Electrolyte disturbance in neonatal.pptx

Neonatalology
Electrolyte disturbance
Most common in neonate
And need more attention and management
We do management
Causes
Risk factors for this problem so its common and need early treatment for the front of the front door and the front door is locked in the door and the front door is locked and the front

1. Electrolyte disturbance

2. 3 day FT male neonate admitted in nursery before 2 days as a case of TTN On IV fluid and feeding by NGT Today notice a puffy eye and baby is apathy , lethargic and vomit milk two times Regarding approach of this case what will you ask?

3. History Examination Investigation

4. What are the causes?

5. most common electrolyte disorder in neonates. It occurs in approximately 33% of very low birthweight infants and is seen in up to 65% of very sick neonates . The most common cause of hyponatremia in the neonate is hypervolemia hyponatremia ( dilutional ) caused by excessive fluid administration or retention of free water .

6. Early-onset hyponatremia normal Na Late-onset hyponatremia low Na

7. SIADH . Weight gain usually occurs without edema. Excessive fluid administration without SIADH results in low urine SG and high urine output. In contrast, SIADH leads to decreased urine output and increased urine osmolarity . Urinary Na excretion in infants with SIADH varies widely and reflects Na intake.

8. c . Therapy. Water restriction is therapeutic unless (i) serum Na concentration is less than approximately 120 mEq /L or (ii) neurologic signs such as obtundation or seizure activity develop. In these instances, hypertonic Na chloride ( NaCl ) (3%) (1 to 3 mL/kg initial dose) should be used. Fluid restriction alone can be used once serum Na concentration is . 120 mEq /L and neurologic signs abate.

9. Investigation US EEG ECG Abd US

10. Management Preventive therapy 1. Use of isotonic fluid is recommended in children but is controversial in newborns. This is due to the risk of hypernatremia since the immature kidneys may not handle the sodium load. 2. Monitor serum electrolytes in any infant 3. Monitor high-risk infants at risk for hyponatremia , 4 . Make sure sodium supplementation is adequate for gestational and postnatal age.

11. Management Intravenous bolus over 10 to 15 minutes (1–2 mL/kg of 3% sodium chloride [513 mEq sodium/L ]) Twenty-four-hour correction. The total body deficit can be calculated and half of that is given over 12 to 24 hours. Recommendations include not to give >8 to 10 mEq /L over the first 24 hours for acute hyponatremia and not to give >6 to 8 mEq /L over 24 hours for chronic hyponatremia . c. Anticonvulsant therapy. Use of routine anticonvulsants for hyponatremic seizures may not be effective and can be associated with severe apnea .

12. General management. Always treat the underlying disorder. 1. Hyponatremia with hypervolemia. Sodium and water restriction while maintaining an effective circulating volume. 2. Hyponatremia with hypovolemia . Volume expansion with sodium and water to replace losses. 3. Hyponatremia with euvolemia . Water restriction.

13. A breastfed term infant who had a birthweight of 3kg present to ER 1 wk after discharge from the newborn nursery with the primary complaint of increasing fussiness. Hx indicates that the infant is a slow feeder and he appears dehydrated His current wt is 2.4kg and his serum Na 180mEq/L A pproach

14. Hypernatremia

15. Hypernatremia with normal or deficient ECF volume a. Predisposing factors include increased renal and IWL in VLBW infants. Skin sloughing can accelerate water loss. ADH deficiency secondary to IVH can occasionally exacerbate renal water loss. b. Diagnosis. Weight loss, tachycardia and hypotension, metabolic acidosis , decreasing urine output, and increasing urine SG may occur. Urine may be dilute if the newborn exhibits central or nephrogenic diabetes insipidus .

16. Therapy. Increase free water administration to reduce serum Na no faster than 1 mEq /kg/hour. If signs of ECF depletion or excess develop, adjust Na intake. Hypernatremia does not necessarily imply excess total-body Na . For example, in the VLBW infant, hypernatremia in the first 24 hours of life is almost always due to free water deficits

17. Hypernatremia with ECF volume excess a. Predisposing factors include excessive isotonic or hypertonic fluid administration, especially in the face of reduced cardiac output. b. Diagnosis. Weight gain associated with edema is observed. The infant may exhibit normal heart rate, blood pressure, and urine output and SG but an elevated FENa . c. Therapy. Restrict Na administration .

