Electrolyte disorders in critically ill patients

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Electrolyte disorders in Critically ill patients : 

Electrolyte disorders in Critically ill patients Ubaidur Rahaman Senior Resident, CCM, SGPGIMS, Lucknow, India

Slide 2: 

“It is the internal environment (not the external world) that provides the physical need for life” CLAUDE BERNARD

BODY FLUID COMPARTMENTS Arrow represents fluid movement : 

BODY FLUID COMPARTMENTS Arrow represents fluid movement Review of Medical Physiology, William F. Ganong

Electrolyte Composition of Body Fluid Compartments : 

Electrolyte Composition of Body Fluid Compartments

Composition of body fluids losing continuously : 

Composition of body fluids losing continuously

Composition of IV fluids in comparison to Plasma : 

Composition of IV fluids in comparison to Plasma

Slide 7: 

Sodium Water disturbances

Slide 8: 

Na is the most abundant molecule in ECF Na is the most osmotically active molecule in ECF S. Osm ( mOsm/kg of water) (2*[Na] + [Glucose/18] + [BUN/2.8] (Na in meq/L, Glucose in mg/dL, BUN in mg/dL) Osmotic pressure and osmolality determines distribution of fluid in body compartments Contribution of Gluc and BUN is 5 mOsm/L

OSMOLALITY : 

OSMOLALITY 24 hour urine sample-500-800 mOsm/kg Extreme range-50-1400mOsm/kg Random urine sample- 300-900mOsm/kg After overnight fluid restriction Urine omolality > 3 times serum osmolality (>800) 280-295 mOsm/kg Serum Urine

Real story in critically ill patients : 

Real story in critically ill patients S. Osm = 2* (140) + 90/18 + 5/2.8 = 280 + 5 + 1.7 = 286.7 S. Osm = 2* (145) + 180/18 + 60/2.8 = 290 + 10 + 21 = 321

Slide 11: 

Na WATER

Slide 12: 

Na / water regulation Thirst ADH RAA Kidney

Epidemiology of electrolyte disorder in ICU : 

Epidemiology of electrolyte disorder in ICU

Slide 14: 

Intensive Care Medicine 2010, 36(2):304-11 Incidence and prognosis of dysnatremias present on ICU admission Funk GC, Lindner G, Druml W, Metnitz B, Schwarz C, Bauer P, Metnitz PG Incidence hyponatremia-17.7%, Hypernatremia-6.9% All types and grades of dysnatremia were associated with increased hospital mortality independent mortality risk rising with increasing severity of both hyponatremia and hypernatremia retrospective study in 77 medical, surgical, and mixed ICUs in Austria, 151,486 adults patients admitted over a period of 10 years (1998-2007). 75% patients had normal sodium levels (Na:135-145) on ICU admission

Slide 15: 

Critical Care 2008, 12:R162 The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia in medical-surgical intensive care units Henry Thomas Stelfox, Sofia B Ahmed, Farah Khandwala, David Zygun, Reza Shahpori, Kevin Laupland Incidence Hyponatremia- 11%, hypernatremia-26% Median time to develop dysnatremia- 2 days Median duration of dysnatremia-2 days More than 1 distinct epi of dysnatremia- 25% (Hyponatremia-16%, hypernatremia-19%) 8142 adults admitted in 3 medical-surgical ICUs Over 6 years documented to have normal S. sodium levels (133 to 145 mmol/L) on the first day of ICU admission hospital mortality increased significantly Independent of SOI ( hypoNa-28%, hyperNa-34%, normoNa-16%) Continued…..

Slide 16: 

Critical Care 2008, 12:R162 The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia in medical-surgical intensive care units Henry Thomas Stelfox, Sofia B Ahmed, Farah Khandwala, David Zygun, Reza Shahpori, Kevin Laupland Continued…..

