Nutritional Support and Fluid Management Flashcards
Which of the following statements is true regarding daily fluid requirements?
A. Premature infants weighing less than 2 kg require only up to 80 mL/kg per day of fluid.
B. Neonates and infants weighing 2 to 10 kg require 200 mL/kg per day of fluid.
C. Infants and children weighing 10 to 20 kg require 1000 mL/day plus 50 mL/kg per day of fluid for every kilogram over 10 kg.
D. Children heavier than 20 kg require 1500 mL/day plus 30 mL/kg per day of fluid for every kilogram over 20 kg.
E. All of the above.
ANSWER: C
COMMENTS: Infants weighing less than 1500 g require 130 to 150 mL/kg per day of fluid.
Those weighing 1500 to 2000 g require 110 to 130 mL/kg per day,
2 to 10 kg require 100 mL/kg per day,
10 to 20 kg require 1000 mL for the first 10 kg and an additional 50 mL/kg for each additional kilogram, and
those weighing more than 20 kg require 1500 mL plus 20 mL/kg for each additional kilogram over 20 kg.
Daily electrolyte requirements include sodium at 2 to 5 mEq/kg and potassium at 2 to 3 mEq/kg.
Dextrose is administered to provide a glucose substrate at a minimum rate of 4 to 6 mg/kg/min.
Fat infusions are started at 0.5 g/kg per day and advanced up to 2.5 to 3 g/kg per day.
Protein requirements are 2 to 3.5 g/kg per day in infants, as opposed to requirements of about 1 g/kg per day in adults.
(Rush Review of Surgery 6th Edition)
What is the daily energy requirement for an 8-month-old healthy baby?
A. 90 to 120 kcal/kg
B. 80 to 100 kcal/kg
C. 75 to 90 kcal/kg
D. 50 to 75 kcal/kg
E. 30 to 50 kcal/kg
ANSWER: B
COMMENTS: Energy requirements are important to consider in the pediatric population.
For premature infants, 90 to 120 kcal/kg are required.
Infants <6 months of age require 85 to 105 kcal/kg,
6 to 12 months require 80 to 100 kcal/kg,
1 to 7 years require 75 to 90 kcal/kg,
7 to 12 years require 50 to 75 kcal/kg,
and >12 years up until 18 years of age require 30 to 50 kcal/kg.
Periods of active growth have higher caloric requirements.
Breast milk provides 0.64 to 0.67 kcal/mL.
When feasible, it is advisable that children have breast milk until 1 year of age. Breast milk additionally helps provide passive immunity with the transmission of both humoral and cellular factors to the baby.
However, breast milk must be supplemented with vitamin D to prevent vitamin D deficiency that is often seen in breastfed infants.
(Rush Review of Surgery 6th Edition)
Total body water of a newborn?
75-80%
During the first week of life, TBW decreases by 4-5%, which is reflected as a normal loss in body weight.
(Pediatric Surgery Secrets)
What is the risk of fluid overload in preterm infants?
Preterm infants with an excess of total body fluids have an increased incidence of:
Patient ductus arteriosus
Left ventricular failure
Respiratory distress syndrome
Necrotizing enterocolitis.
(Pediatric Surgery Secrets)
How does renal fluid physiology differ in newborns and adults?
GFR of the term newborn is 25% of that of an adult.
The GFR rises rapidly during the first week of life and slowly increases to adult levels by 2 years of age.
Despite this low-GFR, the newborn can handle large water loads, because the newborn kidney has a low concentrating capacity.
(Pediatric Surgery Secrets)
What is deficit fluid therapy?
Deficit fluid therapy refers to the management of the fluid losses that occurred before the patient’s presentation.
Deficit therapy has two essential components:
1) An accurate estimation of the severity of dehydration
2) Development of an approach to repair the deficit
(Pediatric Surgery Secrets)
What are the typical signs of dehydration in a child?
The severity of dehydration is estimated from the patient’s history and physical condition.
No single piece of laboratory data can predict the severity of dehydration.
In children with mild dehydration (1-5% total body fluid volume), the usual history is 12-24 hours of vomiting and diarrhea with minimal findings on exam.
Children with moderate dehydration (6-10%) have a history of abnormal fluid losses plus physical findings that include tenting of the skin, weight loss, sunken eyes and fontanel, slight lethargy, and dry mucous membranes.
With severe dehydration (11-15%), the patient develops skin mottling, cardiovascular instability (tachycardia, hypotension), and neurologic involvement (irritability, coma).
Dehydration over a protracted period may be more severe than is clinically evident.
(Pediatric Surgery Secrets)
What are the typical maintenance fluid requirements for a child?
Newborn day 1:
50-60 ml/kg/day of D10W
Newborn day 2:
100 ml/kg/day of D10 1/4NS
Newborn day >7:
100-150 ml/kg/day of D5-10 1/4NS
Older child (0 - 10 kg): 100 ml/kg/day (4 ml/kg/hr)
Older child (10 - 20 kg): 1000 ml/day + 50 ml/kg/day (40 ml/hr + 2 ml/kg/hr)
Older child (>20 kg): 1500 ml/day + 25 ml/kg/day (60 ml/hr + 1 ml/kg/hr)
(Pediatric Surgery Secrets)
How do normal fluid requirements (losses) change for the sick infant?
Normal fluid losses are composed of two parts:
(1) evaporative losses (33% of total losses) and
(2) urinary losses (66% of total losses).
Evaporative losses are free water losses through the skin and lungs and are used for thermal regulation and to humidify inspired air.
The ambient humidity and temperature affect the magnitude of evaporate losses, and patients receiving humidified air have a reduction in fluid requirements.
Similarly, patients with hyperthermia or tachypnea have exaggerated evaporative losses.
Urinary losses are affected by various conditions.
Infants with diabetes insipidus and premature infants have an obligatory production of dilute urine, and appropriate increases in the volume of maintenance fluids must be made.
