Electrolyte Disturbances

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Electrolyte disturbances in PICU:

Electrolyte disturbances in PICU Dr. Isha Deshmukh, Assistant Professor, Department of Pediatrics, MGIMS

Normal Physiology:

Regulation of Na+  ECF volume Regulation of K+  Cellular Electrophysiology Water Regulation  Changes in Serum Osmolality Normal Physiology

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TBF INTRACELLULAR Fluid 40% INTERSTITIAL Fluid 15% Intra- Vascular 5% EXTRACELLULAR

Why are patients in PICU prone for dyselectrolytemias?:

Critical disorders such as severe burns, trauma, sepsis, brain damage, and heart failure reduced perfusion to the kidney due to hypovolemia /hypotension activation of hormonal systems  RAAS and vasopressin tubular damage caused by ischemic or nephrotoxic kidney damage Patients on intravenous fluids Why are patients in PICU prone for dyselectrolytemias?

Basic principles of fluid therapy:

Basic principles of fluid therapy Replace Maintain Repair Abnormal loss: GIT, 3 rd space,Ongoing loss, septic and Hypovolemic shock Insensible water loss + urine Acid base, electrolyte imbalances

Sodium (Na+):

Normal S Na : 135-145 Major component of serum osmolality S osm = (2 x Na + ) + (BUN / 2.8) + (Glu / 18) Normal: 285-295 Alterations in S Na reflect an abnormal water regulation Sodium excretion occurs in stool and sweat, but the kidney regulates sodium balance and is normally the principal site of sodium excretion. Low plasma [Na+]  a relative water excess in conjunction with impaired ability of the kidney to excrete electrolyte-free water. 6 Sodium (Na + )

Pathophysiology:

Na concentration increases  higher plasma osmolality  increased thirst & increased secretion of ADH  renal conservation of water  increase the water content of the body Na concentration returns to normal. During hyponatremia, the decrease in plasma osmolality  stops ADH secretion & consequent renal water excretion  increase in the sodium concentration. Volume depletion takes precedence over osmolality & volume depletion stimulates ADH secretion even if a patient has hyponatremia. Pathophysiology

Hypernatremia - Causes:

EXCESSIVE SODIUM Improperly mixed formula Excess sodium bicarbonate Ingestion of seawater or sodium chloride Intentional salt poisoning (child abuse or Münchhausen syndrome by proxy) Intravenous hypertonic saline Hyperaldosteronism WATER AND SODIUM DEFICITS Gastrointestinal losses Cutaneous losses Renal losses Hypernatremia - Causes

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WATER DEFICIT Nephrogenic diabetes ; Central diabetes insipidus Increased insensible losses Inadequate intake Diarrhea Emesis/ Nasogastric suction Osmotic cathartics (e.g., lactulose) Burns ; Excessive sweating Osmotic diuretics (e.g., mannitol) Diabetes mellitus Chronic kidney disease (e.g., dysplasia and obstructive uropathy) Polyuric phase of acute tubular necrosis Postobstructive diuresis

Sodium (Na+):

Hypernatremia Clinical presentation Dehydration “Doughy” feel to skin Irritability, lethargy, weakness Intracranial hemorrhage Thrombosis: renal vein, dural sinus Seizures Encephalopathy 10 Sodium (Na + )

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Children with hypernatremic dehydration tend to have better preservation of intravascular volume because of the shift of water from the intracellular space to the extracellular space. This maintains BP & UO  less symptomatic initially and potentially become more dehydrated before seeking medical attention. Breast-fed infants with hypernatremia are often profoundly dehydrated. Probably because of intracellular water loss, the pinched abdominal skin of a dehydrated, hypernatremic infant has a "doughy" feel .

