Pediatric iv fluid 1 and electrolyte correction.pptx

Pediatric

1. IV FLUID AND ELECTROLYTE CORRECTION(shortcut) BY OSAMA FATHY AFIFI MASTER DEGREE OF PEDIATRIC NEONATAL EFLLOWSHIP

2. Composition of body fluids total body water as a percentage of body weight declines with age. Early fetal life TBW= 90% At birth TBW= 75-80% By the end of 1st year to puberty about60% - Sensible water loss (SWL ): Easily measured – Urine, stool, NG/OG output, CSF - Insensible water loss (IWL ): Not readily measured –Evaporation from skin (66%) or respiratory tract (33 %)

3. Water loss - Sensible water loss (SWL): Easily measured – Urine, stool, NG/OG output, CSF - Insensible water loss (IWL): Not readily measured Evaporation from skin (66%) or respiratory tract (33%)

4. Total body water is 60 % of body weight. The intracellular fluid volume is 40% of total body weight . The extracellular fluid volume is 20% of total body weight. Plasma volume is 5% of total body weight. Blood is about 8%of total body weight.

5. Serum concentration of k+ may not reflect total body content.k + shift from intracellular space to extra cellular space can maintainnormal or elevated serum k+ despite massive loss Interperitation of k+ related to ph

6. Cell membrane Barrier between ICF and ECF • Freely permeable to water but not to sodium(Na-k atapase pump) • Water moves in either direction depending upon osmolarity Glucose by facilitated diffusion(need carrier can be blocked

7. Osmolarity Osmolarity is the measure of solute concentration per unit VOLUME of solvent. Properity of asolution independant of any Membrane. the cell membranes in general are freely permeable to water, the osmolality of the extracellular fluid (ECF) is approximately equal to that of the intracellular fluid (ICF). Calculated osmolarity = 2 Na + Glucose  + Urea (all in mmol /L). ] + [Glucose]/18 + [ BUN ]/2.8 where [Glucose] and [BUN] are measured in mg/ dL (or urea/6)

8. T onicity Properity of solution in relation to membrane Non penetrating solute throgh basement membrane result in effective osmolarity EX. Urea contribute to total osmolarity but not tonicity as intracellular and extracellular nearly the same

9. Osmolarity and tonicity

10. WATER AND SODIUM HOMEOSTASIS

11. * Stimulated by 1-2% change of plasma osmolarity *Stimulated by moderate volume depletion regardless the osmolarity

12. So sensitive to volume depletion and hypoperrfuion of the kidney To maintain volume regulation by increase N a+ and water reabsorbition and k+ excretion

13. Iv fluid therapy

14. Resuscitation Patients with signs of hypoperfusion should receive fluid resuscitation with boluses of isotonic fluid ( eg , 0.9% saline or Ringer's lactate ). The goal is to restore adequate circulating volume,normal heart rate to restore blood pressure and perfusion. The resuscitation phase should reduce moderate or severe dehydration deficit 20 mL/kg (2% body weight) is given IV over 20 minutes( may need to receive the boluses as fast as possible). If dehydration is severe, 3 boluses of 20 mL/kg (6% body weight) may be required.

15. Maintainnce =UOP+ Insensible water loss normal maintainance

16. chest tube drainge are isotonic replaced by normal saline Replacement Fluids loss

17. Assesment of dehydration

18. Whole plan(type and rate of infusion) Fluid Management of Dehydration Restore intravascular volume: Isotonic fluid (NS or LR): 20 mL/kg over 20 min Repeat as needed Calculate 24 hr fluid needs: maintenance + deficit volume Subtract isotonic fluid already administered from 24 hr fluid needs Administer remaining volume over 24 hr using 5% dextrose NS + 20mEq/L KCl Replace ongoing losses as they occur

19. But in nelson 20 th ed 1- D5 1/2NS + 20 mEq /L KCl is recommended in the child who is NPO and does not have volume depletion or risk factors for nonosmotic ADH production . (.nelson 20 th ed p386 ) 2- Children with volume depletion, baseline hyponatremia , or at risk for nonosmotic ADH production (lung infections such as bronchiolitis or pneumonia ; central nervous system infection) should receive D5 NS + 20 mEq /L KCl . (.nelson 20 th ed p386 ).

