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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 cellsECF space is about 20% of body’s weightInterstitial fluid surrounds the cells and has the same components of plasma, but with less proteinDifference between plasma and interstitial fluid is oncotic pressure- the oncotic pressure (proteins) maintains intravascular volumePlasma 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 potassiumPotassium 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 functionReduced GFR: Acute/Chronic renal failureReduced tubular secretion: Addison’s disease, hypoaldosteronism, potassium sparing diuretics, ACE Inhib, Trimethoprim, Renal tubular acidosisIncreased intake: transfusions, KCl supplementation, sports beverages, IVFs and TPNTranscellular shifts: Cell destruction-trauma, burns, rhabdomyolysis, hemolysis, tumor lysis, catabolismMetabolic acidosis- H shifts inside of cell, K shifts out of cellsAldosterone deficiency: CAH
  • High potassium foodsFigs, 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, tetanyOrder of progression although not always dependent on potassium level
  • TPN and IVFKayexalate- exchange resin that binds K in gutOral is superior to rectal- takes several hours to workDose 1 gram/kg q 4-6 hours
  • Regardless of potassium valueEKG changes occur individually and cannot be correlated with serum K levelLoop diuretics (only work if good renal function)Kayexalate- exchange resin that binds K in gutOral is superior to rectal- takes several hours to workDose 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 osmolalityValues range from 1-159: suggestive of high urine losses-consistent with a renal origin
  • Osmolality is a measure of solute concentrationKidney produces concentrated or dilute urine in response to changes in osmolality Estimate plasma osmolality from this equation: 2 times Na represents Na + Cl90% 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 balanceKidneys 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 waterGain of water in excess of sodiumIVVD from dehydration/AGE or decreased effective circulating volumeCause a decrease in GFR, Proximal tubule increase Na and water reabsorptionDiminished fluid delivery to distal portion of diluting segment and decreased free water excretionMost common electrolyte disturbance in children
  • Relative water excessHypovolemia= loss of salt AND water from ECF
  • Volume overload- dilutionalhyponatremiaHyponatremia in majority of cases is a reflection of relative water excessVolume overload and dilutionalhyponatremiaWater 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 hypovolemicUrine Na 20 mEq/L, >40 in neonate: Renal lossesHigh urine sodium: Renal losses: Salt wasting nephropathy, diuretics, adrenal insufficiencyHave to check urine Na NOT on diureticsIf 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 weightGive one-half replacement over first 8 hours and second half over next 16 hours
  • Think osmolality- think sodiumTreatment of symptomatic hyponatremia with 2cc/kg bolus of 3% saline over 10 min. Max 100 cc. Repeat 1-2 times as needs until symptoms improveRapid correction of hyponatremia- central pontinemyelinolysis (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 hoursCorrection 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 mechanismHyperosmolar-induced thirst sensation kicks in and people drink! Returns sOsm to normal
  • Water deficit=hypernatremic dehydrationDiuresis: osmotic, diuretics, post-obstructive, diuretic phase of ATNNephropathy: inability to concentrate the urine in renal dysplasia, obsturopathy, interstitial disease- leads to excess free water lossGI losses, skin losses
  • Very rareWith insufficient free water intakeSalt poisoning
  • Compare urine volume with fluid intakeWeight loss: diarrheaWeight gain: Increased Na retention- hyperaldosteronismHTN- HyperaldosteronismCNS- lethargy, weakness, irritability, seizures, anxietyRemember skin turgor is well preserved bc it is intracellular water lossIf hypovolemic and most often will be:Identify cause of water deficit and asses kidney’s response by eval renal conc abilityUrine Osm <800 mOsm/kg in hyperNa is a sign of concentrating defect
  • Replace urine volume with hypotonic fluids in addition to deficitNormal saline first if signs of circulatory collapseMeasure electrolytes q 2 hours until neurologically stableOral therapy has less risk of seizures and can tolerate a more rapid rate of correctionCorrection rate not to exceed 1mEq/h unless encephalopathicDo not correct >15mEq/24hr
  • Polyuria from nephrogenic DI

Renal Emergencies: Fluids and Electrolytes Renal Emergencies: Fluids and Electrolytes Presentation Transcript

  • Renal Emergencies
    Caroline Straatmann, MD
  • Outline
    Potassium
    Sodium
    Calcium
    Magnesium
    Hypertension
  • Total Body Water
  • Composition of Electrolytes:ICF and ECF
  • Hyperkalemia
  • Case
    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
  • Case
    What do you do first?
    EKG
    EKG shows peaked T waves
    What do you do next?
    Give calcium gluconate
    Stop his TPN, which has K in it!
  • Case
    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
  • Potassium
    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
  • Hyperkalemia
    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
  • Hyperkalemia
    Symptoms
    Skeletal muscle weakness
    Paralysis
    Parasthesias
    Respiratory failure
  • Hyperkalemia
    Decreased renal excretion
    Reduced GFR
    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
  • Cells
    3 Na
    ECF
    ICF
    Na= 10 mmol/L
    K=140 mmol/L
    Na= 150 mmol/L
    K=4 mmol/L
    2 K
  • Hyperkalemia
    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 and TPN!!!
  • Treatment
    Repeat serum K
    EKG stat
    If EKG shows changes, start treatment immediately
    Progression of changes
    Peaked T waves-Prolonged PR interval-ST depression-Widened QRS-Ventricular fibrillation
  • HyperkalemiaEKG Changes
    Peaked T waves
    Loss of P wave
    Widening of QRS
    ST depression
    Prolonged PR interval
    Ventricular dysrhythmias
    Cardiac arrest
     