CNS changes in Hypernatremia:

Brain develops idiogenic osmoles On correction these take time to decrease Faster correction will cause excessive shift of water into the cells and thus cerebral edema Even though central pontine myelinolysis (CPM) is classically associated with overly rapid correction of hyponatremia, both CPM & EPM can occur in children with hypernatremia. Thrombotic complications occur in severe hypernatremic dehydration and include stroke, dural sinus thrombosis, peripheral thrombosis, and renal vein thrombosis. This is secondary to dehydration and possibly hypercoagulability associated with hypernatremia. CNS changes in Hypernatremia

Cerebral oedema and adaptation to Na:

Cerebral oedema and adaptation to Na

Sodium (Na+):

Management : Use of decreased concentration Na infusate as initial therapy > 165 meq/l. Treatment Rate of correction for Na + 1-2 mEq/L/hr Calculate total body water deficit – children : (correction factor) = 0.6 * wt Correction also depends upon rate of rise in sodium. Correct serum Na over 48-72 hours. 14 Sodium (Na + )

Androuge – Madias formula:

Calculates the amount that plasma sodium will drop following infusion of varying composition: ΔSNa = {[Na] inf − SNa} ÷ (TBW + 1) ΔSNa is a change in SNa by 1 litre of fluid [Na] inf is infusate Na concentration in 1 liter of solution Total body water (TBW) = 0.6 × body weight (for children) Androuge – Madias formula

Beware of Formulas :

Formulas assume body is a closed circuit not accounting for renal/non-renal losses and over/under estimate the correction. Help roughly in deciding initial fluid therapy Frequent measurement of serum Na 2-4 hourly can help decide ongoing correction Moritz and Ayus. Pediatr Nephrol 2005 Beware of Formulas

Treatment of hypernatremic dehydration:

Phase 1: Restoration of intra-vascular volume, 20 ml/kg NS Phase 2: Determine the time of correction 145-157: 24 hrs 158-170: 48 hrs 171-183: 72 hrs 184-196: 84 hrs Replace ongoing losses with N/2 saline with KCl Treatment of hypernatremic dehydration

Type of fluid:

Type of fluid  Does not matter, rate of correction matters N/4 to N/2 saline May run two drips: 1 st : N/2 DNS with KCl 2 nd : Iso P Monitor Na: 6 hourly and adjust the rate Less decrease: increase Iso P More decrease: increase N/2 DNS Type of fluid

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Hypernatremia

Sodium (Na+):

Hyponatremia: Etiology Hypervolemic CHF Cirrhosis Nephrotic syndrome Hypoalbuminemia Septic capillary leak Hypovolemic Renal losses Cerebral salt wasting Extra-renal losses Reduced aldosterone effect GI losses Third space loss 21 Sodium (Na + )

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Removal of excess water by the kidney requires urinary dilution  compromised in patients in ICU: (1) Heart failure, sepsis, shock, and multiple organ dysfunction syndrome -- impair GFR & enhance sodium and water reabsorption at the PCT, thereby diminishing delivery of the filtrate to the diluting segment, i.e., the thick ascending limb of the loop of Henle & DCT (2) loop diuretics, thiazides, osmotic diuretics, and tubulointerstitial pathology reduce the reabsorption of Na and Cl in the diluting segment; (3) and nonosmotic stimuli for vasopressin production such as pain, nausea, medications, and hypovolemia lead to increased water reabsorption in the collecting duct. inappropriate administration of fluids.

SIADH: Important concept to understand:

Caused by various etiologies CNS disease – tumor, infection, CVA, SAH, DST Pulmonary disease – TB, pneumonia, positive pressure ventilation Malignancy – CNS; thymoma, lymphoma Drugs – NSAIDs, diuretics Surgery - Postoperative Idiopathic – most common SIADH: Important concept to understand

Physiology of SIADH:

In SIADH, there is secretion of ADH that is not inhibited by either low serum osmolality/ expanded intravascular volume Unable to excrete water. Dilution of the serum sodium  hyponatremia. In addition, the expansion of the extracellular volume due to the retained water causes a mild increase in intravascular volume. The kidney increases sodium excretion in an effort to decrease intravascular volume to normal and, thus, these patients have a mild decrease in body sodium. Physiology of SIADH

Sodium (Na+):

Sodium (Na + ) Urine Output Serum Na Urine Na Serum Osm Urine Osm DI SIADH CSW

SIADH vs Cerebral Salt Wasting:

Clinical Parameter SIADH Cerebral Salt Wasting Serum Na Low Low Urine output Normal or low High Urine Na High(> 80 mmol/L) Very high(>150 mmol/L) Intravascular volume status Normal or high Low Serum uric acid Low variable Response to NS bolus Hyponatremia persists Hyponatremia improves SIADH vs Cerebral Salt Wasting

