Fluid and electrolyte balance
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    Fluid and electrolyte balance Fluid and electrolyte balance Presentation Transcript

    • FLUID AND ELECTROLYTE BALANCE Dr Shermil Sayd Dept of OMFS KMCT dental college
    • Introduction The prevention and treatment of fluid and electrolyte disturbances are integral parts of surgical care. To achieve homeostasis, the body maintains strict control of water and electrolyte distribution and of acid-base balance. This control is a function of the complex interplay of cellular membrane forces, specific organ activities and systemic and local hormone actions. Pestana C:fluids and electolytes in surgical patients, 2nd ed Baltimore, williams and wilkins, 1981 pp 101-144
    • Total body water and composition • Total body water accounts for 60% or more of the body weight • It varies according to the age, sex and proportion of the body fat • Water is contained mainly in the skeletal muscle
    • FLUID COMPARTMENTS • Two compartments – Intracellular-approx two thirds of water – Extracellular-rest one third of water
    • Extracellular water – Interstitial water-75% of extracellular water – Intravascular water- constitutes 25% of extracellular water vol or 4% to 7%of body wt. • They are separated by a semipermeable membrane Volume (L) % Total body water % Body weight Plasma 3.5 8 4-7 Interstitium 10.5 25 15 Intracellular 28 67 40
    • Electrolytes and proteins in fluid compartments • Balanced concentration of cations and anions maintains electrical neutrality. • In the intracellular compartment, potassium is the dominant cation. • In the interstitial and intravascular compartments, sodium is the dominant cation.
    • • Approximately 7%of plasma is in the form of protein, mostly anionic albumin, which cannot permeate the membrane. • The distribution of ions across the semipermeable membrane is called the Donnan effect. • The forces governing the distribution are expressed as the Gibbs-Donnan equation
    • Osmolarity • Prime determinants of water distribution in the body. • Refers to the number of particles dissolved in a solution. • In plasma, the major determinants of osmolarity are sodium and its accompanying anions, urea and glucose.
    • • Osmolarity expresses the concentration in terms of osmoles of solute per liter of solution. • At the solute concentration of normal body fluids, the osmolality and osmolarity are nearly equivalent • Gennari F:serum osmolality, N Engl J Med 310:102-105, 1984
    • Tonicity • Determines the movement of water across the cellular membrane. • It is calculated by considering only the concentration of the impermeable solutes in the solution. • Normal effective osmolarity of body fluids is 280 mOsm/kg
    • • A reduction in effective osmolarity implies a relative water excess, whereas an increase in effective osmolarity implies relative dehydration
    • Regulation of volume • Kidneys exert the greatest influence on the regulation of intravascular volume. • Osmoreceptors in the posterior pituitary detect small changes in the serum osmolarity, which then regulates the release of ADH. • Baroreceptors in the kidney, carotid, and elsewhere detect small changes in pressure
    • • Other key regulator is the Renin-AngiotensinAldosterone system. • This leads to increase in the sodium reabsorption and potassium excretion.
    • Fluid homeostasis • Maintained under neuroendocrine and renal control. • Urinary losses of water are regulated by renal mechanisms, with 300ml/day the minimal volume required to allow solute excretion. Along with this, insensible loss also occurs through lungs and evaporative water loss • Insensible loss increases by 10% for each 10C increase in body temp
    • Volume excess  Excess of water in the ECC w/ a normal amount of solute or a deficient amount of solute  Occurs in prolonged and excessive diuresis, forcing hypotonic fluids to produce diuresis in the presence of renal impairment  Fluid overload from production of adrenal corticoid hormones [Cushing’s syndrome]
    •  Symptoms  Weight gain & edema  Cough, moist rales, dyspnea [fluid congestion in lungs]  CVP, bounding pulse,neck vein engorgement [fluid excess in the vascular system]  Bulging fontanelles  Hg and Hct  Nausea & vomiting
    •  Management  Restrict fluids to lower fluid volume  Diuretics or hypertonic saline  Continuous assessments to prevent skin breakdown  Record daily weight to assess progress of treatment
    • Volume deficits • May occur from chronic or acute losses
    • Evaluation of chronic volume depletion • Oliguria • Loss of skin turgor • Orthostatic hypotension • Low urine sodium concentration • BUN/creatinine ratio>15:1 • Hematocrit elevated by 5% or 6% per liter of volume deficit
    • Evaluation of acute volume depletion • Hypotension • Tachycardia • Tachypnea • End-organ hypo-perfusion • Skin mottling • Acidosis
    • Treatment • An isotonic solution, such as lactated ringers solution is highly effective in restoring circulating volume. • Normal 0.9% NaCl saline solution is commonly used • Calcium, magnesium, and phosphorous supplements are not required for short-term therapy unless critically ill.
