Renal Emergencies: Fluids and Electrolytes
Transcript of Renal Emergencies: Fluids and Electrolytes
Renal EmergenciesCaroline Straatmann, MD
Total Body Water
0.6 x weight
1/3 ECF
¼ Plasma(Intravascul
ar)¾
Interstitial Fluid
2/3 ICF
Composition of Electrolytes:ICF and ECF
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
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?EKGEKG shows peaked T wavesWhat do you do next?Give calcium gluconateStop 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
causeCan be life-threatening due to
risk of ventricular arrhythmiasNormal 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
ICF
Na= 10 mmol/LK=140 mmol/L
ECF
Na= 150 mmol/LK=4 mmol/L
3 Na
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 KEKG 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
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 = EMERGENCYStabilize myocardium
IV calcium chloride or calcium gluconate (10%)
Shift potassium into cells Beta agonists, insulin/glucose, sodium
bicarbonateRemove excess potassium from the body
Sodium polystyrene sulfonate (SPS) Furosemide Hemodialysis
Hypokalemia
Weakness or paralysis IleusCardiac 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
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
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]
• 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/LLoss of sodiumGain of waterMost 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
HypervolemiaFluid overload
Congestive heart failureWater 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
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 pontine myelinolysis
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 sNa q 2 hoursMoritz et al. Pediatr Nephrol
(2010) 25: 1225-1238
Insufficient Correction
Cerebral Edema
Too aggressive Correction
Demyelination
• Acute hyponatremia=Most dangerous• Symptomatic hyponatremia = Medical
Emergency
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/LAlways abnormal and should be
evaluatedFree water deficit Increased sodium
intake/retention Increased serum OsmDoes 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 DeficitRenal 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 causeCorrect volume disturbance if
presentReplace free water deficit
4mL/kg x (desired change in serum Na (mEq/L))
Risk of cerebral edema from rapid correction
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 significanceTreatment
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
ICUDon’t lower BP too rapidly
Lower no more than 20-25% in 1st 8 hours
Preserve cerebral perfusionAcute 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