Treatment :

Asymptomatic or Chronic SIADH Water restriction Daily fluid intake < 24 hr urinary output + insensible loses Use of frusemide Demeclocycline Inhibits the effects of ADH – causes nephrogenic DI Lithium – inconsistent effect Oral urea – causing osmotic diuresis Cerebral salt wasting- Fludrocortisone Treatment

Redistributive hyponatremia:

Traditional Katz conversion Corrected Na = Observed Na + [(Glucose-100)/100] x 1.6 mEq/L Redistributive hyponatremia

Approach to Hyponatremia:

1 st assess volume status Is the patient volume overloaded, depleted, or euvolemic? 2 nd assess osmolality (hyper, iso, or hypo) Is the blood concentrated? For hypotonic hyponatremia, continue to 3 rd step: 3 rd assess urinary sodium excretion and FeNa % Is the urine concentrated? *Remember VOU – volume status, osmolality, and urine studies Approach to Hyponatremia

STEP 1 – (V) Volume Status:

1 st assess volume status (extracellular fluid volume) Hypotonic hyponatremia has 3 main etiologies : Hypovolemic – both H2O and Na decreased (H20 < Na) Consider obvious losses from diarrhea, vomiting, dehydration, malnutrition, etc Euvolemic – H20 increased and Na stable Consider siADH, thyroid disease, primary polydipsia Hypervolemic – H20 increased and Na increased (H2O > Na) Consider obvious CHF, cirrhosis, renal failure STEP 1 – (V) Volume Status

STEP 2 - (O) Osmolality :

2 nd assess osmolality hyper, iso, or hypo Hypotonic hyponatremia = warrants further workup, especially when there is no obvious fluid overload or depletion Serum Osmolality (mosm/kg) H ypertonic - >295 h yperglycemia, mannitol, glycerol Isotonic - 280-295 pseudo -hyponatremia from elevated lipids or protein Hypotonic - <280 e xcess fluid intake, low solute intake, renal disease, siADH, hypothyroidism, adrenal insufficiency, CHF, cirrhosis, etc. STEP 2 - (O) Osmolality

STEP 3 – (U) Urine Studies:

For euvolemic hyponatremia, check urine osmolality Urine osmolality <100 - excess water intake Primary polydipsia, tap water enemas, post-TURP Urine osmolality >100 - impaired renal concentration siADH, hypothyroidism, cortisol deficiency Check urine sodium & calculate FeNa % A low urine sodium (<10) and low FeNa (<1%) implies the kidneys are appropriately reabsorbing sodium A high urine sodium (>20) and high FeNa (>1%) implies the kidneys are not functioning properly STEP 3 – (U) Urine Studies

Urine Analysis:

Analysis of the urine differentiates renal and nonrenal etiologies When the losses are extrarenal, the kidney responds to volume depletion with low urine volume, a concentrated urine, and sodium retention (urine sodium <20 mEq/L). With renal causes, the urine volume is not appropriately low, the urine is not maximally concentrated, and the urine sodium may be inappropriately elevated Urine Analysis

Key points…….:

A patient with hyponatremia can have a low, normal, or high serum osmolality Child with hypovolemic hyponatremia, the urine sodium is very useful in differentiating between renal & nonrenal causes. The interpretation of the urine sodium is challenging with diuretics because it is high when diuretics are being used but low after the diuretic effect is gone. The urine sodium is not useful if a metabolic alkalosis is present; the urine chloride must be used instead Key points…….

Hyponatremia….:

Clinical manifestations of hyponatremia  cause of the hyponatremia the rapidity of onset. Clinical manifestations of hyponatremia  not seen till the serum Na to 120 - 125 mEq/L May occur in presence of decreased, increased or normal amounts of total body sodium Hyponatremia….