Slide 17: 

Increased risk of hypernatremia Raised S.creatinine Mechanical ventilation Increased risk of both hyper and hyponatremia Length of stay in ICU Increased APACHE II score Dysnatremias develop insidiously over 2 days Difficult to identify as clinicians preoccupied with more acute medical issues and other lab investigations Critical Care 2008, 12:R162 The epidemiology of intensive care unit-acquired hyponatraemia and hypernatraemia in medical-surgical intensive care units Henry Thomas Stelfox, Sofia B Ahmed, Farah Khandwala, David Zygun, Reza Shahpori, Kevin Laupland

Slide 18: 

Critically ill patients prone to electrolyte disturbances

Slide 19: 

Disturbance in fluid and electrolyte homeostasis sepsis, shock, cardiac failure, acute kidney injury, burn, surgery, C.N.S. disorders Activation of neuro hormonal system- SNS, RAAS, Vasopressin Non osmotic release of Vasopressin pain, nausea, medication, hypovolemia Vasopressin deficiency in sepsis Insensitivity to insensible losses Impaired thirst mechanism Inappropriate administration of fluid and electrolytes Diuresis iotrogenic- renal and osmotic diuretics Urea, glucose induced Hypokalemia, hypercalcemia Drug induced- aminoglycoside, ampho B

Slide 20: 

Solute balance= [Na+K]input – [Na+K]output Am J Kidney Dis 2009 Oct, 54:674-679 tonicity balance in patients with Hypernatremia Acquired in the Intensive Care UnitGregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz Continued…

Slide 21: 

Causes of ICU acquired hypernatremia osmotic DI Non oliguric Urea/ glucose Addition of KCl to 0.9%saline led to positive solute balance in 27% patients Hypertonic Osm>150 Am J Kidney Dis 2009 Oct, 54:674-679 tonicity balance in patients with Hypernatremia Acquired in the Intensive Care UnitGregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz Continued…

Slide 22: 

Positive solute balance contributed 56% cases Primary reason was inadequate substitution of hypotonic losses with isotonic or hypertonic fluids Impaired sensorium and inability to express thirst leading to inadequate intake of free water Community acquired hypernatremia- hypovolemic hypernatria ICU- euvolemic or hypervolemic hypernatremia Am J Kidney Dis 2009 Oct, 54:674-679 tonicity balance in patients with Hypernatremia Acquired in the Intensive Care UnitGregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz Continued…

Slide 23: 

Characteristics of patients Am J Kidney Dis 2009 Oct, 54:674-679 tonicity balance in patients with Hypernatremia Acquired in the Intensive Care UnitGregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz Continued…

Slide 24: 

Characteristics of patients Am J Kidney Dis 2009 Oct, 54:674-679 tonicity balance in patients with Hypernatremia Acquired in the Intensive Care UnitGregor L, Nikolaus K, Ulrike Holzinger, Wilfred Druml, christiph schwartz

Slide 25: 

Patients admitted over 1 year medical, surgical or neurological ICU Renal dysfunction, Hypokalaemia, hypercalcemia, mannitol, sodium bicarbonate more common in cases independently associated with hypernatraemia. mortality was higher in case Hypernatremia was independent predictor hypernatremia ≥150 mmol/l in the ICU Nephrol Dial Transplant 2008,23:1562-1568 Hypernatremia in critically ill patients: too little water and too much salt Ewout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse Continued…

Slide 26: 

Approximately half of cases were polyuric, even when fluid balance was negative + Impaired thirst mechanism Inappropriate iv fluid administration with isotonic fluids Aim of treatment- negative solute balance Hypotonic fluid may aggravate fluid overload Diuretic may be considered: combination of loop diuretic and water or thiazide diuretic alone Nephrol Dial Transplant 2008,23:1562-1568 Hypernatremia in critically ill patients: too little water and too much salt Ewout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse Continued…

Slide 27: 

Potential factors contributing to hypernatremia Page 1566 Nephrol Dial Transplant 2008,23:1562-1568 Hypernatremia in critically ill patients: too little water and too much salt Ewout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse

Slide 28: 