18. Hyperkalemia

19. This is the most serious of electrolyte abnormalities because it cancause fatal arrhythmias . Normal potassium levels are generally between 3.5 and 5.5 mEq /L, with a potassium >5.5 mEq /L indicating hyperkalemia. Some reported definitions of hyperkalemia include the following: Serum potassium >7 mEq /L in ELBW Serum potassium >6 mEq /L in full-term neonates. Serum potassium >6.5 mEq /L in premature infants. Moderate hyperkalemia: Serum potassium 6 to 7 mEq /L Severe hyperkalemia: Serum potassium >7 mEq /L

20. Plasma potassium should be monitored in all premature infants <30 weeks postmenstrual age during the first 3 days of life because they can develop nonoliguric hyperkalemia (NOHK) and have serious complications (cardiac arrhythmias, periventricular leukomalacia , brain hemorrhage, and sudden death).

21. How to approach How was the specimen collected ? Is there ECG changes? How much potassium is the infant receiving ? What are the BUN and creatinine levels? What are the urine output and body weight ? Is there associated hyponatremia , hypoglycemia, and hypotension ? Does the infant have any of the common characteristics of premature newborns prone to hyperkalemia?

22. Typical clinical manifestations of symptomatic hyperkalemia include muscular or respiratory paralysis, bradycardia , ventricular arrhythmias (ventricular fibrillation/tachycardia), shock, and cardiac arrest.

23. Differential diagnosis . Pseudo hyperkalemia RBC destruction during phlebotomy or heel stick thrombocytosis or leukocytosis True hyperkalemia

24. Common causes of hyperkalemia Increased potassium administration or intake Pathologic hemolysis of red blood cells . IVH , sepsis Tissue necrosis and breakdown Renal failure/insufficiency Nonoliguric hyperkalemia (NOKH) Metabolic acidosis Dehydration Medications (Penicillin G, digoxin, heparin) Adrenal insufficiency Decreased insulin levels Transfusion

25. Less common causes Neonatal Bartter syndrome Hereditary hyperkalemic disorders Disorders that cause decreased renal excretion of potassium

26. Laboratory studies Serum potassium Serum and urine electrolytes Complete blood count and differential Serum ionized and total calcium levels Serum pH and bicarbonate BUN and creatinine Urine dipstick and specific gravity Abdominal radiograph Electrocardiogram

27. Hypokalemia

28. Hypokalemia is defined as a serum potassium <3.5 mEq /L. Most sources use the following designations: A. Mild hypokalemia is 3.0 to <3.5 mEq /L, B. Moderate hypokalemia is 2.5 to 3.0 mEq /L, C. Severe hypokalemia is <2.5 mEq /L.

29. How to approach What is the central serum potassium? Is the infant on diuretics? How much potassium is the infant receiving? 3rd space loss? What is the infant’s magnesium level? Does the infant have hypertension?

30. Differential diagnosis Pseudohypokalemia True hypokalemia

31. Causes Inadequate intake (rare ) GI loss (by NGT – diarrhea – Vomiting – Medications like Kayexalate ) Renal losses Medications (Diuretic use, Steroids and steroid-like medications, Antibiotics, Magnesium-depleting medications) Any cause of polyuria Renal tubular losses RTA 1 and 2 can cause hypokalemia, Hypomagnesemia , Bartter syndrome Liddle , Gitelman , and Fanconi syndromes

32. Causes Transcellular shifts of K from serum to cells: Alkalosis Insulin therapy Medications Hypothermia Endocrinopathies (CAH, Conn syndrome, Cushing syndrome, SIADH, Hyperthyroidism)

33. Laboratory studies Repeat the serum potassium level Spot check urinary electrolytes . a . Urine potassium is <20 mmol /L: Suspect nonrenal losses. b. Urine potassium is >20 mmol /L: Suspect renal losses and Bartter. c. Urinary chloride level is low (<10 mEq /L): Consider GI losses ( vomiting,drainage , fistulas, ileostomy, diarrhea). d. Urine chloride is normal in Bartter syndrome and diuretic. e. A low urine sodium level with a high urine potassium level is associated with secondary hyperaldosteronism . f . If urine magnesium is high, consider renal magnesium loss . Urinary dipstick for blood