In conditions of excessive secretion of antidiuretic hormone or physiologic stress, the patient may not be able to decrease urine osmolality, and the volume of fluids must be decreased.
(Pediatric Surgery Secrets)
What is the typical dehydration of a child with pyloric stenosis?
Dehydration with pyloric stenosis is based on loss of both fluid and electrolytes, with large losses of hydrogen and chloride ions from gastric secretions.
The degree of dehydration can be estimated by physical exam and serum electrolytes.
After progressive acid and fluid losses, the child develops hypokalemic, hypochloremic metabolic alkalosis.
The degree of dehydration can be estimated by serum chloride and bicarbonate levels.
(Pediatric Surgery Secrets)
Explain paradoxical aciduria.
In children with severe dehydration, the urine pH often demonstrates a paradoxical aciduria, because the renal mechanisms for acid resorption are lost in an attempt to retain both sodium and potassium ions.
The deficit in renal acid resorption contributes to metabolic alkalosis, and this cycle can be broken only by adequate fluid and electrolyte replacement.
Surgery for pyloric stenosis should be deferred until the child is adequately rehydrated.
(Pediatric Surgery Secrets)
How many calories does a newborn infant require?
Most term infants are fed 90-120 kcal/kg/day.
Increased calories are necessary in newborns with increased metabolic demands (e.g., prematurity, increased work of breathing, congenital heart disease).
The overall best measure of adequate caloric support is weight gain (goal of 1%/day).
Gavage feeds may be necessary in tachypneic infants.
(Pediatric Surgery Secrets)
How do you pick the right food for the right baby?
In general, breast milk is the best choice for most infants.
When breast milk is not available, standard formulas (e.g., Enfamil, Similac) are the cheapest, most widely available alternatives and should be used unless there are other concerns.
Premature infants require a special premature formulation.
Soy formulas (e.g., Prosoybee, Isomil) are lactose-free and use soy for the protein source; they are used for infants who are intolerant of milk protein (with malabsorptive symptoms).
Elemental formulas (e.g., Nutramigen, Pregestimil) are lactose-free and have predigested proteins (hydrolyzed casein); they are used for infants with malabsorption, short bowel, and cystic fibrosis.
(Pediatric Surgery Secrets)
What are the major components of total parenteral nutrition?
When possible, enteral feeds are preferable to total parenteral nutrition (TPN).
TPN provides fluids, calories (in the form of carbohydrates and fat), electrolytes, and protein.
Each of these components must be structured carefully for the child requiring parenteral nutrition.
(Pediatric Surgery Secrets)
How should you monitor a child on TPN?
As the child begins TPN, hyperglycemia is poorly tolerated and requires a reduction in glucose infusion: Routine electrolytes, lipid levels, and liver function tests are mandatory.
The major risk to long-term TPN use is cholestatic liver failure.
(Pediatric Surgery Secrets)
What risk is associated with overfeeding a sick child?
Overfeeding calories or substrate in excess of metabolic demands may result in respiratory compromise, hepatic dysfunction, and an increased risk of dying from a particular condition.
(Pediatric Surgery Secrets)
How do energy stores in the body alter with age?
Energy stores are only adequate for ~2 days at 24–25 weeks gestation, increase to ~20 days at term as glycogen and fat stores increase and are in excess of 50 days in the adult, hence the urgent need for adequate caloric intake in preterm infants after birth.
Full-term neonates have higher content of endogenous fat (approximately 600 g) and therefore can tolerate a few days of undernutrition.
(Pearls & Tricks in Pediatric Surgery)
What is the optimum nutritional route for infants?
The optimum nutritional route is oral enteral feeding. However, artificial enteral feeding or parenteral nutrition (PN) may be required if adequate oral feeds cannot be tolerated.
The basic principle underlying choice of feeding routes is that the most physiological route that is safely possible should be used: oral preferred over tube feeding, gastric feeds are preferred over jejunal feeds, enteral feeds are preferred over parenteral feeds etc.
(Pearls & Tricks in Pediatric Surgery)
How should the nutrition of surgical infants and children be monitored?
Effectiveness of nutrition should be assessed.
Growth of all paediatric surgical patients, especially those receiving artificial nutritional support, should be monitored longitudinally using appropriate charts.
Although measurement of weight, height/length, and head circumference is important, it is essential that these are monitored serially, and plotted on centile charts, which are often available on a national basis, or if not, are available from the World Health Organization.
It is especially important to also consider hydration, as over- or under- hydration can be an important contributor to weight change.
(Pearls & Tricks in Pediatric Surgery)
Why can’t premature infants be fed orally?
The swallowing reflex is not fully developed in premature infants so they should be fed by naso- or orogastric tubes until the swallowing reflex is developed and it is safe to give oral feeds.
(Pearls & Tricks in Pediatric Surgery)
Why are gastric enteral feeds preferred over jejunal feeds?
Gastric feeding is preferable to intestinal feeding because it allows for a more natural and complete digestive process i.e. allows action of salivary and gastric enzymes and the antibacterial action of stomach acid, in addition to the use of the stomach as a reservoir.
Gastric feeding is associated with a larger osmotic and volume tolerance and a lower frequency of diarrhea and dumping syndrome.
Thus, transpyloric feeds are usually restricted to infants or children who are either unable to tolerate naso- or oro- gastric feeds, at increased risk of aspiration; or who have anatomical contra-indications to gastric feeds.
(Pearls & Tricks in Pediatric Surgery)
Why is long-term nasogastric or orogastric feeding not recommended?
In infants requiring gastric tube feeding for extended periods (e.g. more than 6–8 weeks) it is advisable to insert a gastrostomy, to decrease the negative oral stimulation of repeated insertion of nasal or oral tubes.
(Pearls & Tricks in Pediatric Surgery)
When should cow’s milk protein allergy be considered?