Use of hypotonic fluid is avoided in ICU Capillary leakiness in sepsis patients Fear of hyponatremia as many patient show non osmotic release of Vasopressin

Slide 29: 

JUST AN ANALYSIS

Nephrol Dial Transplant 2008,23:1562-1568Hypernatremia in critically ill patients: too little water and too much saltEwout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse : 

Nephrol Dial Transplant 2008,23:1562-1568Hypernatremia in critically ill patients: too little water and too much saltEwout J. Hoorn, Mecheil G.H.Betjes, Joachim Weigel, Robert Zietse Tonicity balance illustrating mechanism of hypernatremia 47-year-old male (body weight 95 kg) cystectomy complicated by faecal peritonitis. Hypernatraemia in1day large isotonic volume resuscitation, + hypertonic fluids (NaHCO3) Water loss Renal: renal insufficiency and hyperglycaemia non-renal: wound drains and colostomy

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin : 

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin TBW* ( [S.Na] /140 ) - 1 14 year old male ( weight 40 kg, total body water 24 L) Operated for craniopharyngioma During surgery excreted 4L in 9 hours Over this period P.[Na] rose from 140 to 157 meq/L received 3 L of isotonic saline His urine [Na+K] was 50 meq/L. Free Water deficit: 24* [ (157/140) – 1 ] = 2.9 L 2.9L 2.9L

Slide 32: 

Intensive Care Med 2001;27:921-924 Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremia A.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin 4 L urine with 200meq Na= 1.3 L isotonic saline + 2.7 L of EFW

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin : 

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin Tonicity balance Na 200 mmol

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin : 

Intensive Care Med 2001;27:921-924Tonicity balance, and not electrolyte free water calculations, more accurately guide therapy for acute change in natremiaA.P.C.P. Carlotti, D. Bohn, J.P. Mallie, M.L. Halperin 3 situations with hypernatremia and negative balance of 2.7 L of EFW

Slide 35: 

HYPERNATREMIA

HYPERNATREMIA : 

HYPERNATREMIA True/ Relative water deficit S. Na > 145 meq/L Clinical manifestation Thirst Lethargy, irritability, restlessness Spasticity, hyperreflexia, seizure, coma Death Cerebral Hemorrhage/ ischemia Insulin resistance, impaired gluconeogenesis Cardiac dysfunction Severity of symptoms correlate with rate and magnitude of change in [Na]

Slide 37: 

APPROACH

Slide 38: 

Hypernatremia Hypertonic saline load NaHCO3, 3% saline Hyperaldosteronism Cushing’s syndrome Primary Na gain HYPERVOLEMIA Hypotonic fluid loss HYPOVOLEMIA ISOVOLEMIA Extra renal loss Renal loss Diuresis Osmotic glucose, urea, mannitol, high osmolar feeds Diuretics- frusemide, thiazide Insensible loss Fever, burn Diabetes insipidus CDI NDI renal disease Drugs- amphoterecin, aminoglycosides, lithium Electrolyte disorders- hypokalemia, hypercalcemia Azotemia out of proportion to decrease in GFR Catabolic patients with Moderate renal insuficiency on high protein diet and stress dose steroid

Slide 39: 

Excretion of small volume (<800 ml) Of concentrated urine (Osm U > 800 mOsm/L) Appropriate response to hypernatremia

Slide 40: 

Hypernatremia Insensible losses diuretics Urine volume Hypotonic fluid loss Response to dDAVP Osmotic diuresis + complete CDI _ complete NDI Inherited lithium >1000 ml <800 ml Urine osmolality < 300 300 - 800 HYPOVOLEMIA/ ISOVOLEMIA Urine osmole excretion /day <900 mOsm/day >900 mOsm/day + complete CDI with hypovolemia + Partial CDI - partial NDI Renal tubular disease Drugs electrolyte disturbances Urine osmolality >800 Response to dDAVP Solute diuresis Water diuresis

Slide 41: 

MANAGEMENT

HYPERNATREMIACorrection : 

