Renal Emergencies: Fluids and Electrolytes


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  • We will start with some basic concepts.
    Water is distributed between 2 main components: inside the cells and outside the cells
    ECF space is about 20% of body’s weight
    Interstitial fluid surrounds the cells and has the same components of plasma, but with less protein
    Difference between plasma and interstitial fluid is oncotic pressure- the oncotic pressure (proteins) maintains intravascular volume
    Plasma UF can accumulate in a “third” space and result in edema, ascites, or pleural effusions.
  • Electrolytes inside the cell and outside the cell are different.
    Sodium and chloride are the predominant ECF electrolytes and are responsible for maintaining ECF volume as opposed to potassium
    Potassium and phosphate are principal components of ICF- potassium is primarily intracellular so it is very difficult to estimate total body potassium.
  • Difference between intracellular and extracellular potassium concentrations determines the resting membrane potential of a cell
  • Rare in individuals with normal renal function
    Reduced GFR: Acute/Chronic renal failure
    Reduced tubular secretion: Addison’s disease, hypoaldosteronism, potassium sparing diuretics, ACE Inhib, Trimethoprim, Renal tubular acidosis
    Increased intake: transfusions, KCl supplementation, sports beverages, IVFs and TPN
    Transcellular shifts: Cell destruction-trauma, burns, rhabdomyolysis, hemolysis, tumor lysis, catabolism
    Metabolic acidosis- H shifts inside of cell, K shifts out of cells
    Aldosterone deficiency: CAH
  • High potassium foods
    Figs, molasses, seaweed, dried fruit, nuts, avacodoes, lima beans, spinach, tomatoes, broccoli, carrots, potatoes, cauliflower, bananas, canteloupe, kiwi, oranges, mangoes, ground beef, steak, pork, veal, lamb
  • Associated with weakness, parasthesias, tetany
    Order of progression although not always dependent on potassium level
  • TPN and IVF
    Kayexalate- exchange resin that binds K in gut
    Oral is superior to rectal- takes several hours to work
    Dose 1 gram/kg q 4-6 hours
  • Regardless of potassium value
    EKG changes occur individually and cannot be correlated with serum K level
    Loop diuretics (only work if good renal function)
    Kayexalate- exchange resin that binds K in gut
    Oral is superior to rectal- takes several hours to work
    Dose 1 gram/kg q 4-6 hours
  • Hypernatremia-suggests endocrine cause (increased aldosterone)
    Alkalosis-consistent with primary alkalosis or tubular disorder (Bartter’s)
    TTKG- Urine/serum potassium divided by urine/serum osmolality
    Values range from 1-15
    <5: suggestive of low urine losses-not likely the cause of the hypokalemia
    >9: suggestive of high urine losses-consistent with a renal origin

  • Osmolality is a measure of solute concentration
    Kidney produces concentrated or dilute urine in response to changes in osmolality
    Estimate plasma osmolality from this equation: 2 times Na represents Na + Cl
    90% of your serum osmolality is determined by sodium and chloride
  • Since sodium is the main cation of ECF and primary determinant of osmolality, changes in sodium are linked to changes in ECF volume and associated with disorders of water balance
    Kidneys defend against changes in ECF volume by modulating sodium reabsportion.
    In neonates and growing child, need a positive sodium balance. Otherwise sodium intake equals sodium excretion in a normal kidney at steady state.
    Na requirements in growing child with normal renal function- required for growth- more in infants
  • “Dilutional” effect of glucose: Hyperglycemia increases extracellular osmolality and provides an osmotic force for water to leave the intracellular space for the extracellular space. This results in a decrease in the serum sodium concentration.
  • Loss of sodium in excess of water
    Gain of water in excess of sodium
    IVVD from dehydration/AGE or decreased effective circulating volume
    Cause a decrease in GFR, Proximal tubule increase Na and water reabsorption
    Diminished fluid delivery to distal portion of diluting segment and decreased free water excretion
    Most common electrolyte disturbance in children
  • Relative water excess
    Hypovolemia= loss of salt AND water from ECF
  • Volume overload- dilutional hyponatremia
    Hyponatremia in majority of cases is a reflection of relative water excess
    Volume overload and dilutional hyponatremia
    Water intoxication: radio contest winner in a water drinking contest who died of cerebral edema
  • Physical exam is critical – first step is to determine volume status- hyper or hypovolemic
    Urine Na <20mEq/L , <40 in neonate: Extrarenal losses
    Urine Na >20 mEq/L, >40 in neonate: Renal losses
    High urine sodium: Renal losses: Salt wasting nephropathy, diuretics, adrenal insufficiency
    Have to check urine Na NOT on diuretics
    If the problem is with the kidney (Na losing nephritis, diuretics, adrenal insufficiency) then the kidney does NOT respond approp to the hypovolemia and instead of a concentrated urine with high SG and osm, it is INAPPROPRIATELY LOW.