Hyponatremic seizure:

Treatment Hypertonic saline (3% NaCl) infusion To correct sodium to 125 mEq/L, the deficit is equal to 0.6 X weight[kg] X (125 - measured sodium) 0.6 X 6 X (125-110) = 54 mEq Hyponatremic seizure

Principles of Hyponatremia Management:

Asymptomatic Hyponatremia  Use 0.9%NaCl Symptomatic Hyponatremia Use 3% NaCl Correct only 12mEq/L deficit per day Chronic Hyponatremia or acute hyponatremia with severe symptoms should receive hypertonic saline only to arrest the symptoms and followed by slow correction @ 0.5 mEq/L 5 – 6 ml/kg 3% NaCl  5 meq/l Periodic 1-2 ml/kg/h with frusemide Refractory hyponatremia - minerelocorticoids Principles of Hyponatremia Management

ADH receptor Antagonist:

Conivaptan V1 & V2 receptor antagonist; nonselective; IV limited for 4 days FDA approval for hyponatremia due to SIADH, congestive heart failure and cirrhosis. Tolvaptan (oral) ADH receptor Antagonist

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Hyponatremia

Central Pontine Myelinolysis:

Develops with Aggressive treatment of Chronic hyponatremia Raising Sr.Na >12 meq/L/day. This may occur if there was unrecognized volume depletion with sudden removal of the ADH stimulus during treatment with resulting rapid water diuresis. Thiazide-induced hyponatremia is the classical situation in which this scenario may occur. Central Pontine Myelinolysis

Unfortunately….:

Unfortunately….

CPM:

Focal demyelination in the Pons & extrapontine areas. Causes  dysarthria Spastic Quadriplegia Pseudobulbar palsy Seizures Altered Mental Status Coma & Death CPM

Potassium Homeostasis:

Potassium Homeostasis Most potassium is intracellular Distribution of between the intra- and extracellular compartments alters serum levels Na+, K+-ATPase maintains the high intracellular K+ concentration Pumping Na+ out of the cell and K+ into the cell. Insulin activates the Na+, K+-ATPase- drives K+ into the cell Acidosis (high H+) drives potassium extracellularly; (H+ in for K+ out) Alkalosis drives K+ into the cell β-Adrenergic agonists stimulate the Na+, K+-ATPase, ↑cellular uptake of K+ α-Adrenergic agonists and exercise cause a net movement of K+ out. Potassium is necessary for: Electrical responsiveness of nerve and muscle cells Contractility of cardiac, skeletal, and smooth muscle.

Internal Balance :

Acid-Base 2. Insulin 3. Mineralocorticoids 4. Catecholamines Internal Balance

1. Acid-Base :

With increasing extracellular H+ concentration (acidosis), K+ moves from the intracellular to the extracellular compartment in exchange for H+. The increase in plasma K+ concentration is small at first, but increases for a time, as the acidosis continues. However, K+ is lost in the urine, and one sees a lessening of the effect of acidosis on serum K+. The K+ changes seen with metabolic alkalosis are not well understood and are complicated by the kaliuresis that occurs. Some intracellular shift of K+ does occur, but the decrease in serum K+ is mainly due to renal loss. 1. Acid-Base

Internal Balance :

2. Insulin Insulin stimulates K+ uptake by muscle and hepatic cells. 3. Mineralocorticoids Aldosterone makes cells more receptive to the uptake of K+ and increases renal excretion of K+. Internal Balance

4. Catecholamines :

Epinephrine initially increases plasma K+ because of combined alpha and beta receptor stimulation, which releases K+ from the liver. The response is followed by a decrease in plasma K+ caused by beta-receptor stimulation, which enhances K+ uptake by muscle and liver. The end result is a decrease in serum K+ Propranolol impairs cellular uptake of K+. 4. Catecholamines

External Balance Renal Potassium Excretion :

1. Potassium Intake - An acute or chronic increase in K+ intake leads to increased secretion in the distal convoluted tubule. 2. Sodium Intake and Distal Tubular Flow Rate - A sodium load will increase flow past the distal tubule and cause K+ wasting. The converse is true too. 3. Mineralocorticoids - A mineralcorticoid deficiency leads to K+ retention and Na+ wasting, just as excess leads to opposite changes. External Balance Renal Potassium Excretion

Potassium (K+):

Solvent drag Increase in S osmo  water moves out of cells  K + follows 0.6 S K / 10 of S osmo Evidence of solvent drag in diabetic ketoacidosis Acidosis Low pH  shifts K + out of cells (into serum) Hi pH  shifts K + into cells 0.3-1.3 mEq/L K + change / 0.1 unit change in pH in the opposite direction 51 Potassium (K + )