HYPERNATREMIACorrection Risk : development of brain odema Chronic hypernatramia- brain cells fully adapted Risk is more Acute hypernatremia: 1-2 meq/L/h ( 10-12 meq/L/day) Chronic hypernatremia: 0.5 meq/L/h ( 8-10 meq/L/day) Rate of correction GOAL Na <145

HYPERNATREMIACorrection : 

HYPERNATREMIACorrection TBW* ( [S.Na] /140 ) - 1 EFW deficit calculation (L) Water deficit calculation (L) Madias and Adrogue equation Scan Page 74 JW LEE

Mind it : 

Mind it Formulas assume a closed system Require separate account of ongoing losses as Ongoing loss Must be considered along with calculated water deficit

Slide 45: 

change of 10 meq/L = 4.3L of N/2 saline has to be given in 24 hours 70 kg women Diarrhoea of volume 2 L/ day S.[Na]= 160meq/L , S.[K]= 3.0meq/L But ongoing loss = 0.7 L + 2.0 L = 2.7 L / 24 hours 75 – 160 / (70*50) + 1 = - 2.3 meq/ L Estimated change in S.[Na] with 1 L of N/2 saline Total volume to be given 4.3 L + 2.7 L = 7.0 L / 24 hours

Slide 46: 

Hypernatremia Hypotonic fluid ± diuretic Urine output < water replacement HYPERVOLEMIA Hypotonic fluid loss HYPOVOLEMIA ISOVOLEMIA Osmotic diuresis Insensible loss Diabetes insipidus Hemodynamically unstable Correct volume with isotonic saline Switch over to hypotonic fluid to to correct Na Remove / treat cause of DI Replace losses with hypotonic fluid CDI Ddavp NDI low Na diet + thiazide ± low protein diet ± NSAID

HYPERNATREMIAsummary of management : 

HYPERNATREMIAsummary of management Hemodynamic unstable: resuscitate with isotonic fluid (0.9% saline or RL) Switch over to hypotonic fluid once resuscitated Hypovolemic hypernatremia: AIM- positive EFW and solute balance isovolemic hypernatremia: AIM- positive EFW balance Replace losses with Hypotonic fluid Treatment of cause: DI Hypervolemic hypernatremia: AIM- negative EFW and solute balance Na restriction + Hypotonic fluid + frusemide CDI: ADH analogue dDAVP: 10-20 ug intranasal bd or 1-2ug sc bd NDI remove/ correct causative agent Thiazide/ indomethacin

Slide 48: 

hypernatremia Duration of hypernatremia Absent/ mild neurologic signs [Na] ≥155 meq/L Severe neurologic compromise 5% dextrose Initial goal Fall of [Na] by 1.5-2.0 meq/L/h for 3-4 hours or until symptoms resolve Change in [Na] can occur rapildly Immediate attainment to normal Is not goal Initial acute management of [Na] <155 meq/L < 2 days > 2 days Change in [Na] should not exceed 10 meq/L in first 24 hours Search for alternative cause of neurologic compromize

DIABETES INSIPIDUS : 

DIABETES INSIPIDUS Hypotonic urine in face of hyperosmolar plasma CDI- Osm U <200 NDI- Osm U 200-500 Water restriction: failure of Osm U to rise by 50 mOsm/ L in first few hours Vasopressin- CDI Osm U rise by atleast 50% immediately

Slide 50: 

HYPONATREMIA

HYP0NATREMIA : 

HYP0NATREMIA True/ Relative water excess S. Na < 135 meq/L Clinical manifestation headache, nausea lethargy, disorientation, restlessness Muscle cramp, weakness, depressed reflexes, seizures, coma Death Chronic hyponatremia: developing over >48 hours Adaptative mechanism minimize symptoms Severity of symptoms correlate with rate and magnitude of fall in [Na]

Slide 52: 