Cow’s milk protein allergy can be acute (IgE-mediated) or delayed (non-IgE medi- ated).
Gastrointestinal symptoms are usually present (reflux, colic, constipation etc.), and intolerance in the absence of anatomical reasons may be a manifestation of Cow’s milk protein allergy.
It can be present even in exclusively breast-fed infants, as bovine antigens may be passed from the mother.
(Pearls & Tricks in Pediatric Surgery)
What are the advantages of minimal enteral (trophic) feeding?
Minimal feeds may prevent gut mucosal atrophy, increase intestinal blood flow, improve activity of digestive enzymes and thus ‘prime’ the gut for subsequent higher volume, nutritive feeds.
In addition, oral stimulation may prevent later oral aversion.
(Pearls & Tricks in Pediatric Surgery)
If infants and children are tolerating full feeds, should weight monitoring cease?
Tolerance is not the same as absorption, as infants and children may require a significant period of time for intestinal adaptation to allow complete absorption of administered feeds.
Growth monitoring should continue and be checked against centile charts at outpatient follow-up.
(Pearls & Tricks in Pediatric Surgery)
What might explain poor growth in an infant with a stoma?
Sodium is essential for growth, so that infants with a stoma may have inadequate sodium intake.
Low urinary sodium with normal serum sodium suggests active sodium conservation, and sodium supplementation may be appropriate.
(Pearls & Tricks in Pediatric Surgery)
When should parenteral nutrition (PN) be given to a surgical infant or child?
PN is given when enteral feeding is impossible, inadequate, or hazardous, but should be given for the shortest period of time possible and the proportion of nutrition given enterally increased as tolerated.
Energy reserves are such that stable term infants can tolerate 3–4 days without enteral feeds, and older children 7–10 days, before starting PN, if it is anticipated that enteral nutrition may be resumed within this time.
Premature neonates have smaller energy reserves and the time before introducing PN is much shorter.
The most frequent indications in paediatric surgery are intestinal obstruction due to congenital anomalies, although acquired conditions such as post-operative ileus, necrotizing enterocolitis, short-bowel syndrome, gastroenterological indications, and respiratory co-morbidity may require PN for variable lengths of time.
(Pearls & Tricks in Pediatric Surgery)
Why should PN not be administered peripherally?
Peripheral administration gives significant risk of complications from hyperosmolar glucose, which can cause vascular irritation or damage and thrombosis.
PN should be administered via centrally placed catheters (including peripherally inserted central catheters (i.e. PICC lines), surgically placed central catheters or centrally-placed umbilical catheters) dependent on the vascular access already available and the length of time that PN is anticipated to be needed for [2].
(Pearls & Tricks in Pediatric Surgery)
Which are the components of PN that should be considered as making up the energetic requirements?
The caloric requirements for PN are provided by carbohydrate and lipid.
Protein is required for growth and is not used as a source of calories.
The ideal PN regimen therefore, should provide enough amino acids for protein turnover and tissue growth, and sufficient calories to minimize protein oxidation for energy.
(Pearls & Tricks in Pediatric Surgery)
What lipid emulsions should be used in PN of infants and children?
Although pure soybean lipid emulsions can be used short-term, composite lipid emulsions with or without fish oils should be used for PN lasting more than a few days, as this is thought to help prevent cholestasis, one of the major complications of PN.
(Pearls & Tricks in Pediatric Surgery)
Are the energy requirements on PN similar to EN?
No, energy requirements are approximately 10% lower because calorie losses in stool etc. are minimal.
(Pearls & Tricks in Pediatric Surgery)
Why does weight often drop in the first few days after birth?
This is a normal physiological change in fluid compartments, resulting in diuresis and weight loss of 5–10%.
(Pearls & Tricks in Pediatric Surgery)
How are hyponatremia and hypernatremia defined?
Hyponatremia is a serum sodium less than 128 mEq/L in the neonate and less than 135 mEq/L in children; hypernatremia is a serum sodium greater than 150 mEq/L.
(Pearls & Tricks in Pediatric Surgery)
Why are post-operative infants and children at risk of hyponatremia?
Anti-diuretic hormone is secreted for several days in response to operative stress, which can lead to hyponatremia.
In addition, gastrointestinal fluid losses also lead to electrolyte losses. Isotonic rather than hypotonic fluids should be administered to decrease risk of hyponatremia, and gastrointestinal electrolyte losses measured and replaced.
(Pearls & Tricks in Pediatric Surgery)
Which neonatal acquired emergency of term infants is typically accompanied by dehydration and electrolyte disturbances?
Pyloric stenosis typically presents with dehydration together with hyponatremia, hypokalemia, and metabolic alkalosis, so that appropriate resuscitation and correction of electrolyte balance are essential before surgery is performed.
(Pearls & Tricks in Pediatric Surgery)
How are respiratory and metabolic acidosis/alkalosis differentiated?
In respiratory acidosis/alkalosis, PaCO2 is >45 mmHg (acidosis) or <35 mmHg (alkalosis) and treatment is via appropriate respiratory support.
In metabolic acidosis/alkalosis, bicarbonate <21 mmol/l (acidosis) or >26mmmol/l (alkalosis).
In metabolic acidosis it is useful to check the anion gap [=Na+−(Cl−+HCO3−), which is normally 12 ± 2 mEq/l] to understand the underlying cause and correct the existing deficits.
It is also important, before treatment with sodium bicarbonate bolus, to check the volemic status because of this condition can be due to a tissue hypo-perfusion.
(Pearls & Tricks in Pediatric Surgery)
When should hypotonic fluids be administered?
Hyponatremia at admission, or post-operatively is relatively common in children, so administration of hypotonic fluids should be reserved only for those with a demonstrated hypernatremia >145–150 mEq/L.
(Pearls & Tricks in Pediatric Surgery)
Which of the following is an appropriate treatment for persistent hypercalcemia in pediatric surgical patients?