  • 0.6 L/kg= distribution factor as a fraction of body weight
    Give one-half replacement over first 8 hours and second half over next 16 hours
  • Think osmolality- think sodium
    Treatment of symptomatic hyponatremia with 2cc/kg bolus of 3% saline over 10 min. Max 100 cc. Repeat 1-2 times as needs until symptoms improve
    Rapid correction of hyponatremia- central pontine myelinolysis (rehydration leads to brain dehydration)
  • More than 50% of children with serum Na <125 mEq/L will develop hyponatremic encephalopathy due to children’s larger brain to intracranial volume ratio. Children has less room available in their rigid skulls for brain expansion and are likely to develop brain herniation at higher sNa concentration than adults
  • Stop further therapy when awake, alert, responding to commands, resolution of headache and nausea or acute rise in Na of 10 mEq/L if in first 5 hours
    Correction in first 48 hours should not excees 15-20 mEq/L and should avoid normo- or hypernatremia
  • As opposed to hyponatremia which can sometimes be normal in certain physiologic states
  • Body has two defenses to protect against developing hyperNa: ability to prod a concentrated urine (ADH release) and powerful thirst mechanism
    Hyperosmolar-induced thirst sensation kicks in and people drink! Returns sOsm to normal
  • Water deficit=hypernatremic dehydration
    Diuresis: osmotic, diuretics, post-obstructive, diuretic phase of ATN
    Nephropathy: inability to concentrate the urine in renal dysplasia, obst uropathy, interstitial disease- leads to excess free water loss
    GI losses, skin losses
  • Very rare
    With insufficient free water intake
    Salt poisoning
  • Compare urine volume with fluid intake
    Weight loss: diarrhea
    Weight gain: Increased Na retention- hyperaldosteronism
    HTN- Hyperaldosteronism
    CNS- lethargy, weakness, irritability, seizures, anxiety
    Remember skin turgor is well preserved bc it is intracellular water loss
    If hypovolemic and most often will be:
    Identify cause of water deficit and asses kidney’s response by eval renal conc ability
    Urine Osm <800 mOsm/kg in hyperNa is a sign of concentrating defect
  • Replace urine volume with hypotonic fluids in addition to deficit
    Normal saline first if signs of circulatory collapse
    Measure electrolytes q 2 hours until neurologically stable
    Oral therapy has less risk of seizures and can tolerate a more rapid rate of correction
    Correction rate not to exceed 1mEq/h unless encephalopathic
    Do not correct >15mEq/24hr
  • Polyuria from nephrogenic DI
  • Renal Emergencies: Fluids and Electrolytes

    1. 1. Caroline Straatmann, MD
    2. 2. 0.6 x weight 1/3 ECF ¼ Plasma (Intravascular) ¾ Interstitial Fluid 2/3 ICF
    3. 3. Intracellular (mEq/L) Extracellular (mEq/L) Na 20 135-145 K 150 3-5 Cl ____ 98-110 HCO₃ 10 20-25 PO₄ 110-115 5 Protein 75 10
    4. 4.  A 12 year old boy with chronic renal insufficiency secondary to obstructive uropathy is admitted for pancreatitis. He cannot tolerate enteral feeds and is on TPN. He complains of his legs feeling weak. Labs show 144 120 60 7.4 15 4.7
    5. 5.  What do you do first?  EKG  EKG shows peakedT waves  What do you do next?  Give calcium gluconate  Stop hisTPN, which has K in it!