    • • If the patient is febrile maintenance fluid must be increased by 10%for each degree above 37.20C
    • IV fluid composition Solution Na+ K+ Ca+ Mg+ Cl- HCO3 Glu Osm 0.9%NaCl(NS) 154 - - - 154 - - 308 D5/0.9%NaCl 154 - - - 154 - 50 560 0.45%NaCl(1/2NS) 77 - - - 77 - - 560 D5/0.45% NaCl 77 - - - 77 - 50 406 0.225% NaCl(1/4) 38.5 - - - 38.5 - - 77 D5/0.225% NaCl 38.5 - - - 38.5 - 50 329 LR 130 4 3 - 109 28 - 273 3.0% NaCl(hypertonic) 513 - - - 513 - - 1026
    • SODIUM HOMEOSTASIS • Normal dietary intake is 6-15g/day. • Sodium is excreted in urine, stool, and sweat. • Urinary losses are tightly regulated by renal mechanisms.
    • Sodium abnormalities Hypernatremia: • Defined as a serum sodium concentration that exceeds 150mEq/L. • Always accompanied by hyperosmolarity
    • Etiology • Excessive salt intake • Excessive water loss • Reduced salt excretion • Reduced water intake • Administration of loop diuretics • Gastrointestinal losses
    • Evaluation • With history, physical examination and assessment of volume status • Very young and the very old and the debilitated are more susceptible • Symptoms: malaise, lethargy, vomiting, generalized seizures and coma
    • • Most severe cases : bridging intracranial vessels rupture, causing intracerebral and pericerebral hemorrhage • In chronic hypernatremia, more time is available for cerebral adaptation by the intracellular accumulation of organic osmolites, called as cerebral osmoregulation. The brain is the only organ with this potential.
    • Treatment: • Restore circulating volume with isotonic saline solution • After intravascular vol. correction hypernatremia is corrected using free water in the form of D5W. • The free water deficit can be calculated as the difference between NTBW and CTBW.
    • Hyponatremia • Serum sodium concentration less than 135mEq/L
    • Etiology • Excessive water intake • Impaired renal water excretion • Loss of renal diluting capacity
    • Symptoms: • Mostly neurologic and due to cellular swelling induced by ECF hypo-osmolality • Cerebral swelling leads to lethargy, confusion, vomiting, seizures and coma • Symptoms rarely occur until serum sodium concentration goes below 120mEq/L • Severity related to rate of decrease
    • Classification: • Hypervolemic • Normovolemic • Hypovolemic • Pseudohyponatremia
    • Hypervolemic • Have edema • Cause: renal failure, CHF, COPD with hypercarbia, and severe liver disease
    • Normovolemic : • Cause: Syndrome of Inappropriate secretion of ADH(SIADH) • SIADH is seen in patients with stroke or injury and in pulmonary conditions such as tuberculosis and cancer • Plasma vol. is normal or slightly elevated
    • Hypovolemic • Have renal or extrarenal loss of sodium greater than that of the water losses. • Urinary sodium level – >20mEq/L-renal loss associated with diuretic use, aldosterone deficiency, salt losing nephritis, renal failure and subarachnoid hemorrhage. – <10mEq/L- normal tubular response to hyponatremia
    • • Extra renal loss occurs as vomiting, fistula or diarrheal loss
    • Pseudohyponatremia • Two situation – in hyperlipidemia or hyperproteinemia – Osmotically active glucose • 100 mg/dl increase in the serum glucose will suppress serum sodium by 1.6mEq/L
    • Treatment : • Hypervolemia- volume restriction and loop diuretics. In patients with renal failure, dialysis might be required. • SIADH patients usually responds to fluid restriction • Hypovolemia- salt and water replacement • If due to endocrine deficiencies, hormonal replacement indicated
    • • Asymptomatic- should be treated slowly. Isotonic saline preferred. Addition of loop diuretics will hasten water excretion, provided plasma volume is restored • Fluid restriction, loop diuretic and correction of the underlying cause is sufficient in normovolemic or hypervolemic states
    • • Symptomatic- associated with seizures or coma. Danger of neurologic damage exists if sodium level increased rapidly. Central pontine myelinosis has been shown to occur in rapid correction of hyponatremia. • Current recommendation is, no faster than 0.5mEq/L/hr. • A concentration of 120mEq/L is sufficient. After the symptoms have abated, sodium correction should occur at a still slower rate.