APPROACH

Slide 53: 

hyponatremia hypotonic Hypovolemic hyponatremia Hypertonic HypoNa Hyperglycemia Hypertonic sodium free sol (mannitol) Hypotonic HypoNa Isotonic HypoNa Pseudohyponatremia Hyperlipidemia hyperproteinemia Normal serum osmolality low serum osmolality high serum osmolality Assess serum osmolality Assess volume status isovolemic hypovolemic hypervolemic hypotonic isovolemic hyponatremia hypotonic Hypervolemic Hyponatremia Cirrhosis Congestive heart failure Nephrotic syndrome Renal falire Discussed in next pages

Slide 54: 

Diuresis Osmotic- glucose, urea, mannitol Diuretics- thiazide, frusemide Electrolytes-Hypokalemia, hypercalcemia Drugs- aminoglycoside, ampho B Salt wasting nephropathy Cerebral salt wasting GI loss naso gastric aspirate, abdominal Drains/ fistula third space loss (pancreatitis, ileus, obstruction) Vomiting, diarrhea Non renal loss hypotonic Hypovolemic Hyponatremia Skin loss fever open wounds, burns hemorrhage Adrenal deficiency Mineralocorticoid deficiency Renal loss LOSS (both water and Na) = Negative water and Na balance

Slide 55: 

Acute psychosis CNS disorders hypothyroidism Hypotonic Isovolemic Hyponatremia Drug induced Opiods NSAIDS Antipsychotics- haloperidol SSRI- fluoxetine, sertraline TCA Carbamezapine antineoplastics Pain, nausea, stress Pulmonary disease Infections malignancy SIADH Cortisol deficiency Impaired free water loss in urine Normal Na loss in urine

Slide 56: 

CORRECTION

PRECAUTION IN CORRECTION : 

PRECAUTION IN CORRECTION Absolute magnitude of correction in 24 hours more important than rate central pontine myelinosis Initial rapid rate of correction tapering off after several hours incurs less risk than slow steady correction that exceeds 12 meq/L in 24 hours Increased risk Hypoxemia, hypokalemia, malnutrition, alcoholism

HYPONATREMIA : 

HYPONATREMIA 1-2 meq/L/h ( 10-12 meq/L/day) Rate of correction Symptomatic or Acute hyponatremia (change >0.5 meq/L/h or onset in < 48 hours) 0.5 meq/L/h ( 8-10 meq/L/day) Chronic hyponatremia (Change over > 48 hours or unknown duration) Increased risk of CPM as adaptive mechanism has occured 120-130 meq/L Lower iin patients with s.Na<105 GOAL of Correction

Slide 59: 

Any saline solution that is hyperosmolar to urine can increase [Na] when oral water intake is restricted Mind it RULE FOR CORRECTION A crystalloid with an osmolarity less than urine osmolarity may actually worsen hyponatremia, even if the fluid [Na] is greater than serum [Na] CONTINUED….

Slide 60: 

Na=154 Water=1000 Water= 300 Na=154 Na=115 Na=118 Gain of 154 mOsm will be lost in 300 ml urine Gain of 700 ml of EFW (154* 1000/500= 300 ml, OsmU > 500) 60 years male, febrile encephalopathy Body weight: 60 kg, TBW: 36 L Develops SIADH S.[Na]= 118, urine Osm > 500 mOsm/L Given 1 L of 0.9% saline ONE RULE FOR CORRECTION Simultaneous IV loop diuretic can counteract this phenomenon By promoting free water excretion

HYPONATREMIACALCULATION OF [Na] deficit : 

HYPONATREMIACALCULATION OF [Na] deficit TBW* ( 140 – s.Na) Na deficit (meq) Anticipated change in s.Na with 1L of fluid (Madias and Adrogue equation) Scan Page 74 JW LEE

HYPONATREMIA : 

HYPONATREMIA Remove or treat cause of hypertonicity Repeat lab Use newer method of lab Hypertonic HypoNa Hyperglycemia Hypertonic sodium free sol (mannitol) Isotonic HypoNa Pseudohyponatremia Hyperlipidemia hyperproteinemia Fluid shift to ICF compartment does not take place Neuronal cell swelling does not occur

