Caroline Straatmann, MD

Caroline Straatmann, MD
Renal Emergencies

Outline Potassium Sodium Calcium Magnesium Hypertension

Total Body Water We will start with some basic concepts.
0.6 x weight 1/3 ECF (Intravascular) ¼ Plasma ¾ Interstitial Fluid 2/3 ICF 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.

Composition of Electrolytes: ICF and ECF
Intracellular (mEq/L) Extracellular (mEq/L) Na 20 K 150 3-5 Cl ____ 98-110 HCO₃ 10 20-25 PO₄ 5 Protein 75 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.

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

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 Difference between intracellular and extracellular potassium concentrations determines the resting membrane potential of a cell

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 Common Drugs Increased intake
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 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

Cells 3 Na 2 K ECF ICF Na= 10 mmol/L K=140 mmol/L Na= 150 mmol/L

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!!! 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

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

Hyperkalemia EKG Changes
Peaked T waves Loss of P wave Widening of QRS ST depression Prolonged PR interval Ventricular dysrhythmias Cardiac arrest Associated with weakness, parasthesias, tetany Order of progression although not always dependent on potassium level

Treatment 1. Stop K intake 2. Protect myocardium (any EKG changes)
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)

Hyperkalemia Treatment
Eliminate source of potassium intake or offending drugs K⁺ < 6 mEq/L Low potassium diet Diuretics K⁺ > 6 mEq/L Cation exchange resin: SPS 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

Hyperkalemia Treatment
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 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

Hypokalemia

Hypokalemia Weakness or paralysis Ileus Cardiac dysrhythmias
Delayed depolarization Flat/absent T waves U waves

Hypokalemia U waves BMP Renin Aldosterone Cortisol Hypernatremia
Alkalosis Bartter’s Renin Aldosterone Cortisol 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

Hypokalemia Treatment
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= 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] 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 2.8 18

Serum osmolality is tightly regulated
Sodium 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 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

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 “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.

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 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

Hyponatremia Loss 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) Relative water excess Hypovolemia= loss of salt AND water from ECF

Hyponatremia Gain of Water
Hypervolemia Fluid overload Congestive heart failure Water intoxication Diluted formula Hypotonic fluids SIADH 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

Hyponatremia Evaluation
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 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.

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 Actively seizing or impending resp failure
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 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 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

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 pontine myelinolysis 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)

Hyponatremic Encephalopathy
Early ADVANCED Headache Nausea and vomiting Lethargy Weakness Confusion Altered consciousness Agitation Gait disturbances Seizures Coma Apnea Pulmonary edema Decorticate posturing Dilated pupils Anisocoria Papilledema Cardiac arrhythmias Central diabetes insipidus 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

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 sNa q 2 hours Moritz et al. Pediatr Nephrol (2010) 25: 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 mEq/L and should avoid normo- or hypernatremia

Acute hyponatremia=Most dangerous
Insufficient Correction Too aggressive Correction Cerebral Edema Demyelination 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 As opposed to hyponatremia which can sometimes be normal in certain physiologic states

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 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

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 Extrarenal loss Diuretic use
Nephropathy with renal concentrating defect Diabetes insipidus Extrarenal loss Vomiting/Diarrhea Skin losses 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

Increased Sodium Intake/Retention
Hypernatremia Increased Sodium Intake/Retention Salt poisoning Exogenous sodium Hypertonic feeding/saline NaHCO3 administration Mineralcorticoid excess Hyperaldosteronism Very rare With insufficient free water intake Salt poisoning

Hypernatremia Evaluation
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⁺ 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

Hypernatremia Treatment
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 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

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 Bones Moans Groans Renal calculi Bone pain
Depression Groans Constipation

Hypercalcemia Symptoms Differential diagnosis
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 Polyuria from nephrogenic DI

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 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 Rarely of clinical significance Treatment
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. 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 IV Enalapril (Enalaprilat) IV hydralazine
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 Isradipine Labetalol
Short-acting- see effects in min 0.25 mg/kg initial dose 10 mg capsules Isradipine Short-acting: effects within one hour mg/kg/dose Labetalol Heart rate is dose limiting factor

Thank You

Caroline Straatmann, MD

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