    • • Total sodium deficit(TSD): TSD=0.6XWEIGHT IN KG X (140-MEASURED Na+) • In patients with stupor and coma, hypertonic saline(3%NaCl) solution is used. Objective is to restore sodium rapidly to 120mEq/L, at a correction no greater than 0.5mEq/L/hr. thereafter correction may be at a slower pace with isotonic saline. Oh M, Corrol H: disorders of sodium metabolism: hypernatremia and hyponatremia. Crit care Med 20:94103, 1992
    • Potassium homeostasis • Principal intracellular cation in the body • Quantity in avg. sized adult is 3800mEq/L or 55mEq/Kg. • Located mostly in the skeletal muscle • Paramount for the function of excitable tissue. • Normal plasma conc. Is 3.5 to 5mEq/L. • Internal factors responsible for the maintenance include insulin, aldosterone, catecholamine and acid base balance
    • Potassium abnormalities Hyperkalemia • Serum potassium > 5.5mEq/L
    • Etiology • Renal or adrenal insufficiency • Metabolic acidosis • Iatrogenic causes – Medications(NSAID, ACE inhibitors) – Excessive administration of potassium • • • • Intravascular hemolysis Rhabdomyolysis Seizures Severe GI bleeding
    • Pseudohyperkalemia: • In vitro hemolysis due to excessive agitation of the sample before reaching the lab. • Prolonged tourniquet time and fist clenching during blood draw(increase by 1.6mEq/L) • Thrombocytosis and leukocytosis • True K levels are measured using plasma
    • Evaluation: • Myocardial effects – Conc. Increase to 6mEq/L • Peaking of the T-wave • Prolonged PR interval • RR interval increases – Above 6mEq/L • Loss of P waves • Widening of the QRS complex
    • – Final outcome • Complete heart block • Ventricular tachycardia • Cardiac standstill • Extracardiac symptoms – Paresthesias – Flaccid paralysis – ileus
    • Treatment: • Reversal of cardiac toxicity • 10-20ml 10% calcium gluconate should be administered. Action starts in 1-5mins and lasts for 30mins. • Concurrent treatment with insulin or sodium bicarbonate moves the potassium into the cells
    • • Administering 10unts of insulin in5oml of a 50% dextrose solution will elicit a response in 15 to 45mins and lasts for 4-6 hrs • K can be removed from the body by – Cation exchange resin kayexalate (50-100mg) as enema – 40gm orally with sorbitol, each gm removes approx. 0.5 to 1mEq of K. onset of action os slow and lasts for 4-6hrs – Effective method-dialysis
    • Hypokalemia: • Serum potassium level<3.5mEq/L
    • Etiology: • GI losses from vomiting, diarrhea, or fistula and use of diuretics
    • Evaluation: • Metabolic alkalosis often co-exists with hypokalemia, decreases serum K level. • Generalized weakness and fatigue • ECG – Flattened T-wave – Diminished QRS voltage and U waves In digoxin taking patients hypokalemia will cause life threatening arrhythmias
    • Treatment: • Correction of the underlying condition • K should be given orally unless severe(<2.5mEq/L), patient is symptomatic or the enteral route is contraindicated • Oral K supplements (60-80mEq/L) coupled with normal diet is sufficient. • ECG monitoring along with frequent assessment of serum K level is reqiured
    • Calcium homeostasis • Body contains approx. 1400gm of calcium • Reduction in calcium level leads to PTH secretion which increases calcium reabsorption from the bone. It increases calcium reabsorption from the DCT and stimulates the formation of the active metabolite of vit. D that increases gut reabsorption of elemental calcium and facilitates the PTH action on the bone
    • Calcium abnormalities: Hypercalcemia: • Ionized calcium conc. > 5.3mg/dL
    • Etiology: • Hyperparathyroidism • Cancer • Paget's disease • Pheochromacytoma • Hyperthyroidism • Thiazide diuretics