Slide 63: 

hypotonic hyponatremia Primary polydypsia Beer potomania Post TURP urine osmolality <100 mOsm/L Assess urine osmolality Assess volume status EFW restriction ± loop diuretic Correct hypokalemia Urine [Na] <10meq/L Urine [Na] >20meq/L Renal loss Non renal loss hypovolemic urine osmolality > 100 mOsm/L Treatmentc Isotonic saline to correct hypovolemia Correct hypokalemia if present hypervolemic Isovolemic Continued on next page Continued….

Slide 64: 

hypotonic hyponatremia Assess volume status Urine [Na] <10meq/L Urine [Na] >20meq/L Renal failure Cirrhosis Congestive heart failure Nephrotic syndrome hypervolemic urine osmolality > 100 mOsm/L EFW restriction (restriction less than urine output) Urine [Na] >20meq/L Isovolemic SIADH Hypothyroidism Cortisol deficiency, Administer saline with osmolality more than urine osmolality Loop diuretic ADH antagonist Treat underlying disease Stop drug causing increased ADHsecretion Correct hypokalemia if present TREATMENT

HYPONATREMIAsummary of management : 

HYPONATREMIAsummary of management Replace calculated Na deficit with isotonic saline or RL hypotonic Hypovolemic hyponatremia AIM- positive water and Na balance hypotonic isovolemic hyponatremia AIM- negative EFW and positive Na balance Symptomatic frusemide ivi + 3% saline Asymptomatic Water restriction ± Intermittent frusemide ± enteral salt hypotonic Hypervolemic hyponatremia AIM- negative EFW and Na balance Na and EFW restriction + frusemide ADH antagonist ( for chronic SIADH as delayed onset of action) demeclocycline HCL: 600-1200mg PO daily Phenytoin sod: 200-300mg PO daily Lithium: 600-1200mg PO daily

Slide 66: 

hyponatremia Duration of hyponatremia Absent/ mild neurologic signs [Na] < 125 meq/L Severe neurologic compromise 3% saline ivi Initial goal increase [Na] by 1.5-2.0 meq/L/h for 3-4 hours or until symptoms resolve Change in [Na] can occur rapildly Immediate attainment to normal Is not goal Initial acute management of [Na] >125 meq/L < 2 days > 2 days Change in [Na] should not exceed 10 meq/L in first 24 hours and 18 meq/L in first 48 hours Search for alternative cause of neurologic compromize

SOLUTION= SOLUTE+ SOLVENT : 

SOLUTION= SOLUTE+ SOLVENT Molality: number of moles of a solute per kilogram of solvent Molarity: number of moles of solute per litre of solution Osmolality: number of osmoles of solute per kilogram of solvent Osmolarity: number of osmoles of solute per litre of solution Tonicity = effective osmolality sum of the concentrations of the solutes which have the capacity to exert an osmotic force across the membrane.

Slide 68: 

Free water (FW) Calculated base on osmolality (Na, Glucose, BUN) As urea is freely permeable across all cell membrane Does not contribute to effective osmolality ie tonicity Electrolyte free water (EFW) Calculation based on S.[Na} Modified Electrolyte free water (MEFW) Calculation takes into consideration Glucose along with s.[Na]

Slide 69: 

HYPOKALEMIA

Slide 70: 

HYPERKALEMIA

Slide 71: 

PHOSPHORUS abnormality

Slide 72: 

Hypophosphatemia Normal phosphate balance

Phosphorus : levels : 

Phosphorus : levels

Hpophosphtemia : causes : 

Hpophosphtemia : causes Iatrogenic 65% Iatrogenic + fasting 15% Septicemia 09% Iatrogenic + septicemia 08% Iatrogenic + GI losses 06% Iatrogenic + hypokalemia 04% Iatrogenic includes glucose infusions, re-feeding syndrome, & drugs