34. Laboratory studies Serum electrolytes and creatinine . ABG Serum Mg Drug screen Serum adrenocorticotropic hormone, cortisol, renin activity, and aldosterone levels. Serum insulin and C-peptide tests Genetic testing in Bartter syndrome Genetic testing in Bartter syndrome Imaging and other studies ( abd x-ray/US, ECG, MRI)

35. Management Prevent life-threatening cardiac and muscular complications first Rapid correction of hypokalemia is not recommended Bolus intravenous potassium administration is not recommended Oral replacement is always preferred. If an infant is unable to tolerate oral replacement (ileus, emesis) IV potassium is recommended . The maximum recommended intravenous concentration is 40 mEq /100 mL(400 mEq /L) of potassium chloride in patients with a central line. Peripheral intravenous (IV) line should be limited to 20 mEq /L .

36. Management Serum potassium levels should be monitored every 4 to 6 hours . If alkalosis is present, treatment is potassium chloride to replenish chloride. If the infant is acidotic, preferred treatment is potassium acetate (IV) or potassium bicarbonate (oral). Rapid correction of acidosis may worsen hypokalemia. Correct low magnesium before treating with potassium Do not dilute potassium salts in a dextrose-containing solution Remember that excessive correction of hypokalemia may result in hyperkalemia .

37. Management Oral potassium supplements are available as chloride, bicarbonate, citrate, gluconate , and phosphate salts. Recommendations for treatment with oral potassium supplements are as follows: a. Potassium bicarbonate: Used in infants with hypokalemia with metabolic acidosis ( eg , RTA or diarrhea). b. Potassium phosphate: Used only in infants with hypokalemia and hypophosphatemia ( eg , proximal RTA with Fanconi syndrome or phosphate wasting ). c. Potassium chloride: Used in infants with hypokalemia, hypochloremia , and metabolic alkalosis ( eg , diuretic therapy–induced hypokalemia, vomiting ).Used in infants with hypovolemia .

38. Emergency treatment Limited to infants with life-threatening symptoms of hypokalemia (cardiac arrhythmias, severe respiratory depression/distress, extreme muscle weakness/paralysis) or for a serum potassium level <2.0 to 2.5 mEq /L ( controversial as to what critical level to treat regardless of clinical signs; varies from 1.5 to 2.5 mEq /L). Aggressive treatment with IV potassium requires ECG monitoring. Never give a bolus of potassium; give potassium chloride 0.5 to 1 mEq /kg/dose over1 hour (some sources suggest 2 hours) with continuous ECG monitoring ( maximum infusion rate: 1 mEq /kg/h ).

39. C . Moderate symptomatic hypokalemia. Use IV potassium with ECG monitoring. 1. Abnormal electrocardiogram: ST-segment depression, T-wave depression, U-wave elevation: Treat with potassium chloride 0.5 to 1 mEq /kg IV over 3 to 4 hours with ECG monitoring. 2. Normal electrocardiogram: Add 20 mEq of potassium chloride per liter to peripheral vein IV fluids. If higher concentrations are needed a central line is necessary. Otherwise increase the amount in the IV fluids (preferred) or a slow correction over 24 hours

40. Mild asymptomatic hypokalemia. May resolve without treatment.

41. Hypocalcemia

42. hypocalcemia is <2.0 mmol /L (<8.0 mg/ dL ) for a term infant or <1.75 mmol /L (<7.0 mg/ dL ) for a preterm infant. iCa levels of <1.2 mmol / dL (4 mg/ dL ) are considered hypocalcemic .

43. Risk factors Early-onset neonatal hypocalcemia . a. A full-term infant receiving 100 to 120 mL of normal formula b. Premature (especially <28 weeks) or sick infants c. Calcium levels (both iCa 2+ and tCa 2+ ) usually return to normal within 48 to 72 hours regardless of whether supplemental Ca 2+ is given Perinatal stress. Infant of diabetic mother. Intrauterine growth restriction . Nutritional deprivation. Hypomagnesemia . Congenital abnormalities. Maternal hyperparathyroidism.