    • Evaluation: • Moderate hypercalcemia(5.3-6.5mg/dL) tend to be asymptomatic or complain only of malaise • Severe hypercalcemia– Neurologic symptoms • Lethargy->stupor and coma – CV manifestation • Arrythmia • Shortened QT interval
    • – GI effects • • • • Anorexia Constipation Pancreatitis Hyperacidity – Renal defect • Polyuria
    • Treatment: • Severe hypercalcemia– If hyperparathyroidism-surgery – Initial supportive therapy includes furosamide to increase calcium excretion • Calcitonin reduces bone resorption and has an immediate effect and lasts for 48 hrs. prolongation can be done by using corticosteroids
    • • Bisphosphonates are effective in inhibition of osteoclastic activity, but onset of action is very slow( 2-3 days) • Mithramycin has rapid onset of action, but is associated with renal and hepatic toxicity. • Dialysis is required in patients with renal failure
    • Hypocalcemia: • Ionized calcium conc. < 4.4mg/dL
    • Etiology: • Parathyroid or thyroid surgery – onset immediate(hrs) or delayed(1-2 days) • Severe pancreatitis • Magnesium deficiency • Massive blood transfusion
    • Evaluation: • Mild or moderate – Asymptomatic • Severe – Neuromuscular • • • • • Paresthesia Muscular spasm Seizures Tetany weakness
    • • Laryngospasm • Bronchospasm • Chvostek sign – CV symptoms • • • • • Arrythmias Heartblock Bradycardia Refractory hypotension ECG- prolongation of the QT interval and T-wave inversion
    • Treatment: • Treatment of the underlying disorder • Asymptomatic – Calcium supplementation is not required • Symptomatic – IV calcium therapy- initially 100mg elemental calcium over a period of 5-10mins.susequently, a calcium infusion of 0.5-2mg/kg/hr is given
    • • Once calcium conc. is corrected, enteral therapy with elemental calcium is begun at a dosage of 14gm/day Kobrin S, goldfarb s: hypocalcemia and hypercalcemia. In adrogue H acid base and electrolyte disorders. Newyork, churchill, livingstone, 1991, pp69-96
    • Magnesium homeostasis • 2nd most plentiful intracellular cation • Adult body contain 2000mEq of magnesium(Mg) • Normal concentration range 1.6 mEq to 2.1mEq/L • Daily consumption-25 mEq • Excretion- one third by stool and the rest by renal excretion
    • Magnesium abnormalities: Hypermagnesemia: • Serum magnesium level >2.1 mEq/L
    • Etiology: • Decreased GFR • Addison’s disease
    • Evaluation: • Symptomatic when serum Mg>4 mEq/L • Neuromuscular sequelae – Loss of deep tendon reflex – Somnolence – Apnea • Cardiac effects – Bradycardia – Heart block – Cardiac arrest( extreme elevation)
    • Treatment: • Symptomatic– Antagonizing using calcium infusion(5-10 mEq ) – Followed by immediate dialysis – If renal function normal, saline diuresis • Long term therapy- remove all exogenous Mg intake
    • Hypomagnesemia: • Serum Mg concentration<1.6 mEq/L
    • Etiology: • GI losses • Reduced absorption(short bowel syndrome) • Excessive urinary losses – Alcoholism – 10 aldosteronism – Diuretics
    • Evaluation: • Neuromuscular effects – Tremor – Ataxia – Carpopedal spasm – Tetany • Cardiotoxicity – Prolonged QT interval->ventricular tachycardia
    • Treatment: • Symptomatic – Mg infusion(8-16 mEq over a 5-10 min period, followed by 48 mEq/day) • If asymptomatic- Mg supplements given orally
    • Phosphate homeostasis • • • • Dietary intake-800-1200mg/day Reabsorbed in the jejunum Kidney acts as the principle regulator Normal serum P conc. Is 2.5-4.5mg/dL
    • Phosphate abnormalities: Hyperphosphatemia: • Serum phosphate level>4.5mg/dL
    • Etiology: • Renal insufficiency • Thyrotoxicosis • Malignant hyperthermia • Hypoparathyroidism