A. Potassium supplements
B. IV fluid administration
C. Diuretic therapy
D. Bisphosphonate therapy
Calcium plays important roles in enzyme activity, muscle contraction and relaxation, the blood coagulation cascade, bone metabolism, and nerve conduction.
Calcium is maintained at a total serum concentration of:
1.8 to 2.1 mmol/L in neonates
2 to 2.5 mmol/L in term infants
It is divided into three fractions. Thirty to fifty percent is protein bound, and 5% to 15% is complexed with citrate, lactate, bicarbonate, and inorganic ions.
The remaining free calcium ions are metabolically active and concentrations fluctuate with serum albumin levels.
Hydrogen ions compete reversibly with calcium for albumin binding sites and therefore free calcium concentrations increase in acidosis.
Calcium metabolism is under the control of many hormones but primarily 1,25-dihydroxycholecalciferol (gastrointestinal absorption of calcium, bone resorption, increased renal calcium reabsorption), parathyroid hormone (bone resorption, decreased urinary excretion), and calcitonin (bone formation and increased urinary excretion).
Calcium is actively transported from maternal to fetal circulation against the concentration gradient, resulting in peripartum hypercalcemia.
There is a transient fall in calcium postpartum to 1.8 to 2.1 mmol/L and a gradual rise to normal infant levels over 24 to 48 hours.
Hypocalcemia
In addition to the physiologic hypocalcemia of neonates which is usually asymptomatic, other causes of hypocalcemia are hypoparathyroidism, including DiGeorge syndrome, and parathyroid hormone insensitivity in infants of diabetic mothers, which may also be related to hypomagnesemia.
Clinical manifestations are tremor, seizures, and a prolonged QT interval on electrocardiography.
Hypercalcemia
This is less common than hypocalcemia but can result from inborn errors of metabolism such as familial hypercalcemic hypocalcuria or primary hyperparathyroidism.
Iatrogenic causes are vitamin A overdose or deficient dietary phosphate intake.
Less common causes in children are tertiary hyperparathyroidism, paraneoplastic syndromes, and metastatic bone disease.
Coran
—
Initial treatment of hypercalcemia involves hydration to improve urinary calcium output.
Isotonic sodium chloride solution is used, because increasing sodium excretion increases calcium excretion.
Addition of a loop diuretic inhibits tubular reabsorption of calcium, with furosemide having been used up to every 2 hours. Attention should be paid to other electrolytes (eg, magnesium, potassium) during saline diuresis.
These treatments work within hours and can lower serum calcium levels by 1-3 mg/dL within a day.
Bisphosphonates serve to block bone resorption over the next 24-48 hours by absorbance into the hydroxyapatite and by shortening the life span of osteoclasts.
Administered intravenously (IV), they decrease serum calcium in 2-4 days with a nadir at 4-7 days.
These medications have been studied more in adults than in children; however, many studies have established safety and efficacy in children, particularly with etidronate and pamidronate.
Medscape
Which of the following is an appropriate method for monitoring electrolyte balance in pediatric surgical patients with persistent electrolyte imbalances?
A. All of the above
B. EKG monitoring
C. Urine electrolyte levels
D. Serum electrolyte levels
A. All of the above
Which of the following is an appropriate method for preventing persistent electrolyte imbalances in pediatric surgical patients?
A. All of the above
B. Regular electrolyte monitoring
C. Diuretic therapy
D. IV fluid restriction
.
Which of the following is a common cause of persistent hyponatremia in pediatric surgical patients?
A. Excessive IV fluid administration
B. Diabetes insipidus
C. Hypernatremia
D. Adrenal insufficiency
A. Excessive IV fluid administration
Which of the following is a potential complication of IV fluid therapy in postoperative pediatric patients?
A. Hypocalcemia
B. Hyperkalemia
C. Hypoglycemia
D. Hyponatremia
D. Hyponatremia
Which of the following is a common indication for IV fluid therapy in postoperative pediatric patients?
A. Hypovolemia
B. Hypokalemia
C. Hypernatremia
D. Hypertension
A. Hypovolemia
What is the appropriate rate of fluid administration for a neonatal surgical patient?
A. 180 mL/kg/day
B. 100 mL/kg/day
C. 150 mL/kg/day
D. 120 mL/kg/day
D. 120 mL/kg/day
Which of the following is a potential complication of persistent hyperkalemia in pediatric surgical patients?
A. Hypoglycemia
B. Cerebral edema
C. Hypotension
D. Cardiac arrhythmia
D. Cardiac arrhythmia
Which of the following is an appropriate method for correcting hyperkalemia in a neonatal surgical patient?
A. Sodium bicarbonate
B. All of the above
C. Insulin and glucose
D. Calcium gluconate
Hyperkalaemia is defined as a serum potassium concentration greater than 7 mmol/L.
Hyperkalaemia is common when capillary blood samples are haemolysed. The first step should be to confirm high serum K⁺ with a non-haemolysed venous or arterial sample.
ECG changes (peaked T waves, broad QRS complexes, and arrhythmias) indicate significant hyperkalaemia and require urgent treatment with calcium gluconate.
Hyperkalaemia in the NICU is most commonly associated with non-oliguric hyperkalaemia in the first 72 hours of life of the very preterm infant. Immature function of the erythrocyte Na/K - ATPase is believed to be the reason for non-oliguric hyperkalaemia.
Oliguric renal failure (e.g.: due to hypoxic event, drug error or renal tubular acidosis) or haemolysis are other causes for hyperkalaemia.
Hyperkalaemia is believed to be exacerbated by:
- metabolic acidosis, due to exchange of intracellular K⁺ with extracellular H⁺
- renal impairment and hypovolaemia
Complications
ECG changes:
Peaked T-waves
Prolonged PR interval
Broadened QRS complexes
Disappearing of the P-wave
Arrhythmias
Ventricular tachycardia and impaired AV conduction.