Hypokalemia:

Usually secondary to: GI loss (vomiting, diarrhea) Urinary losses (diuretics, RTA) Also think about : co-existing electrolyte abnormality (hypomagnesemia), hyperaldosteronism, insulin therapy, albuterol, alkalosis) Indications for replacement: Evidence of potassium loss Significant deficit in body potassium Acute therapy in redistributive disorders (periodic paralysis, thyrotoxicosis) Hypokalemia

Causes Transcellular Shift:

 Blockers, Digoxin Insulin deficient states Hyperglycemia/hypertonic-severe Metabolic acidosis Ischemic gut NSAID!!! Sepsis- inc catecholamine states Adrenal insufficiency Hyporenin/Hypoaldo states Type 4 RTA, sickle cell, intestinal nephritis, obstructive uropathy Causes Transcellular Shift

Hypokalemia:

Symptoms: usually manifest when serum K <3.0 Muscle weakness (K <2.5), cramps, rhabdomyolysis Respiratory muscle weakness GI symptoms: anorexia, nausea, vomiting Cardiac arrhythmias: atrial tachycardia, junctional tachycardia, AV block, ventricular tachycardia or fibrillation EKG abnormalities: PAC, PVC, sinus bradycardia, ST segment depression, decreased amplitude of T-wave, increased amplitude of U-wave (mostly in V4-V6) If prolonged hypokalemia: functional changes in the kidney and glucose intolerance Hypokalemia

ECG changes ::

The typical finding of hypokalemia include: 1) depression of the T wave. 2) elevation of the U wave. ECG changes :

Management:

The underlying cause should be identified and treated. If the problem is mainly one of redistribution of K into cells, reversal of the cause (e.g. correction of alkalosis) may be sufficient If hypokalemia is mild : oral K supplements are given. If the patient is severely hypokalemic: the cautious infusion of intravenous K should be considered (but not more than 20 mmol per hour). Management

Formulations:

Potassium Chloride : PREFERRED AGENT Most patients with hypokalemia and acidosis are also chloride depleted Raises serum potassium at a faster rate Available as salt substitute, liquid, slow release tablet or capsule, and IV Oral tab: 20- 40meq Oral syp. – 5ml = 13 meq Intravenous KCl. Potassium Bicarbonate/Citrate/Acetate: can be used in patients with hypokalemia and metabolic acidosis Potassium Phosphate: Rarely used (Fanconi syndrome with phosphate wasting) Formulations

Hyperkalemia:

Normal serum potassium 3.5-5.5 mEq/L Hyperkalemia is a serum potassium greater than 5.5 mEq/L Hyperkalemia

Hyperkalemia:

DIAGNOSIS. Spurious hyperkalemia is very common in children, get repeat value! Basic Metabolic Panel- renal fxn and acid-base status. If Hyponatremia and volume depletion due to salt wasting- think low aldosterone Phosphorus and Uric Acid If Hyperphosphatemia and hyperuricemia- think causes of cell death Tumor lysis syndrome Rhabdomyolysis- Elevated creatinine phosphokinase (CPK) level and ↓Ca Hemolysis- Hemoglobinuria and a decreasing hematocrit When no clear etiology - differentiating decreased potassium excretion from the other etiologies Measuring urinary potassium to assess renal excretion of potassium. The transtubular potassium gradient (TTKG) = [K]urine/[K]plasma × (plasma osm/urine osm) urine osmolality > serum osmolality for the result to be valid. TTKG should be >10 in hyperkalemia (<8 suggests a defect in renal K+ excretion) Aldosterone level Hyperkalemia

What to Do??:

Is the value accurate?? Are there EKG changes?? Is there evidence of Hemolysis on lab specimen?? Recheck blood Associated systemic dysfunction ABG changes What to Do??