44. Clinical presentation Early-onset hypocalcemia (first week of life) a. Apnea b . Stridor c . Irritability, jitteriness, tremors, or hyperreflexia d. Clonus, tetany , or seizures e. Arrhythmia secondary to prolonged QT interval Late-onset hypocalcemia (any time after first week) a. Lethargy, apnea b . Feeding intolerance c. Abdominal distention d . Bone demineralization, increased alkaline phosphatase e . Skeletal fractures Paradoxically , neonatal hypocalcemia is often asymptomatic. Only an index of suspicion based on risk factors will lead to a correct diagnosis .

45. Diagnosis Laboratory studies a. Total and ionized calcium levels b . Serum magnesium levels of <1.5 mg/ dL are indicative of hypocalcemia because they often coexist. c. Elevated alkaline phosphatase levels. d. Urinary calcium losses of >4 mg/kg/24 h Imaging studies for bone demineralization, metaphyseal lucencies , and rib and long bone fractures Electrocardiographic studies will identify arrhythmias due to QT interval changes .

46. Management Acute treatment. Reserved for the symptomatic hypocalcemic infants with apneic spells, seizures, or cardiac failure with arrhythmia. Dosage is 100 to200 mg/kg of 10% calcium gluconate slowly by peripheral IV over 15 to 20 minutes with constant cardiac monitoring (see Chapter 155 for dosing information ). Maintenance treatment. IV dosage of 20 to 60 mg/kg/d of elemental calcium Vitamin D supplementation. Hypocalcemia secondary to blood/exchange transfusions. Hypocalcemia secondary to diuretic therapy .

47. Hypercalcemia

48. Definition. iCa 2 + serum level >1.35 mmol /L (5.4 mg/ dL ) for any infant, irrespective of a tCa serum level . Although tCa2+ is indicative of hypercalcemia at levels >2.75 mmol /L(11 mg/ dL ), it is not a reliable measure.

49. Risk factors Congenital hyperparathyroidism a. Primary. Due to genetic defects as either familial hypocalciuria , hypercalcemia , or severe neonatal hyperparathyroidism. b. Secondary. Due to maternal hypoparathyroidism . 2. Maternal hypocalcemia 3. Subcutaneous fat necrosis 4. Therapeutic hypothermia 5. Idiopathic infantile hypercalcemia 6. Williams syndrome 7. Hypophosphatasia 8. Hyper- or hypothyroidism 9. Malignancy (very rare in the newborn) 10. Distal renal tubular acidosis, Jansen metaphyseal chondrodysplasia 11. Iatrogenic

50. Clinical presentation 1. Feeding intolerance, constipation, failure to thrive 2. Polyuria, dehydration 3. Hematuria, nephrocalcinosis , nephrolithiasis 4. Lethargy, hypotonia , seizures (rare, only in the most severe hypercalcemia ) 5. Bradycardia , short QT interval, hypertension

51. Diagnosis Laboratory studies a. Serum calcium for levels as given previously b. Serum total protein and albumin-globulin ratio for hypoproteinemia c. Blood gases for acid-base status d. Serum phosphorus for hypophosphatemia e. Urine calcium and phosphorus f. Parathyroid hormone, 25-hydroxy (OH) vitamin D, 1, 25-OH vitamin D g. Thyroid studies h. Alkaline phosphatase for hypophosphatasia i. Serum creatinine Imaging studies a. Renal ultrasound for calcifications b. Long bone x-rays for demineralization secondary to hyperparathyroidism or osteosclerotic lesions secondary to hypervitaminosis

52. Management Acute symptomatic hypercalcemia a. Discontinue any parenteral intake of calcium. b. Increase fluid intake as intravenous normal saline. c. Augment calcium loss Less acute but severe hypercalcemia . Consider: a. Calcitonin (limited newborn/neonatal experience). b. Glucocorticoids are effective on a short-term basis but are not recommended. c. Intravenous bisphosphonates

53. Management Refractory hypercalcemia . In extreme situations, parathyroidectomy has been the last resort.