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