EKG Changes Peaked T Waves:

EKG Changes Peaked T Waves

EKG Changes Widening of QRS Complex:

EKG Changes Widening of QRS Complex

EKG Changes Ventricular Tachycardia/Torsades:

EKG Changes Ventricular Tachycardia/Torsades

Treatment :

1- Stabilize myocardial membrane 2- Drive extracellular potassium into the cells 3- Removal of Potassium from the body 4 –prevent further hyperkalemia. Treatment

Treatment Stabilize the Myocardial Membrane:

Elevations in the extracellular potassium concentration will result in a decrease in membrane excitability that may be manifested clinically by impaired cardiac conduction and/or muscle weakness or paralysis Calcium antagonizes the cellular effects of Hyperkalemia Treatment Stabilize the Myocardial Membrane

Treatment Stabilize the Myocardial Membrane:

Types of Calcium Calcium Gluconate  can be given central or peripherally Calcium Chloride  can only be given via central line Has higher concentration of calcium and if given peripherally will cause local sclerosis and gangrene Treatment Stabilize the Myocardial Membrane

Treatment Drive Extracellular Potassium Into the Cells:

1-  2 Agonists (albuterol) Drives K 2+ intracellular by increasing Na-K ATPase in skeletal muscle Usual dose for asthma 0.5 cc/3cc NSS Dose for hyperkalemia 5cc over 10 min 10X more potent Effects occur in 20-30 min ADR-palpitations/arrhythmia Treatment Drive Extracellular Potassium Into the Cells

Treatment Drive Extracellular Potassium Into the Cells :

2- Insulin and Glucose Drives K 2+ intracellular by increasing Na-K ATPase in skeletal muscle 1 amp D50 with 5-10 units of regular insulin IV Effects seen in 30 min with peak in 60 min Duration several hours ADRs: hypoglycemia Treatment Drive Extracellular Potassium Into the Cells

Treatment Drive Extracellular Potassium Into the Cells:

3- Sodium Bicarbonate (NaHCO 3 ) Causes an alkalosis leading to potassium wasting Only works if hyperkalemia 2 o to ongoing severe metabolic acidosis Onset few minutes but effects are not long lasting Treatment Drive Extracellular Potassium Into the Cells

Treatment Removal of Potassium From the Body:

1- Loop Diuretic Leads to loss of K + in urine by inhibiting NA-K-2CL transporter in Loop of Henle Need renal function and volume to get filtrate to Loop of Henle Treatment Removal of Potassium From the Body

Treatment Removal of Potassium From the Body:

2- Sodium Polystyrene Sulfonate (Kayexalate ) Exchanges Na + for K + and binds it in gut, primarily in large intestine, decreasing total body potassium K removed from body 8-12 hours after administration in stool Given PO/PR ADRs: intestinal necrosis/gangrene DO NOT GIVE INDISCRIMINATLY Treatment Removal of Potassium From the Body

Disorders of calcium homeostasis:

Factors affecting calcium met: Changes in protein binding & chelation (with PO4/ other anions) Excessive /deficient hormonal action. Protein binding is Ph dependent. Acidic ph decreases calcium binding & increases ionized ca Alkalosis increases binding & reduces ca. Direct measurement of ca  ICU Disorders of calcium homeostasis

Hypocalcemia :

Determination of free ionized calcium – diagnostic. Rate of decline contributes to severity of symptoms Correction for protein binding Correction of underlying cause – respiratory alkalosis, chemotherapy, blood product transfusion. Drugs – calcitonin, EDTA, theophylline. Hypocalcemia

Treatment :

Appropriate efforts to reduce serum phosphate levels, as intravenous calcium causes deposition of calcium – phosphate salts. Urgency of therapy – determined by child’s clinical status Intravenous calcium chloride/ gluconate – infusion under cardiac monitoring Asymptomatic hypocalcaemia – oral supplements. Treatment

Hypercalcemia :

Serum total calcium > 15 mg/dl Renal , CVS, CNS disturbances predominate & reflect both the degree & duration of calcium elevation Alteration in cardiac conduction system include shortened QT interval and a tendency to Dysrhythmias Less common in children Increased bone reabsorption, increased intestinal calcium absorption, decreased renal excretion of calcium Hypercalcemia

Treatment :

Hydration with isotonic saline solution (200 – 250 ml/kg/day) and furosemide diuresis ( 1 mg/kg) results in calciuresis and amelioration of hypercalcemia . Drugs inhibit bone resorption – calcitonin, mithramycin, & indomethacin. Treatment