    • Evaluation: • Few symptoms associated • Commonly discovered by lab testing • Chronic hyperphosphatemia leads to metastatic calcifications and arterial obstruction(calciphylaxis)
    • Treatment: • Treatment of the underlying renal failure • Chronic- phosphate binding antacids are effective • Acute- end stage renal disease. Dialysis is required
    • Hypophosphatemia: Serum phosphate level <2.5mg/dL
    • ETIOLOGY: • Transcellular shifts • excessive urinary losses • Decreased dietary intake • Decreased intestine absorption • Diuretics • Hyperparathyroidism • Malabsorption • Hypomagnesemia • Vit. D deficiency
    • • Severe hypophosphatemia – Chronic respiratory alkalosis – Chronic alcoholism – Severe burns – Treatment of diabetic ketoacidosis
    • Evaluation: • Mild/moderate reduction- no signs • Severe hypophosphatemia – Myalgias – Muscle weakness – CHF – Respiratory insufficiency
    • Treatment: • Oral or parenteral phosphate repletion and correction of the underlying disorders
    • Electrolyte Disorders Signs and Symptoms Electrolyte Excess Deficit Sodium (Na) •Hypernatremia •Thirst •CNS deterioration •Increased interstitial fluid •Hyponatremia •CNS deterioration Potassium (K) •Hyperkalemia •Ventricular fibrillation •ECG changes •CNS changes •Hypokalemia •Bradycardia •ECG changes •CNS changes
    • Electrolyte Disorders Signs and Symptoms Electrolyte Excess Deficit Calcium (Ca) •Hypercalcemia •Thirst •CNS deterioration •Increased interstitial fluid •Hypocalcemia •Tetany •Chvostek’s, Trousseau’s • Hypermagnesemia • Loss of deep tendon •Hypomagnesemia •Hyperactive DTRs •CNS changes Magnesium (Mg) reflexes (DTRs) • Depression of CNS • Depression of neuromuscular function signs •Muscle twitching •CNS changes •ECG changes
    • Acid-Base Balance • Usually present clinically as – Tissue malfunction due to disturbed pH – 20 changes in respiration as a response to the underlying metabolic changes. • Clinical picture is dominated by the cause of the acid-base change, such as uncontrolled diabetes mellitus or primary lung disease • Only becomes evident when the venous plasma bicarbonate conc. Is noted to be abnormal, or when a full arterial blood gas analysis shows abnormalities in the pH, PCO2 or bicarbonate
    • • In metabolic disturbances, respiratory compensation is almost immediate to achieve the predicted PCO2 immediately after the onset of the metabolic disturbance.
    • Metabolic Acidosis Etiology and assessment • Occurs when acids other than carbonic acid accumulates in the body resulting in ↓ plasma bicarbonate
    • Causes of metabolic acidosis Disorder A. Normal anion gap • Inorganic acid addition • GI base loss • Renal tubular acidosis B. Increased anion gap Endogenous acid load Diabetic ketoacidosis Starvation ketosis Lactic acidosis Renal failure Exogenous acid load Aspirin poisoning Methanol poisoning Ethylene glycol poisoning Mechanism -Therapeutic infusion of or poisoning with NH4Cl, HCl -Loss of HCO3 in diarrhea, small bowel fistula, urinary diversion procedure. -Urinary loss of HCO3 in proximal RTA; impaired tubular acid secretion in distal RTA -Accumulation of ketones with hyperglycemia -Accumulation of ketones without hyperglycemia -Tissue hypoxia or liver disease -Accumulation of organic acids -Accumulation of salicylate -Accumulation of formate -Accumulation of glycolate, oxalate
    • • Two patterns are seen – Pattern A-when a mineral acid accumulates or when there is a primary loss of bicarbonate buffer from the ECF, there is no addition of the acidic anion. In this case anion gap occurs, which is normal, since the plasma chloride increases to replace the depleted bicarbonate levels. – Usually occurs due to diarrhea, where the clinical generally obvious or to RTA.