  • Treatment
    1. Stop K intake
    IVFs, TPN
    2. Protect myocardium (any EKG changes)
    10 % Calcium gluconate infusion
    1 ml/kg/dose
    3. Shift K into the cells (K>7)
    Insulin 0.1 unit/kg/hr with D25W 1-2 mL/kg/hr (15 min)
    High dose inhaled beta agonists (albuterol) (30 min)
    Na Bicarbonate 1-2 meq/kg IV over 5-10 min (3-4hour)
  • HyperkalemiaTreatment
    Eliminate source of potassium intake or offending drugs
    K⁺ < 6 mEq/L
    Low potassium diet
    Diuretics
    K⁺ > 6 mEq/L
    Cation exchange resin: SPS
  • HyperkalemiaTreatment
    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
  • Hypokalemia
  • Hypokalemia
    Weakness or paralysis
    Ileus
    Cardiac dysrhythmias
    Delayed depolarization
    Flat/absent T waves
    U waves
  • Hypokalemia
    U waves
    BMP
    Hypernatremia
    Alkalosis
    Bartter’s
    Renin
    Aldosterone
    Cortisol
  • HypokalemiaTreatment
    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
  • Hyponatremia
  • Case
    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
  • Case
    What is the most likely diagnosis?
    Pseudohyponatremia
    SIADH
    Psychogenic polydipsia
    Hypoaldosteronism
    How would you raise the plasma sodium concentration?
  • Osmolality of Body Fluids
    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]
    2.8
    18
    • 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
    Sodium
  • Factitious Hyponatremia
    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
  • Hyponatremia
    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
  • HyponatremiaLoss of Sodium
    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)
  • HyponatremiaGain of Water
    Hypervolemia
    Fluid overload
    Congestive heart failure
    Water intoxication
    Diluted formula
    Hypotonic fluids
    SIADH
  • HyponatremiaEvaluation
    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
  • Treatment
    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
  • Treatment
    Symptomatic
    CNS manifestations, encephalopathic
    Use 3% NaCl (513 mEq/L) via infusion pump
    1 mL/kg/hr of 3%NaCl will raise serum Na by 1 mEq/L/hr
    Continue until patient is alert and seizure free
    Na has increased by 20 meq/L or to 125-130 mEq/L
    Actively seizing or impending resp failure
    Increase t0 4-8 mL/kg/hr
  • Hyponatremic Dehydration
    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) X Wt (kg)
    Desired Na⁺ is 135 mEq/L
    Maintenance and ongoing losses
    Replace over 24 hours
  • Hyponatremia
    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 pontinemyelinolysis
  • Hyponatremic Encephalopathy
    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
  • Hyponatremic Encephalopathy
    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 sNaq 2 hours
    Moritz et al. PediatrNephrol (2010) 25: 1225-1238
  • Insufficient Correction
    Too aggressive Correction
    Demyelination
    Cerebral Edema
    • Acute hyponatremia=Most dangerous
    • Symptomatic hyponatremia = Medical Emergency
  • Hypernatremia
  • Question
    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
  • Hypernatremia
    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
  • Hypernatremia
    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
  • Question
    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
  • Hypernatremia
    Water Deficit
    Renal loss
    Diuretic use
    Nephropathy with renal concentrating defect
    Diabetes insipidus
    Extrarenal loss
    Vomiting/Diarrhea
    Skin losses
  • Hypernatremia
    Increased Sodium Intake/Retention
    Salt poisoning
    Exogenous sodium
    Hypertonic feeding/saline
    NaHCO3 administration
    Mineralcorticoid excess
    Hyperaldosteronism
  • HypernatremiaEvaluation
    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⁺
  • HypernatremiaTreatment
    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
  • Hypercalcemia
  • Case
    A 19yo female with renal failure in in the ER. She c/o polyuria x 6 months and HA and constipation x 6 weeks. She is on HCTZ for HTN. BP is 140/92, P 86
    BUN/Cr=61/3
    Na=140
    Ca=13.8, Ph=3.9, Mg=1.9, Alb=4.2
    What do you do next?
    Calcitonin
    IV saline
    Loop diuretics
    Surgical consult
    Bisphosphonates
  • Hypercalcemia
    Stones
    Renal calculi
    Bones
    Bone pain
    Moans
    Depression
    Groans
    Constipation
  • Hypercalcemia
    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
  • Treatment
    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
  • Hypermagnesemia
    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
  • Hypermagnesemia
    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
  • Hypermagnesemia
    Symptoms
    Decreased DTRs, lethargy, confusion
    Hypocalcemia (hypermagnesemia suppresses PTH)
    Rarely of clinical significance
    Treatment
    Stop supplemental Mg
    Diuresis
    Dialysis
  • Hypertensive Emergencies
  • Case
    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?
  • Hypertensive Emergency
    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
  • Hypertensive Emergency
    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
  • Treatment of HTN Emergency
    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
  • Case
    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)
  • Treatment of HTN Emergency
    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
  • HTN Emergency
    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
  • On call
    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
  • HTN Urgency
    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
  • HTN Urgency
    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
  • Thank You