20. NO big difference In one study of children admitted with hypovolemia caused by gastroenteritis, patients were assigned randomly to receive either hypotonic or isotonic intravenous fluid . The administration of hypotonic solution (0.45 percent saline) did not alter the mean sodium level of children who were hyponatremic (from 132 to 133 mEq /L) but decreased the mean sodium level of children who were initially normonatremic (from 137 to 135 mEq /L). The use of isotonic solution increased mean serum sodium levels of initial hyponatremic patients (from 132 to 134 mEq /L) but there was no change in mean sodium levels in the initial normonatremic patients (from 137 to 138 mEq /L). ( up-to-date 2013)  So that we can safely use D5 1/2NS +20mEq/l KCL in hyponatrimec dehydration without fear of decreasing already decreased plasma NA.

21. Conclusion Deficit therapy :- Amount :- according to degree of dehydration Type: D5 1/2NS +20mEq/l KCL How to give In mild hyponatremic and iso natremic dehydration:- deficit +maintenance fluid of 24hr –shock therapy over 24 hr In hypernatremic dehydration: - according level of NA correct not more 0.5mleq/l of NA per hour or 12 mleq / l per day

22. Electyrolyte defecit

23. Monitoring and Adjusting Therapy Measurement of serum electrolyte levels at least daily is appropriate for any child who is receiving IV rehydration . . It is always important to look at trends. For example , a sodium concentration ([Na + ]) of 144 mEq /L is normal; but if the[Na + ] was 136 mEq /L 12 hr earlier, there is a distinct risk that the child will be hypernatremic in 12 or 24 hr. It is advisable to be proactive in adjusting fluid therapy . . The patient with an elevated creatinine value and K + level of 5 mEq /L does not receive any potassium until the serum K + level decreases .

24. Hyponatremia It is a serum sodium level <135 mEq /L. Hyponatremia exists when the ratio of water to Na+ is increased. This condition can occur with low, normal, or high levels of body Na+ . Similarly, body water can be low, normal, or high . Pseudohyponatremia  defined by a serum sodium concentration of less than 135 mEq /L in the setting of a normal serum osmolality (280 to 300 mOsm /kg) when the plasma contains very high concentrations of protein (multiple myeloma, IVIG infusion) or lipid ( hypertriglyceridemia,hypercholesterolemia ). Hyperosmolality , as may occur with hyperglycemia, causes a low [Na+ ] because water moves down its osmotic gradient from the ICS into the ECS, diluting the [Na+ ]. However, because the manifestations of hyponatremia are a result of the low plasma osmolality, patients with hyponatremia resulting from hyperosmolality do not have symptoms of hyponatremia . When the etiology of the hyperosmolality resolves, such as hyperglycemia in diabetes mellitus, water moves back into the cells, and the [Na+ ] rises to its “true” value ,

25. Hypovolemic hyponatremia Sodium loss > water loss (renal and extrarenal loss) • Usually a combination of sodium loss and water retention due to ADH synthesis, resulting in renal water retention . Gastroenteritis is the most common cause in children hyponatremia if patient takes in hypotonic fluid, either intravenously or enterally , Burns: cause massive losses of isotonic fluid,sweat , Third space losses, diuretics, RTA-II, CAH , pseudohypoaldosteronism CSW : CNS injury (production of natriuretic peptide -- renal salt wasting) , • In diseases associated with urinary sodium loss, the urine sodium level is >20 mEq /L despite volume depletion there is a Renal sodium loss

26. Hypervolemic hyponatremia Excess of TBW and sodium, increase in water > increase in sodium as in Heart failure Cirrhosis Nephrotic syndrome Acute , chronic kidney injury Capillary leak caused by sepsis Hypoalbuminemia caused by gastrointestinal disease ( protein-losing enteropathy ) • Conditions with hypervolemic hyponatremia – A decrease in effective blood volume (Regulatory systems sense decrease in effective blood volume – Attempt to retain water and sodium to correct problem, ADH causes renal water retention – Aldosterone and other intrarenal mechanisms retains sodium • In these disorders, there is a low urine sodium (<10 mEq /L) and excess of both total body water and sodium