Hypophosphatemia : causes : 

Hypophosphatemia : causes Inadequate input GI phosphate binders Starvation Vomiting , NG suctioning Malabsorption syndrome Relative or absolute VIT.D def. Transcellular shift Alkalosis CHO load Drugs (insulin, epinephrine, steroids, β2agonists) Excessive losses Phosphaturic agents Acute volume expansion Massive diuresis Diuretic phase of ARFprimary or secondary hyperparathyroidism Dialysis, osteomalacia

Hypophosphatemia : Clinical manifestations : 

Cardiac Decreased contractility Possible cardiomyopathy Respiratory Respiratory failure Failure to wean Skeletal muscle/ bone Osteomalacia Myalgia Rhabdomyolysis Hematological Granulocyte, platelet & leucocyte dysfunction CNS Weakness numbness Seizures Renal -ATN Hypophosphatemia : Clinical manifestations

Hypophosphatemia : replacement therapy : 

IV therapy when severe hypophosphatemia (S.PO4 <1mg/dl) & pts. With symptoms with a S. PO4 < 2mg/dl. Oral dose 1200-1500mg daily when S. PO4 > 2mg/dl Maintenance therapy 1200mg PO & 800mg/day IV Hypophosphatemia : replacement therapy

Hypophosphatemia : replacement therapy : 

Hypophosphatemia : replacement therapy In patients with renal failure slower correction

Hypophosphatemia : replacement therapy : 

Hypophosphatemia : replacement therapy

Hyperphosphatemia : causes : 

Hyperphosphatemia : causes Decreased renal excretion CRF Increased tubular reabsorption in hypoparathyroidism, acromegaly, hyperthyroidism Transcellular shift Metabolic or respiratory acidosis Tumor lysis syndrome Sepsis, acute hemolysis Malignant hyperpyrexia, rhabdomyolysis Increased phosphate intake Laxatives or enema Injudicious IV phosphate therapy

Hyperphosphatemia : clinical sequel : 

Hyperphosphatemia : clinical sequel Hypocalcemia Skeletal muscle tetany Seizure activity Prolongation of QT interval Arrhythmias Hypotension Metastatic calcification Others Secondary hyperparathyroidism Progression of CRF

Hyperphosphatemia : management : 

Hyperphosphatemia : management GI dialysis Phosphate binding drugs Sucralfate Aluminium containing antacids Hemodialysis Treatment of underlying cause Treatment of hypocalcemia

Definition : 

Definition Severe fluid and electrolyte shifts and related metabolic complications in malnourished patients undergoing refeeding.

Consequences of Starvation : 

Consequences of Starvation Decreased insulin and increased glucagon secretion. With a switch from glucose towards ketone bodies as a source of energy Glycogen stores used BMR decreases Brain adapts to using ketones Atrophy of all organs Reduced Lean Body Mass Abnormal liver function

Consequences of starvation : 

Consequences of starvation Deficiency of vitamins and trace elements Whole body depletion of potassium, magnesium and phosphate Increased intracellular and whole body sodium and water Impaired cardiac, intestinal and renal reserve, leading to reduced ability to excrete excess sodium and water Serum concentrations of electrolytes maintained within normal limits

Refeeding : 

Refeeding Increased insulin release leads to increased uptake of glucose, phosphate and potassium into cells. Magnesium is used as a co-factor for cellular pump activity Reactivation of the Na/K membrane pump leads to further movement of K into cells with a simultaneous movement of sodium and fluid out of cells

Refeeding : 

Refeeding Reduced phosphate is associated with increased urinary magnesium excretion Stimulation of protein synthesis leads to increased anabolic tissue growth which in turn leads to increased cellular demand for phosphate, potassium, glucose and water

Refeeding : 

Refeeding Excess glucose can lead to hyperglycaemia and fat abnormalities Reduced sodium and water excretion Increased cellular thiamine utilisation due to its role as a co-factor for carbohydrate metabolism

Consequences of electrolyte abnormalities : 

