for meningeal signs. There is no focal neurological deficit, no papilledema. He weighs 60 kg. Labs: 110 80 Uosm=275mOsm/kg UNa=50 mEq/L 3.5 22 CSF: 100WBC: 75%mononuclear

  29. CASE STUDY 5 • Is ADH present? (hint: look at Uosm) • Why is this man hyponatremic?

  30. (present TBW) (present SNa) =present TBS (normal TBW) (normal SNa) =normal TBS (0.6)(60kg) x (110) = (???) x (140) (36L)(110)/(140) = (???) = 28L 36 – 28 = 8 liters excess water

  31. SYMPTOMS OF HYPONATREMIA • Mainly neurologic • Symptoms of cerebral edema • Nausea and malaise • followed by headache, lethargy, obtundation, seizures, coma and death • The rate at which the hyponatremia develops determines the degree and severity of the symptoms • Several protective responses which act to minimize cell swelling • Within four hours of hyponatremia developing the cells start to lose solutes & as intracellular solute amount decreases, water moves back out of the cells, returning the cell volumes toward normal

  32. CASE STUDY 5 • How would you treat this man? • For rapid correction of symptomatic euvolemic hyponatremia, hypertonic (3%) saline is used • Hypertonic (3%) saline has about 0.5mEq/ml. (500mEq/L) • What are your goals and end points? • Goal for rapid/initial SNa is to increase SNa to 120-125mEq/L or until symptoms improve-whichever is lower • Overly rapid correction of hyponatremia can lead to an osmotic demylination state • Patients should have plasma serum sodium concentrations increased at less than 12 mEq/L/day (0.5mEq/L/hr)

  33. The amount of sodium needed to raise the serum sodium can be estimated by the sodium deficit. Multiply the total body water (0.5xlean body weight in kg in women, 0.6x weight in men) by the plasma sodium deficit per liter. 36L x 15 mEq/L = 540 mEq Na need At <0.5mEq/L/hour need to change over 30 hours 1000mL/30hours  30 mL/hour

  34. CASE STUDY 6 A 30 year old man comes in complaining of polyuria and polydipsia for the previous two weeks. He has a history of sarcoidosis diagnosed 10 years ago for which he has been on Prednisone intermittently. Except for bilateral pulmonary crepitants and for uveitis, the physical exam is normal. Labs: 152 120 30 4 25 1.0 U/A: neg glucose, acetone Uosm=75 mOsm/kg H2O

  35. What are the causes of polyuria? • Diabetes mellitus • Diabetes insipidus • Hypokalemia • Hypercalcemia • Psychogenic water drinking

  36. HYPERNATREMIA BY DEFINITION, HYPERNATREMIA IS A HYPERTONIC STATE. YOU STILL DON’T KNOW THE VOLUME STATUS WITHOUT EXAMINING THE PATIENT. IN A VOLUME CONTRACTED STATE, WATER AND SODIUM ARE LOST-JUST MORE WATER THAN SODIUM. IN AN APPARENTLY EUVOLEMIC PATIENT, PURE WATER IS LOST. THERE ARE FEW SIGNS OF VOLUME DEPLETION AS MOST OF THE WATER LOSS IS INTRACELLULAR. VOLUME EXPANDED STATES ARE THOSE IN WHICH HYPERTONIC VOLUME EXPANSION TAKES PLACE.

  37. CENTRAL DIABETES INSIPIDUS: Idiopathic Trauma Hypoxic encephalopathy Posthypophysectomy Neoplastic 1:craniopharyngioma, pinealoma, cyst metastatic: breast, lung Misc: sarcoidosis,aneurysm, Histiocytosis X, encephalitis, meningitis NEPHROGENIC DIABETES INSIPIDUS: Hereditary: usually X-linked, very rare AR form Drugs: lithium, cidofovir, foscarnet Electrolyte disorders: hypokalemia, hypercalcemia Misc: sickle cell anemia or trait, renal amyloidosis, Sjögren’s syndrome, transient DI in pregnancy

  38. DIABETES INSIPIDUS THERAPY • DDAVP • a 2 amino acid substitute of ADH with potent antidiuretic effect but little to no pressor effects • Mild volume depletion(1-2 kg), a low salt diet and a thiazide diuretic • increases proximal sodium and water resorption and decreases water delivery to the ADH sensitive collecting tubule • Don’t use loop diuretics • induce a relative resistance to ADH by decreasing the maximal interstitial concentration • NSAIDs • potentiate ADH and are additive to the thiazide effect(renal prostaglandins oppose ADH effects)

  39. CASE STUDY 7 A 78 year old woman was admitted with right hemiparesis. She had a 9 year history of hypertension. PE: Her BP was 190/95 mm Hg. Pulse 80 beats per min.

  40. CASE STUDY 7 LABS: Hct 40%. Urine: SpGr 1.025, negative for protein and glucose. Sediment: Occasional WBC and RBC. BUN 17, Creat. 1.0 mg/dl. Glucose 140 mg/dL, Na 140 mEq/L, K 3.7 mEq/L, CO2 24 mEq/L and Cl 103 mEq/L. After admission she was managed with tube feedings and eventually transferred to a nursing home.

  41. Three weeks later she was readmitted because of vomiting and tachypnea. PE: Wt. 67 kg., BP 115/80. P=120, Temp. = 101.6 F. She was unresponsive and had poor skin turgor. LABS Urine: SpGr 1.022, protein 1+, glucose neg. Sediment: Few hyaline casts. BUN 120 mg/dl, creatinine 3 mg/dl, glucose 150 mg/dL, Na 160 mEq/L, K 5.9 mEq/L, Cl 125 mEq/L, CO2 18 mEq/L. Hct 48%.

  42. CASE STUDY 7 Is total body sodium increased, normal or decreased? It total body water increased, normal or decreased? How did this occur?

  43. Is total body sodium increased, normal or decreased? Is total body water increased, normal or decreased? BP 115/80 P=120 Normal Our patient Water Sodium poor skin turgor

  44. How did this occur? Loss of sodium and water-more water than sodium Water losses: insensible (temp 101F), urine (conc.), GI Sodium losses: poor intake and vomiting

  45. THE TRAGEDY OF THE VERY YOUNG & VERY OLD • Mobile people lose salt and water (N/V) but as IVV , ADH and they become thirsty/seek out fluids. • fluid intake with ADH present can lead to hyponatremia • Non-mobile people (playpens, restraints, strokes) cannot respond to thirst • if they lose more water than sodium, they become hypernatremic

  46. CASE STUDY 7 • What is the first priority in her therapy? • IVV resuscitation • What IV would you first order? • 0.9% NaCl • How much would you give? • Until she is better

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