    6. 6.  In addition to this treatment, which one of the following would be the most effective therapy for his hyperkalemia?  Subcutaneous insulin and slow infusion of glucose  Intravenous beta – 2 agonist  Intravenous insulin  Intravenous sodium bicarbonate  Oral sodium polystyrene sulfonate
    7. 7.  Growing child requires 1-2 mEq/kg/day  Avoid potassium deficiency  Cellular growth  Serum potassium concentration does not reflect total body potassium content  Ex: Diabetic ketoacidosis  Disturbance in serum K⁺ can affect cell membrane resting potential  Muscle paralysis  Ventricular arrhythmias
    8. 8.  Serum K >5 mmol/L (5 meq/L)  Kidney failure is the leading cause  Can be life-threatening due to risk of ventricular arrhythmias  Normal renal response to hyperkalemia  Stimulate aldosterone secretion which then stimulates urinary potassium excretion
    9. 9.  Symptoms  Skeletal muscle weakness  Paralysis  Parasthesias  Respiratory failure
    10. 10.  Decreased renal excretion  ReducedGFR  Reduced tubular secretion  Increased intake  Transcellular shifts  Metabolic acidosis  Tumor Lysis Syndrome  Rhabdomyolysis  Aldosterone deficiency or resistance  Common Drugs  Amiloride  Spironolactone  Cyclosporine/Tacrolimus  Heparin  ACE inhibitors/ARBs  Pentamidine  Trimethoprim- Sulfamethoxazole
    11. 11. ICF Na= 10 mmol/L K=140 mmol/L ECF Na= 150 mmol/L K=4 mmol/L 3 Na 2 K
    12. 12.  Reason for K to have shifted outside the cells?  K shift to outside the cell after the blood was collected?  Hemolysis  Tissue hypoxia distal to tourniquet  Heel stick  Are the kidneys excreting K appropriately?  GFR  Drugs  Aldosterone  Excessive dietary K intake contributing to the problem?  IVFs andTPN!!!
    13. 13.  Repeat serum K  EKG stat  If EKG shows changes, start treatment immediately  Progression of changes  PeakedT waves-Prolonged PR interval-ST depression-Widened QRS-Ventricular fibrillation
    14. 14.  PeakedT waves  Loss of P wave  Widening of QRS  ST depression  Prolonged PR interval  Ventricular dysrhythmias  Cardiac arrest
    15. 15.  Eliminate source of potassium intake or offending drugs  K⁺ < 6 mEq/L  Low potassium diet  Diuretics  K⁺ > 6 mEq/L  Cation exchange resin: SPS
    16. 16.  EKG changes = EMERGENCY  Stabilize myocardium  IV calcium chloride or calcium gluconate (10%)  Shift potassium into cells  Beta agonists, insulin/glucose, sodium bicarbonate  Remove excess potassium from the body  Sodium polystyrene sulfonate (SPS)  Furosemide  Hemodialysis
    17. 17.  Weakness or paralysis  Ileus  Cardiac dysrhythmias  Delayed depolarization  Flat/absentT waves  U waves
    18. 18. U WAVES  BMP  Hypernatremia  Alkalosis  Bartter’s  Renin  Aldosterone  Cortisol
    19. 19.  If > 2.0 mEq/L and no EKG changes, treat orally with KCl, minimum 2 mEq/kg/day  If < 2.0 and/or EKG changes, treat intravenously, with KCl 40 mEq/L into IV fluids  “Potassium runs”: not recommended unless cardiac/ICU patient  Monitor potassium values until normal value is established
    20. 20.  A 7 yo male with cystic fibrosis and obstructive lung disease is admitted for a 2 week h/o progressive lethargy. He is obtunded.  Labs: Na=105, K=4, Cl=72, HCO3=21  Plasma osmolality= 222mOsm/kg H20  Urine osmolality= 604 mOsm/kg H20  Urine Na= 78 mEq/L
    21. 21.  What is the most likely diagnosis?  Pseudohyponatremia  SIADH  Psychogenic polydipsia  Hypoaldosteronism  How would you raise the plasma sodium concentration?