Consequences of electrolyte abnormalities

Incidence : 

Incidence 0.2-5% hospital patients have hypophosphataemia Incidence is increased in certain groups Incidence in patients receiving nutrition support has been reported to be 30-40%

Patients at Risk of Refeeding : 

Patients at Risk of Refeeding Those who have had very little or no food intake for >5 days especially if already undernourished (BMI <20 kg/m2, unintentional weight loss >5% within the last 3-6 months)

Patients at High Risk of Refeeding : 

Patients at High Risk of Refeeding Patients with any of the following: BMI < 16 kg/m2 Unintentional weight loss >15% within the last 3-6 months Very little or no nutrition for >10 days Low levels of potassium, magnesium or phosphate prior to feeding

Patients at High Risk of Refeeding : 

Patients at High Risk of Refeeding Patients with 2 or more of the following: BMI < 18.5 kg/m2 Unintentional weight loss >10% within the last 3-6 months Very little or no nutrition for >5 days A history or alcohol abuse or some drugs including insulin, chemotherapy, antacids or diuretics

Feeding patients who are at risk : 

Feeding patients who are at risk Introduce feeding at maximum 50% of total energy requirements for the first 2 days before increasing to full requirements if no biochemical abnormalities Meet full requirements for fluid, electrolytes, vitamins and minerals from day 1 of feeding Monitor appropriate biochemistry including potassium, phosphate and magnesium (see chapter on monitoring)

Feeding patients who are at high risk : 

Feeding patients who are at high risk Consider starting nutrition at maximum 10 kcal/kg and increase slowly to meet full requirements by 4-7 days. Any increase in feed should be dependent on trends in biochemistry

Feeding patients who are at high risk : 

Feeding patients who are at high risk Potassium, magnesium and phosphate supplementation from the outset (unless blood levels are already high): Potassium (likely requirement 2-4 mmol/kg/day) Magnesium (likely requirement 0.2 mmol/kg/day IV, 0.4 mmol/kg/day oral) Phosphate (likely requirement 0.3-0.6 mmol/kg/day)

Feeding patients who are at high risk : 

Feeding patients who are at high risk Immediately before and during first 10 days of feeding: Oral thiamine 200-300mg/day Vitamin B co strong 1-2 tds or full dose IV vitamin B Multivitamin and trace element supplement Restore circulatory volume and monitor fluid balance closely Monitor appropriate biochemistry including, potassium, phosphate and magnesium

Feeding patients who are at high risk : 

Feeding patients who are at high risk In extreme case eg BMI<14 kg/m2 Very little or no nutrition for > 15 days Pre-feeding Hypokalaemia, hypophosphataemia or hypomagnesaemia Consider starting feed at 5kcal/kg It is not necessary to correct electrolyte levels prior to feeding if this cautious approach is used

Feeding patients who are at high risk : 

Feeding patients who are at high risk Beware of very malnourished, dehydrated patients with renal impairment and consequently normal or high potassium and phosphate levels. It is also easy to overlook significant renal impairment in patients with very low BMI and recent starvation who have very low creatinine and urea production.

References : 

References Brook M.J. & Melnik G 1995. The Refeeding Syndrome: An approach to understanding its complications and preventing it occurrence. Pharmacotherapy 15(6):713-26. Crook M.A. et al 2001. The importance of the Refeeding Syndrome. Nutrition 17:632-7. Keys A. et al 1950. The Biology of Human Starvation vols 1,2. Minneapolis University of Minnesota Press. Marinella M.A. 2003. The Refeeding Syndrome and Hypophosphataemia. Nutrition Reviews 61(9):320-3. NICE 2006 Nutrition Support in Adults Solomon S.L. et al 1990 The Refeeding Syndrome: A Review. J. Parent. & Enteral Nutrition 14(1):90-7. Terelevich A. et al 2003. Refeeding Syndrome: Effective and safe treatment with phosphates polyfusor. Aliment. Pharmacol. Ther. 17:1325-1329.

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