Treatment
1) 10% Calcium gluconate
Dose: 0.5 mL/kg IV (0.1 mmoL/kg) over 10-30 min. The dose of calcium gluconate may be repeated.
Effect: Stabilizes myocardial membrane potential, should be given if the infant is at risk of, or has ECG changes and/or arrhythmias.
Side effects: Cardiac arrhythmias and seizures with severe hypercalcaemia
2) Stop IV K⁺
Remove K⁺from IV (i.e.: replace TPN with 10% glucose with Na+).
3) IV Glucose and Insulin
Glucose: 8-16 mg/kg/min (e.g.: 2.5-5 ml/kg/hr
20% glucose (20 ml of 50% glucose and 30 ml of water in a 50 ml syringe))
in addition to maintenance fluid, aim for blood glucose concentration (BGC) > 12 mmol/l.
When BGC >12 mmol/L, start insulin infusion (0.1-0.6 units/kg/hr).
Effect: Shift of ionized K+ from the extracellular to the intracellular space. K+ is transported over the membrane in combination with glucose.
SE: Hypoglycaemia, hyperglycaemia
4) Salbutamol
Intravenous: 4 micrograms/kg over 10 min or
nebulized via ETT: 400 micrograms/dose (made up to a total of 4 ml with normal saline) up to 2 hrly.
Be aware: salbutamol comes in two different preparations, for IV administration and as sterinebs: they are not interchangeable!
Effect: Salbutamol is a beta-adrenergic agonist and stimulates the membrane Na+/K+ - ATPase. Singh et al report a small randomized trial of nebulized salbutamol compared with saline for very preterm infants. Nebulized salbutamol reduced plasma K+ rapidly with no adverse effects noted.
SE: Tachycardia, hypertension, tremor, hypokalaemia, hyperglycaemia. Inhaled Salbutamol seems to be generally well tolerated.
5) Sodium bicarbonate
Correction of an existing metabolic acidosis can be considered
Dose: Sodium bicarbonate dose (mL) = base deficit x 0.6 x weight (kg).
Effect: May facilitate shift of K+ from the extracellular to the intracellular space.
SE: Increased vascular volume, serum osmolarity, serum sodium, hypercapnia and respiratory acidosis, hypocalcaemia, oedema, congestive heart failure, hyperirritability, intraventricular haemorrhage.
6) Resonium
Should be avoided in preterm infants
Dose: 0.5 - 1 g/kg rectally
Effect: Binds intestinal K+ and prevents intestinal absorption.
SE: Intestinal perforation and constipation in preterm infants. IV Salbutamol seems more effective than resonium.
7) Exchange transfusion or peritoneal dialysis.
Starship
https://starship.org.nz/guidelines/hyperkalaemia-in-the-neonate/
Which of the following is a potential complication of overhydration in postoperative pediatric patients?
A. Hypertension
B. Pulmonary edema
C. Hypoglycemia
D. Hypernatremia
B. Pulmonary edema
Which of the following is an appropriate indication for fluid restriction in a neonatal surgical patient?
A. Hyponatremia
B. Hypernatremia
C. Hypokalemia
D. Hypocalcemia
.
What is the most common electrolyte abnormality in neonatal surgical patients receiving parenteral nutrition?
A. Hypermagnesemia
B. Hyperkalemia
C. Hypokalemia
D. Hypocalcemia
C. Hypokalemia
How to diagnose and correct hyponatremia?
Normal sodium: 135-140mmol/L
Hyponatremia
- Serum sodium <135mmol/L
- Symptoms start at <120mmol/L (cerebral edema sx: apathy, nausea, vomiting, headache, fits, coma)
- Management
1) Correct fluid status first (check if hyper or hypovolemic).
2) When normovolemic, start gradual NaCl infusion not exceeding 0.8mEq/kg/hr.
3) Urine sodium
<10mmol/L: appropriate renal response to euvolemic hyponatremia
>20mmol/L: sodium leakage from damaged renal tubules or hypervolemia
How is neonatal feeding administered?
Oral feeding:
Start at 2-5cc/kg, q3-4h
Advance in increments of 2-5cc/kg every 2 feedings.
Breastmilk:
0.64-0.67kcal/mL
Term infants should receive 20kcal/oz formula.
Dextrose contains 3.4kcal/g.
During the first 8 hours postoperatively, a 1-kg premature infant has 0.3 mL/kg/h of urine output. Specific gravity is 1.025. Previous initial volume was 5 mL/kg/h. Serum BUN has increased from 4 mg/dL to 8 mg/dL; hematocrit value has increased from 35% to 37%, without transfusion.
How will you manage this patient?
This child is dehydrated.
The treatment is to increase the hourly volume to 7 mL/kg/h for the next 4 hours and to monitor the subsequent urine output and concentration to reassess fluid status.
Depending on the degree of dehydration and the child’s underlying cardiopulmonary status, it may be prudent to bolus the child with 10–20 mL/kg of 0.9% normal saline—all the while carefully monitoring physiologic responsiveness.
During the first 8 hours postoperatively, a 3-kg newborn with congenital diaphragmatic hernia (CDH) has 0.2 mL/kg/h of urine output and a urine osmolarity of 360 mOsm/L. The previous fluid volume was 120 mL/kg/day (15 mL/h). The serum osmolarity has decreased from 300 mOsm/L preoperatively to 278 mOsm/L; BUN has decreased from 12 mg/dL to 8 mg/dL.
How will you manage this patient?
The inappropriate antidiuretic hormone response requires reduction in fluid volume from 120 mL/kg/day to 90 mL/ kg/day for the next 4–8 hours.
Repeat urine and serum measurements will allow for further adjustment of fluid administration.