    22. 22. 2.8 18  Normal=280-295 mOsm/kg  Osmotic equilibrium tightly regulated between ECF and ICF compartments  Water moves between compartments in response to alterations in osmolality of either compartment  2 [Na⁺] + [BUN] + [Glucose]
    23. 23. • Serum osmolality is tightly regulated • Sodium is the major determinant of serum osmolality • Sodium balance is regulated by the kidney • Serum sodium does not reflect total body sodium content • Na requirements in growing child • 2-3 mEq/kg/day
    24. 24.  Drawn from an indwelling catheter  Hyperlipidemia  Normal plasma Osm  Hyperglycemia  Drives water into extracellular space, diluting the Na concentration ▪ Plasma osm will be high ▪ Na decreases 1.6 mEq/L for each 100 mg/dL rise in glucose
    25. 25.  Serum Na < 130 mEq/L  Loss of sodium  Gain of water  Most common cause is intravascular volume depletion from gastroenteritis  After volume expansion, will be able to regulate free water excretion
    26. 26.  Lose more salt relative to water but still hypovolemic  Hyponatremic dehydration  GI losses (prolonged AGE/hypotonic intake)  Renal losses  Chronic diuretic therapy  Salt wasting nephropathy  Adrenal insufficiency  Skin losses  Cystic fibrosis (hyponatremic/hypochloremic)
    27. 27.  Hypervolemia  Fluid overload  Congestive heart failure  Water intoxication  Diluted formula  Hypotonic fluids  SIADH
    28. 28.  History and Physical  Determine volume status  Estimate sodium intake and output  If hypovolemic:  Renal or Extrarenal losses?  Urine Na⁺  Does kidney respond appropriately to hypovolemia?  Urine specific gravity  Urine osmolality
    29. 29.  Correct underlying cause  Hyponatremic dehydration  SIADH ▪ Fluid restriction (insensible water losses) until Na levels normalize  Rate of correction depends on how quickly it developed  Acute hyponatremia is more dangerous  Increased risk of herniation or apnea from increased ICP from rapid, unbalanced water movement into brain cells  In general, correction with hypertonic saline in unnecessary unless there are neurological manifestations of hyponatremia
    30. 30.  Sodium deficit (mEq) = Fluid deficit (L) X 0.6 X [Na⁺] in ECF (mEq/L) PLUS  Excess sodium deficit = (Desired Na⁺ - Actual Na⁺) X (0.6 L/kg) XWt (kg)  Desired Na⁺ is 135 mEq/L  Maintenance and ongoing losses  Replace over 24 hours
    31. 31.  As sOsm falls, water moves into cells, and risk of cerebral edema  If severe (<120 mEq/L), may observe seizures, altered mental status, vomiting  For Na⁺ < 120 mEq/L, raise Na⁺ to 125 mEq/L by giving 3% saline  Rapid correction of hyponatremia : central pontine myelinolysis
    32. 32. EARLY  Headache  Nausea and vomiting  Lethargy  Weakness  Confusion  Altered consciousness  Agitation  Gait disturbances ADVANCED  Seizures  Coma  Apnea  Pulmonary edema  Decorticate posturing  Dilated pupils  Anisocoria  Papilledema  Cardiac arrhythmias  Central diabetes insipidus
    33. 33.  2 ml/kg bolus of 3% NaCl, max 100 ml over 10 min  Repeat 1-2 times until symptoms improve  Goal of correction is 5-6 mEq/L in first 1-2 hours  Recheck sNa q 2 hours  Moritz et al. Pediatr Nephrol (2010) 25: 1225-1238
    34. 34. Insufficient Correction Cerebral Edema Too aggressive Correction Demyelination •Acute hyponatremia=Most dangerous •Symptomatic hyponatremia = Medical Emergency
    35. 35.  A 9 yr old boy who has cerebral palsy is admitted to CHNOLA following 4 days of diarrhea. His initial serum Na level is 174mEq/L. Once circulatory volume is restored, the primary focus of the fluid management must be to provide appropriate amounts of:  Chloride  Free water  Glucose  Phosphate  Potassium
    36. 36.  Serum sodium >150 mEq/L  Always abnormal and should be evaluated  Free water deficit  Increased sodium intake/retention  Increased serum Osm  Does not imply total body sodium overload
    37. 37.  Rarely develops in those who have access to free water  Most often from inability to access free water  At risk  Ineffective breastfeeding  Critically ill patients  Infants  Neurologically impaired
    38. 38.  Children who have hypernatremic dehydration often appear minimally dehydrated on exam. This is due to maintenance of:  Extracellular fluid volume  Intracellular fluid volume  Total body glucose  Total body sodium concentration  Total body water balance
    39. 39. Water Deficit  Renal loss  Diuretic use  Nephropathy with renal concentrating defect  Diabetes insipidus  Extrarenal loss  Vomiting/Diarrhea  Skin losses
