Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Renal Emergencies: Fluids and Electrolytes

2,010 views

Published on

  • Be the first to comment

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

×