A 3-kg baby, 24 hours following operative closure of gastroschisis, had an average urine output of 3 mL/kg/h for the past 4 hours. During that time period, the infant received fluids at a rate of 180 ml/kg/ day. The specific gravity of the urine has decreased to 1.006; serum BUN is 4 mg/dL; hematocrit value is 30%, down from 35% preoperatively. The total serum protein concentration is 4.0 mg/dL, down from 4.5 mg/dL.
How will you manage this patient?
This child is overhydrated. The treatment is to decrease the fluids to 3 mL/kg/h for the next 4 hours and then to reassess urine output and concentration.
A 5-kg infant with severe sepsis secondary to Hirschsprung enterocolitis has had a urine output of 0.1 mL/kg/h for the past 8 hours. The specific gravity is 1.012; serum sodium, 150; BUN, 25 mg/dL; creatinine, 1.5 mg/dL; urine sodium, 130; and urine creatinine, 20 mg/dL.
How will you manage this patient?
FE Na less than 1% usually indicates a prerenal cause of oliguria, whereas greater than 3% usually implies a renal cause (e.g., acute tubular necrosis).
This patient is in acute renal failure.
The plan is to restrict fluids to insensible losses plus measured losses for the next 4 hours and to then reassess the plan using both urine and serum studies.
Of note, while the FE urea may be a better predictor of prerenal failure in this population, both FE urea and the FE Na have limited utility in neonates, reflecting the relative immaturity of neonatal renal function.
When does the greatest growth rate occur in a neonate?
The greatest growth rate occurs during fetal life.
In fact the passage from one fertilized cell to a 3.5-kg neonate encompasses an increase in length of 5000-fold, an increase in surface area of 61 x 10^6, and an increase in weight of 6 x 10^12.
The greatest postnatal growth rate occurs just after birth.
It is not unusual in neonates undergoing surgery to notice a period of slow or arrested growth during critical illness or soon after surgery.
What is IUGR?
The definition of IUGR is often confused and unclear in the medical literature.
IUGR is usually defined as a documented decrease in intrauterine growth noted by fetal ultrasonography.
IUGR can be temporary, leading to a normal-sized neonate at birth.
There are two types of IUGR: symmetric and asymmetric.
Symmetric IUGR denotes normal body proportions (small head and small body) and is considered a more severe form of IUGR.
Asymmetric IUGR denotes small abdominal circumference, decreased subcutaneous and abdominal fat, reduced skeletal muscle mass, and head circumference in the normal range.
Infants with asymmetric IUGR show catch-up growth more frequently than do infants with symmetric IUGR, although 10% to 30% of all infants with IUGR remain short as children and adults.
Premature infants are expected to have catch-up growth by 2 years of age.
Those born after 29 weeks of gestation usually exhibit catch-up growth, whereas those born before 29 weeks of gestation are more likely to have a decreased rate of length and weight gain, which may be noted in the first week after birth and last up to 2 years.
What parameters are used in Ballard Scoring?
What are major causes of mortality in neonates undergoing surgery?
What is the body water composition of a neonate?
The content and distribution of intracellular and extracellular water in the human body is defined as total body water (TBW) and it changes with age.
TBW also varies with body fat content.
Fat cells contain very little water; therefore children with more body fat have a lower proportion of body water than children with less fat.
The water in body tissues includes the intracellular fluid, which represents the water contained within the cells, and extracellular fluid.
Extracellular fluid is further subdivided into intravascular fluid (plasma), interstitial fluid (fluid surrounding tissue cells), and transcellular fluid (e.g., cerebrospinal, synovial, pleural, peritoneal fluid).
During the first trimester, when only 1% of body mass is fat, 90% of body mass is TBW, with 65% of body mass made up of extracellular fluid.
However these ratios alter throughout gestation as the amount of body protein and fat increases.
TBW as a proportion of body mass declines and is approximately 70% to 80% by term.
TBW continues to decline during the first year of life reaching 60% of total body mass, which is consistent with adult age.
This is accompanied by a decrease in the extracellular compartment fluid (ECF)/intracellular compartment fluid (ICF) ratio.
The ECF is 60% of total body mass at 20 weeks’ gestation, declining to 40% at term, whereas ICF increases from 25% at 20 weeks’ gestation to 35% of body mass at term and then to 43% at 2 months of age.
Because extracellular fluid is more easily lost from the body than intracellular fluid and infants have a larger surface area/body mass ratio, they are more at risk of dehydration than are older children and adults.
Among preterm infants, those who are SGA have a significantly higher body water content (approximately 90%) than appropriate for full-term infants (approximately 80%).
Blood volume can be estimated as:
106 mL/kg in preterm infants,
90 mL/kg in neonates,
80 mL/kg in infants and children and
about 65 mL/kg in adults.
Adequate systemic perfusion depends on adequate intravascular volume, as well as many other factors.
However infants and children can compensate for relatively large losses in circulating volume, and signs and symptoms of shock may be difficult to detect if a child has lost less than 25% of the circulating volume.
The movement of fluid between the vascular space and the tissues depends on osmotic pressure, oncotic pressure, hydrostatic pressure, and changes in capillary permeability.
Understanding these factors is important when trying to anticipate changes in the child’s intravascular volume.
What happens in the neonate’s fluid balance intrapartum to postpartum?
Before labor, pulmonary fluid production decreases while existing fluid is reabsorbed, and efflux through the trachea increases and accelerates during labor, thereby drying out the lungs.
During labor, arterial pressure increases and causes shifts in plasma from the vascular compartment and a slight rise in hematocrit values.
Placental transfusion can occur if there is delayed clamping of the cord and the neonate is placed at or below the level of the placenta, resulting in up to 50% increase in red blood cells and blood volume.
This polycythemia may have severe consequences such as neurologic impairment, thrombus formation, and tissue ischemia.
One day postpartum the neonate is oliguric.
Over the following 1 to 2 days, dramatic shifts in fluid from the intracellular to extracellular compartment result in a diuresis and natriuresis that contributes to weight loss during the first days of life.