    40. 40. Increased Sodium Intake/Retention  Salt poisoning  Exogenous sodium  Hypertonic feeding/saline  NaHCO3 administration  Mineralcorticoid excess  Hyperaldosteronism
    41. 41.  Determine volume status  Blood pressure  Renal water loss  Kidney does not appropriately respond to hypovolemia  Low urine s.g and osmolality  High urine Na⁺  Extrarenal water loss  Kidney responds appropriately to hypovolemia  High urine s.g.  Low urine Na⁺
    42. 42.  Treat cause  Correct volume disturbance if present  Replace free water deficit  4mL/kg x (desired change in serum Na (mEq/L))  Risk of cerebral edema from rapid correction
    43. 43.  Stones  Renal calculi  Bones  Bone pain  Moans  Depression  Groans  Constipation
    44. 44.  Symptoms  Weakness, irritability, abdominal cramping, n/v, polyuria, polydipsia, renal stones, pancreatitis, shortened QT interval  Differential diagnosis  Hyperparathyroidism, excessive calcium intake, malignancy, thiazides, prolonged immobilization, sarcoidosis
    45. 45.  Most hypercalcemic patients are also volume depleted  Hydration to increase UOP and Ca excretion  NS with potassium at 2-3x maintenance if renal function and BP allow  Forced diuresis  Furosemide  Calcitonin  Bisphosphonates  Dialysis
    46. 46.  A 18 month old with ESRD secondary to renal dysplasia on chronic peritoneal dialysis has a serum Mg of 3.2. He is asymptomatic. All other values are normal except his BUN/Cr.  What is your next step in management?  Change to hemodialysis  Increase phosphate binders  Increase vitamin D  Continue peritoneal dialysis
    47. 47.  Etiologies  Renal failure ▪ Common in CKD due to decreased excretion ▪ Levels in AKI parallel potassium and are derived from the intracellular pool ▪ Rapid cell lysis  Excessive administration
    48. 48.  Symptoms  Decreased DTRs, lethargy, confusion  Hypocalcemia (hypermagnesemia suppresses PTH)  Rarely of clinical significance  Treatment  Stop supplemental Mg  Diuresis  Dialysis
    49. 49.  You are called to the floor at 2 am to see a 16 yo orthopedic post-op patient because his BP is 160/100  What do you do?  A 5 yo boy is brought to the ER because of new-onset generalized seizure which has subsided by the time he arrives. He is postictal with BP of 160/100.  What do you do?  Is this HTN urgency or emergency?
    50. 50.  HTN Emergency is elevated SBP and DBP with acute end-organ damage  Stroke (ischemic/hemorrhagic)  Pulmonary edema  HTN encephalopathy  HTN urgency does not have end organ damage.  HA, Nausea, Blurred vision
    51. 51.  In children, 75% of cases of HTN emergency will be secondary to renal or renovascular causes  What do you need to do before treatment?  Rule out increased ICP as etiology of HTN  Get plasma renin activity level  If the patient is bleeding or coagulopathic, treat the elevated BP urgently  Worry about hemorrhagic stroke
    52. 52.  ICU  Don’t lower BP too rapidly  Lower no more than 20-25% in 1st 8 hours  Preserve cerebral perfusion  Acute goal is a mildly elevated BP
    53. 53.  A 5 yo boy is brought to the ER because of new-onset generalized seizure which has subsided by the time he arrives. He is postictal with BP of 160/100.  What would you start?  What would be your immediate BP goal?  Goal around 130/85 (20% reduction)
    54. 54.  Nitroprusside  Arterial and venous vasodilator  Very short-acting  Easily titrated  Cyanide toxicity  Don’t use in renal or liver failure  IV Calcium channel blockers  Nicardipine  Can cause increased ICP
    55. 55.  IV Labetalol  Alpha and beta blocker: decreases peripheral vascular resistance  Continuous or intermittent dosing  Do not use in asthmatics, lung disease, CHF, diabetics  IV Enalapril (Enalaprilat)  IV hydralazine  Potent arterial vasodilator  Infants
    56. 56.  You are called to the floor for a 8 yo child with PIGN who is seizing. His BP is 155/98  What do you do for immediate treatment?  IV labetalol bolus dose  Transfer to PICU for nicardipine or labetalol infusion  Goal is to decrease his BP by 20-25% in first 8 hours  What other therapy might be helpful?  Lasix- PIGN is assoc with volume overload
    57. 57.  Severe asymptomatic HTN  May have headache  Most commonly due to non-adherence or ingestion of large amounts of salt  Reduce BP over several hours to days  Oral medications
    58. 58.  Oral medications  Nifedipine ▪ Short-acting- see effects in 15-20 min ▪ 0.25 mg/kg initial dose ▪ 10 mg capsules  Isradipine ▪ Short-acting: effects within one hour ▪ 0.05-1 mg/kg/dose  Labetalol ▪ Heart rate is dose limiting factor