Hypomagnesemia :

Hypomagnesemia is associated with a 2-3 fold increased mortality in critically ill & postoperative patients Clinically hypomagnesemia is often associated with hypokalemia & hypocalcemia. Because of the role of magnesium in transmembrane potassium transport, simultaneous correction of hypomagnesemia is required to correct hypokalemia. Hypomagnesemia

Symptoms of hypomagnesemia:

Symptoms of hypomagnesemia include respiratory muscle weakness Fasciculations , convulsions cramps, tetany coronary artery vasospasm, and supra- and ventricular arrythmias. Symptoms of hypomagnesemia

PowerPoint Presentation:

In intensive care, the preferred administration route is IV in the form of slow infusions of magnesium sulfate of up to 25-50 mg/kg to correct a magnesium deficit. Hypermagnesemia is an infrequent and dangerous complication of magnesium administration  patients with renal insufficiency. Magnesium is a first line treatment of torsades de pointes and arrythmias induced by digitalis.

Hyperphosphatemia:

Causes Increased intake Decreased excretion Transcellular shifts Hyperphosphatemia

Increased Intake:

Enemas and laxatives Sodium phosphorus laxatives Increased in ileus and hirschprung’s disease Cow's milk in infants Higher phosphorus content than human breastmilk Treatment of hypophosphatemia Overly aggressive treatment Vitamin D intoxication Excessive GI absorption of calcium and phosphorus Hypercalcemia suppresses PTH release Phosphorus excretion is then decreased at kidney ↑phos resorption at proximal convoluted tubule Increased Intake

Transcellular Shifts:

Tumor lysis syndrome Cellular breakdown with release of contents ↑phos, ↑ K+, ↑uric acid, ↓calcium Rhabdomyolysis Muscle cell breakdown with myoglobin release ↑phos, ↑ K+, ↑CPK) Acute hemolysis Red blood cell breakdown ↑phos, ↑ K+, ↑ indirect bilirubin, ↑LDH Diabetic ketoacidosis and lactic acidosis During acidosis, phosphorus is shifted from the intracellular to the extracellular space Transcellular Shifts

Clinical Manifestations:

Hypocalcemia Tissue deposition of calcium-phosphorus salt Inhibition of 1,25-dihydroxyvitamin D production Decreased bone resorption. Symptomatic hypocalcemia is most likely when phosphorus increases rapidly diseases predisposing to hypocalcemia are present chronic renal failure rhabdomyolysis). Systemic calcification Solubility of phosphorus and calcium in the plasma is exceeded. Inflamed conjunctiva- foreign body feeling, erythema, and injection. (BOBBY) Hypoxia from pulmonary calcification Renal failure from nephrocalcinosis. Clinical Manifestations

Diagnostic Testing:

Assess renal function: Bun and creatinine. Focus history on intake of phosphorus and the presence of chronic disease. If suspect rhabdomyolysis, tumor lysis, or hemolysis Check potassium, uric acid, calcium, LDH, bilirubin, and CPK If mild hyperphosphatemia and sign. hypocalcemia check serum PTH level Distinguishes between hypoparathyroidism and pseudohypoparathyroidism. Diagnostic Testing

Treatment:

Depends on its severity and etiology. Dietary phosphorus restriction- in mild hyperphosphatemia Intravenous fluids- enhance renal excretion if kidney function is intact. Oral phosphorus binder- in significant hyperphosphatemia Prevents absorption of dietary phos Removes phos from the body by binding what is normally secreted and absorbed by GI tract Binders containing aluminum hydroxide or use calcium carbonate if also hypocalcemic. Aluminum-containing binders NOT used in CRF because of aluminum toxicity. Esp if taking oral citrate, which ↑ gastrointestinal absorption of aluminum. Preservation of renal function-high urine flow permits continued excretion Dialysis directly removes phosphorus from the blood in ESRD only an adjunct to dietary restriction and phosphorus binders dialysis is not efficient enough to keep up with normal dietary intake . Treatment

Thank you for your attention……… :

Thank you for your attention……… ALL SUGGESTIONS ARE WELCOME

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