This is approximately 5% to 10% in the term neonate and 10% to 20% in the premature newborn.
The proportion of contributions from ECF and ICF to fluid loss is controversial and the mechanism is yet to be determined.
This diuresis occurs regardless of fluid intake or insensible losses and may be related to a postnatal surge in atrial natriuretic peptide.
Limitations in the methodology of measuring ECF and ICF have limited our understanding of the processes.
It has been demonstrated however that large increases in water and calorie intake are required to reduce the weight loss.
Higher caloric intake alone reduces weight loss but the ECF still decreases.
Subsequent weight gain appears to be the result of increases in tissue mass and ICF per kilogram of body weight but not ECF per kilogram of body weight.
By the fifth day postpartum, urinary excretion begins to reflect the fluid status of the infant.
Why does a neonate have less tolerance for fluid imbalance?
The kidneys in neonates have small immature glomeruli and for this reason the glomerular filtration rate (GFR) is reduced (about 30 mL/min/1.73m2 at birth to 100 mL/min/1.73m2 at 9 months).
Eventually renovascular resistance decreases, resulting in a rapid rise in GFR over the first 3 months of life followed by a slower rise to adult levels by 12 to 24 months of age.
Premature and low-birth-weight infants may have a lower GFR than term infants, and the initial rapid rise in GFR is absent.
Urine osmolality is controlled by two mechanisms.
Urine is concentrated in the loop of Henle using a countercurrent system dependent on the osmolality of the medullary interstitium.
In neonates, the low osmolality in the renal medulla means the countercurrent system is less effective and urine concentration capacity is between 50 and 700 mOsm/kg compared with 1200 mOsm/kg in the adult kidney; therefore there is less tolerance for fluid imbalance.
What is the normal range for sodium in the neonate?
Serum sodium is the major determinant of serum osmolality and therefore extracellular fluid volume.
Urinary sodium excretion is dependent on the GFR and therefore is low in neonates when compared with adults.
Normal neonatal serum sodium levels are 135 to 140 mmol/L, controlled by moderating renal excretion.
During the period of oliguria on the first day of life, sodium supplementation is not normally required.
The normal maintenance sodium requirement after normal diuresis is 2 to 4 mmol/kg/day.
How do you manage hyponatremia?
Hyponatremia is defined when serum sodium concentrations are less than 135 mmol/L.
Treatment depends on the fluid status of the patient and in case of hypovolemia or hypervolemia, fluid status should be corrected first.
When normovolemic, serum sodium levels should be gradually corrected with NaCl infusion, but at a rate not exceeding 0.8 mEq/kg/hr.
Symptoms are not reliable for clinical management because they are not often apparent until serum sodium levels fall to less than 120 mmol/L, and their severity is directly related to the rapidity of onset and magnitude of
hyponatremia.
If not promptly recognized, hyponatremia may manifest as the effects of cerebral edema: apathy, nausea, vomiting, headache, fits, and coma.
Urine sodium concentrations can be useful to help determine the underlying cause of hyponatremia because the kidneys respond to a fall in serum sodium levels by excreting more dilute urine, but the secretion of antidiuretic hormone (ADH)/vasopressin in response to hypovolemia affects this.
Urine sodium concentrations less than 10 mmol/L indicates an appropriate renal response to euvolemic hyponatremia.
However if the urinary sodium concentration is greater than 20 mmol/L this can indicate either sodium leakage from damaged renal tubules or hypervolemia.
How do you manage hypernatremia?
Hypernatremia (serum sodium concentrations >145 mmol/L) may be due to hemoconcentration/ excessive fluid losses (e.g., diarrhea).
Symptoms and clinical signs include dry mucous membranes, loss of skin turgidity, drowsiness, irritability, hypertonicity, fits, and coma.
Treatment is again by correction of fluid status with appropriate electrolyte-containing solutions.
Other causes of hypernatremia are renal or respiratory insufficiency, or it can be related to drug administration.
What is the normal range for potassium?
In the 24-72h postpartum, a large shift of potassium from intracellular to extracellular compartments occurs, resulting in a rise in plasma potassium levels.
This is followed by an increase of potassium excretion until the normal serum concentration of 3.5 to 5.8 mmol/L is achieved.
Therefore supplementation is not required on the first day of life, but after neonatal diuresis a maintenance intake of 1 to 3 mmol/kg/day is required.
How do you manage hypokalemia?
Hypokalemia is commonly iatrogenic, either due to inadequate potassium intake or use of diuretics but can also be caused by vomiting, diarrhea, alkalosis (which drives potassium intracellularly) or polyuric renal failure.
As a consequence, the normal ion gradient is disrupted and predisposes to muscle current conduction abnormalities (e.g., cardiac arrhythmias, paralytic ileus, urinary retention, and respiratory muscle paralysis).
Treatment employs the use of KCl.
How do you manage hyperkalemia?
Hyperkalemia can be iatrogenic or due to renal problems but can also be caused by cell lysis syndrome (e.g., from trauma), adrenal insufficiency, insulin-dependent diabetes mellitus, or severe hemolysis or malignant hyperthermia.
As in hypokalemia, hyperkalemia alters the electrical gradient of cell membranes and patients are vulnerable to cardiac arrhythmias, including asystole.
Treatment is with insulin (plus glucose to avoid hypoglycemia) or with salbutamol.
What is the normal range for calcium?
Calcium plays important roles in enzyme activity, muscle contraction and relaxation, the blood coagulation cascade, bone metabolism, and nerve conduction.
Calcium is maintained at a total serum concentration of 1.8 to 2.1 mmol/L in neonates and 2 to 2.5 mmol/L in term infants and is divided into three fractions.
Thirty percent to 50% is protein bound, and 5% to 15% is complexed with citrate, lactate, bicarbonate, and inorganic ions.
The remaining free calcium ions are metabolically active and concentrations fluctuate with serum albumin levels.