27. Euvolemic hyponatremia • Hyponatremia + no evidence of volume overload or volume depletion • Patients typically have an excess of TBW and a slight decrease in total body sodium • Some of these patients have an increase in weight, implying that they are volume-overloaded • SIADH: Inappropriate secretion of ADH , Secretion of ADH is not inhibited by either low serum osmolality or expanded intravascular volume • Unable to excrete water • Dilution of the serum sodium Kidney increases sodium excretion in an effort to decrease IV volume to normal     Diagnostic criteria for SIADH Hyponatremia : Absence of – renal , adrenal , thyroid insufficiency , heart failure , nephrotic syndrome or cirrhosis ,Diuretic ingestion , Dehydration • Urine osmolality > 100mosm/kg , Serum osmolality < 280mosm/kg , serum sodium <135 and Urine sodium >30 meq /L

28. Symptom of hyponatremia

29. Diagnosis 1st step: determination of plasma osmolality and urine osmolality • Normal osmolality: pseudohyponatremia • High osmolality: Glucose or effective osmole ( mannitol ) • Low osmolality: – Indicates true hyponatremia – These patients are at risk for neurological complication • 2nd step : clinically evaluate the patient's volume status , hypervolemic , euvolemic ? or hypovolemic hyponatremia :( renal or nonrenal ) • 3rd step: Urine sodium • Useful in differentiating between renal and nonrenal causes • Nonrenal losses: (kidney is working properly) renal retention of sodium Urinary sodium low (typically <10 mEq /L) • Renal losses: Urine sodium >20 mEq /L,

30. Treatment of hyponatremia Symptomatic hyponatremia A patient with severe symptoms (seizures), no matter the etiology, should be given a bolus of hypertonic saline to produce a small, rapid increase in serum sodium. Hypoxia worsens cerebral edema, and hyponatremia may exacerbate hypoxic cell swelling . Therefore, pulse oximetry should be monitored and hypoxiaaggressively corrected. 3 % hypertonic saline given in a dose of 5 cc/kg is expected to raise the serum sodium approximately 5 mEq /L  For symptomatic cases give 3%NS 3-5 ml/kg over 1-2 hr. (increases serum Na by 5-6mEq/l)  Stop further therapy with 3%NS when patient is symptom free or acute rise in serum sodium is 10mEq/l in first 5 hour . Duration of correction not more than 2mEQ per hour

31. Treatment of hyponatremia (Asymptomatic)    Rapid correction may cause central pontine myelinolysis (CPM ), Maximum limit of 10-12 mEq /L for first 24 hours and 18 mEq /L over first 48 hours hypovolemichyponatremia : The cornerstone of therapy is to replace the Na+ deficit and any water deficit present. complete restoration of intravascular volume suppresses ADH production. hypervolemic hyponatremia is difficult; patients have an excess of both water and Na+ . Administration of Na+ leads to worsening volum overload and edema The cornerstone of therapy is water and Na+ restriction , ttt of the cause ,diuretics may help by causing excretion of both Na+ and water. Vasopressin antagonists ( vaptans ), by blocking the action of ADH and causing a water diuresis, are effective in correcting the hypervolemic hyponatremia caused by heart failure. Vaptans are contraindicated if there are moderate to severe CNS symptoms.

32. Treatment of hyponatremia euvolemic hyponatremi ( SIADH) Fluid restriction (60-75%) Treat underlying cause Occasionally loop diuretics to lower urine osmolality Therapy with saline can create problems Temporarily increase sodium concentration Causes kidneys to eliminate almost all of the sodium, eliminating any benefit from therapy Water contained in the saline is retained – Hyponatremia may actually worsen

33. Hypernatremia Hypernatremia is a [Na+ ] >145 mEq /L, although it is sometimes defined as >150 mEq /L . Etiology Excessive Sodium intake unproperly mixed formula, Excess sodium bicarbonate, Ingestion of seawater or sodium chloride, Intentional salt poisoning (child abuse or Munchausen syndrome by proxy), Intravenous hypertonic saline, Hyperaldosteronism Water Deficit Nephrogenic Diabetes Insipidus Central Diabetes Insipidus Increased Insensible Losses Premature infants, Radiant warmers, Phototherapy, Inadequate intake:

34. Clinical Manifestations Hypernatremia, even without dehydration, causes central nervous system (CNS) symptoms that tend to parallel the degree of Na+ elevation and the acuity of the increase. Patients are irritable, restless, weak, and lethargic. ,high-pitched cry and. , thirst sensation , Hypernatremia is associated with hyperglycemia and mild hypocalcemia ; the mechanisms are unknown . Brain hemorrhage is the most devastating consequence decrease in brain volume, This decrease result in tearing of intracerebral veins and bridging blood vessels as the brain moves away from the skull and the meninges. Patients may have subarachnoid, subdural , and parenchymal hemorrhages.