    • – Pattern B- accumulating acid is accompanied by its corresponding anion, which adds to the unmeasured anion gap, while the chloride level remains normal. – Cause is usually apparent from the clinical signs such as diabetes mellitus, renal failure or shock. – Other causes include alcoholism, starvation ketosis, lactic acidosis and intoxication by methanol
    • Management: • Identify and correct the cause • IV fluid resuscitation is needed due to associated water and sodium depletion • Bicarbonate infusions can be started in cases where the underlying cause cannot be identified and the acidosis level is critical(H+ >100nmol/L, pH < 7).
    • Metabolic alkalosis • It’s the inability of the kidney to excrete the excess bicarbonate ions or to retain hygrogen ion. • Usually accompanied by respiratory compensation • PCO2 increases 5-7mmHg for each 10 mEq/L of increase in plasma concentration.
    • Etiology: • Two types – Chloride responsive metabolic alkalosis • Have contracted ECF vol. and chloride deficit and urinary chloride<10 mEq/L • Vomiting and high nasogastric output are the common causes • Deficit chloride gap is filled by bicarbonate • In late stages, H is exchanged for Na.
    • – Chloride-unresponsive metabolic alkalosis • Are normovolemic or hypovolemic • Urinary chloride conc. >10 mEq/L. • E.g.:- cushing’s syndrome • High metabolic alkalosis is associated with a cerebral hypoperfusion, a leftward shift of the oxyhemoglobin dissociation curve and hypokalemia
    • Treatment: • Correction of the underlying defect • Contraction alkalosis treated with saline • With chloride unresponsive metabolic alkalosiscarbonic anhydrase inhibitor, acetazolamide. • Severe alkalemia treated with an infusion of 0.1N HCl. • The source of mineralocorticoid, if possible, should be corrected
    • Respiratory acidosis • Present when the pH is low and the PCO2 is elevated • Two types based upon etiology, time of evolution of the disorder and the degree of renal compensation – Acute – Chronic
    • Etiology : • Due to ineffective alveolar ventilation • Decompensation of pre existing respiratory disease • Asthma • Neuromuscular disorders • CNS depression • Airway obstruction
    • Evaluation: • In acute, resp. acidosis, the expected response is only 1 mEq increase in HCO3- for each 10 mm Hg rise in PCO2 • In chronic respiratory acidosis, renal adaptation is substantial • Plasma bicarbonate concentration increases 3 to 4 mEq/L for each 10mm Hg rise in PCO2 • Renal compensation never restores the pH to the normal levels
    • Treatment: • Improve alveolar ventilation – By intubation – By mechanical ventilation • Chronic respiratory acidosis the goal is the restoration of a compensated steady state because the underlying defect is usually uncorrectable
    • Respiratory alkalosis • Present when the pH is high and PCO2 is low • May be acute or chronic
    • Etiology: • Alveolar hyperventilation • In surgical patients – Hypoxia – CNS lesions – Pain – Hepatic encephalopathy – Mechanical ventilation
    • Evaluation: • In acute respiratory alkalosis(ARA), renal compensation is minimal. • In chronic respiratory alkalosis(CRA) , kidney responds by decreasing the excretion of the hydrogen ion • Serum bicarbonate conc. Is expected to decrease by 4-5 mEq/L for each 10mm Hg decrease in the PCO2 • Usually patient asymptomatic
    • • Severe alkalosis may have carpopedal spasm, circumoral numbness, cramps and confusional states. • Hyperventilation is particularly dangerous in patients with subarachnoid hemorrhage because it exacerbates vasospasm
    • Treatment: • Correction of the underlying problem.
    • Summary • Fluid compartments in the body must balance • Body systems regulate F&E balance • Assessment of body fluid is important to determine causes of imbalance • Interventions for imbalances are based on the cause
    • References • Oral and maxillofacial surgery-Daniel M Laskin • Essentials of surgery-Becker and Stucchi • Adrogue H, madias N: management of life threatening acid base disorders. N Engl J Med 338:26-34, 1998 • Gennari F:serum osmolality, N Engl J Med 310:102-105, 1984 • Kobrin S, goldfarb s: hypocalcemia and hypercalcemia. In adrogue H acid base and electrolyte disorders. Newyork, churchill, livingstone, 1991, pp69-96
    • • Oh M, Corrol H: disorders of sodium metabolism: hypernatremia and hyponatremia. Crit care Med 20:94-103, 1992 • Pestana C:fluids and electolytes in surgical patients, 2nd ed Baltimore, williams and wilkins, 1981 pp 101-144