35. Treatment of hypernatremia Correct deficit over 48 to 72 hours. Recommended rate of drop is 0.5mEq/l/ hr (10-12mEq/l/day) to avoid brain edema  Hypotonic infusates are used as N/4 or N/5 saline, avoid sodium free fluids .). Seizures during correction of hypernatremia are treated using 3%NS as 5-6ml/kg infusion over 1-2 hr - 3 -treatment of the cause

36. H ypokalemia Hypokalaemia is defined as a plasma potassium level less than 3.5mmol/L Eatiology : Transcellular Shifts a Alkalemia,Insulin Drugs/toxins (theophylline, hydroxychloroquine ), refeeding syndrome and hypomagnesimia Extrarenal Losses Diarrhea,Laxative abuse, Sweating, Sodium polystyrene sulfonate ( Kayexalate ) Renal loss Gitelman syndrome, Bartter syndrome, Distal renal tubular acidosis ,Proximal renal tubular acidosis , Diabetic ketoacidosis

37. H ypokalemia Clinical manifestation CVS : ECG change( flattened T wave , Q-T interval prolongation,  a depressed ST segment, and the appearance of a U wave ,), arrhythmia( digitalis-induced arrhythmias) Other :constipation ,ileus, urinary retention, muscle cramp upto paralysis

38. Hypokalemic ECG changes

39. Treatment of hypokalemia Severe, symptomatic hypokalemia requires aggressive treatment with kcl infused with saline . Supplementation is more cautious if renal function is decreased because of the kidney's limited ability to excrete excessive K+ (call nephro team.)

40. H yperkalemia a potassium level greater than 5.5 mEq /L. Eatiology : Pseudo hyperkalemia : hemolysis of drawn blood Leukocytosis (white blood cell count >50,000/mm3 or thrombocytosis [platelets >1,000,000/mm3 ]) redistribution : acidosis, especially inorganic endogenous Extensive tissue injury, burns, heat stroke, or trauma Hemolysis Rhabdomyolysis Tumor lysis syndromes Tissue necrosis Hemolytic uremic syndrome Increased potassium load exogenous : Banked blood transfusions Decreased excretion with or without increased intake Acute renal failure and severe chronic renal failure Mineralocorticoid deficiency — Addison’s disease ,CAH, Selective aldosterone deficiency , Tubulo -interstitial disease , Type IV renal tubular acidosis

41. Hyperkalemia Although hyperkalemia is defined as a serum potassium concentration of > 5.5 mEq /L, it is moderate (6 to 7 mEq /L) and severe (> 7 mEq /L) cases of hyperkalemia that are life threatening and require immediate therapy Changes in the electrocardiogram (ECG) begin with peaking of the T waves . This is followed, as K+ level increases, by ST-segment depression, an increased PR interval, flattening of the P wave, and widening of the QRS complex( QRS(increased risk of arrhythmia)

42. ECG

43. Hperkalemia Treatment 1-stop infusion of k and hyperkalemic drug 2- Calcium Gluconate 10%: 0.5 ml/kg slow IV injection over 2-5 minutes if unstable(under monitoring), over 20min if stable. Onset of action less than 3 minutes, should see normalization of ECG. If not can be repeated.duration of action 30 minute. 3- Salbutamol nebulization: onset of effect 20 -30 minute ,duration of action 2hours 4- INSULIN/GLUCOSE to be given at the same time (0.1 regular insulin per kg+0.5GM glucose(5ml G10% /KG) together at 15-30 minute peak 60 minutes till 2hours. 5-NAHCO3 especially with acidosis 6-DIURETIC(FUROSAMIDE) 7- Kayexalate  (Sodium polystyerene sulfonate ) 8-Dialysis