Hydrogen ions compete reversibly with calcium for albumin-binding sites and therefore free calcium concentrations increase in acidosis.
Calcium metabolism is under the control of many hormones but primarily 1,25-dihydroxycholecalciferol (gastrointestinal absorption of calcium, bone resorption, increased renal calcium reabsorption), parathyroid hormone (bone resorption, decreased urinary excretion), and calcitonin (bone formation and increased urinary excretion).
Calcium is actively transported from maternal to fetal circulation against the concentration gradient, resulting in peripartum hypercalcemia.
There is a transient fall in calcium postpartum to 1.8 to 2.1 mmol/L and a gradual rise to normal infant levels over 24 to 48 hours.
How do you manage hypocalcemia?
In addition to the physiologic hypocalcemia of neonates which is usually asymptomatic, other causes of hypocalcemia are hypoparathyroidism, including DiGeorge syndrome, and parathyroid hormone insensitivity in infants of diabetic mothers, which may also be related to hypomagnesemia.
Clinical manifestations are tremor, seizures, and a prolonged QT interval on electrocardiography.
How do you manage hypercalcemia?
This is less common than hypocalcemia but can result from inborn errors of metabolism such as familial hypercalcemic hypocalcuria or primary hyperparathyroidism.
Iatrogenic causes are vitamin A overdose or deficient dietary phosphate intake.
Less common causes in children are tertiary hyperparathyroidism, paraneoplastic syndromes, and metastatic bone disease.
What is the role of magnesium in neonatal physiology?
As an important enzyme cofactor, magnesium affects adenosine triphosphate (ATP) metabolism and glycolysis.
Only 20% of total body magnesium is exchangeable with the biologically active free ion form.
The remainder is bound in bone or to intracellular protein, RNA, or ATP, mostly in muscle and liver.
Gastrointestinal absorption of magnesium is controlled by vitamin D, parathyroid hormone, and sodium reabsorption.
As previously stated, hypomagnesemia is often related to hypocalcemia and should be considered.
What are the two phases of the metabolic stress response?
The metabolic response to illness due to stressors such as trauma, surgery, or inflammation has been well described, and the magnitude of the response varies according to illness severity.
Cuthbertson was the first investigator to realize the primary role that whole-body protein catabolism plays in the systemic response to injury.
Based on his work, the metabolic stress response has been conceptually divided into two phases.
The initial, brief “ebb phase” is characterized by decreased enzymatic activity, reduced oxygen consumption, low cardiac output, and core temperature that may be subnormal.
This is followed by the hypermetabolic “flow phase” characterized by increased cardiac output, oxygen consumption, and glucose production.
During this phase, fat and protein mobilization is manifested by increased urinary nitrogen excretion and weight loss.
This catabolic phase is mediated by a surge in cytokines and the characteristic endocrine response to trauma or surgery that results in an increased availability of substrates essential for healing and glucose production.
What makes the metabolic stress response of children different from that of adults?
Neonates and children share similar qualitative metabolic responses to illness as adults, albeit with significant quantitative differences.
The metabolic stress response is beneficial in the short term, but the consequences of sustained catabolism are significant because the child has limited tissue stores and substantial nutrient requirements for growth.
Thus, the prompt institution of nutritional support is a priority in sick neonates and children.
The goal of nutrition in this setting is to augment the short-term benefits of the metabolic response to injury while minimizing negative consequences of persistent catabolism.
In general, the metabolic stress response is characterized by an increase in net muscle protein degradation and the enhanced movement of free amino acids through the circulation. These amino acids serve as the building blocks for the rapid synthesis of proteins that act as mediators for the inflammatory response and structural components for tissue repair.
The remaining amino acids not used in this way are channeled through the liver, where their carbon skeletons are utilized to create glucose through gluconeogenesis.
The provision of additional dietary protein may slow the rate of net protein loss, but it does not eliminate the overall negative protein balance associated with injury.
Carbohydrate and lipid turnover are also increased severalfold during the metabolic response.
Although these metabolic alterations would be expected to increase overall energy requirements, data show that such an increase is quantitatively variable, modest, and evanescent.
Overall, the energy needs of the critically ill or injured child are governed by the severity and persistence of the underlying illness or injury.
Accurate assessment of energy requirements in individual patients allows optimal caloric supplementation and avoids the deleterious effects of both underfeeding and overfeeding.
Children with critical illness demonstrate a unique hormonal and cytokine profile.
A transient decrease in insulin levels is followed by a persistent elevation, the anabolic effects of which are overcome by increased levels of catabolic hormones (glucagon, cortisol, catecholamines).
This overall catabolic state is marked by increases in specific inflammatory cytokines (interleukin [IL]-6, tumor necrosis factor [TNF]-α).
Novel ways to manipulate these hormonal and cytokine alterations with an aim to minimize the deleterious consequences induced by the stress response are a focus of research.
How does the body composition of a neonate differ from that of an adult, in terms of nutrition?
The body composition of the young child contrasts with that of the adult in several ways that significantly affect nutritional requirements.
Carbohydrate stores are limited in all age groups and provide only a short-term supply of glucose. Despite this fact, neonates have a high demand for glucose and have shown elevated rates of glucose turnover compared with those of the adult. This is thought to be related to the neonate’s increased ratio of brain-to-body mass because glucose is the primary energy source for the central nervous system.
Neonatal glycogen stores are even more limited in the early postpartum period, especially in the preterm infant.
Short periods of fasting can predispose the newborn to hypoglycemia.
Therefore, when infants are burdened with illness or injury, they must rapidly turn to the breakdown of protein stores to generate glucose through the process of gluconeogenesis.
In premature infants, gluconeogenesis is sustained despite provision of parenteral nutrition (PN) with glucose infusion rates higher than endogenous glucose production rate.
Lipid reserves are low in the neonate, gradually increasing with age.
Premature infants have the lowest proportion of lipid stores because the majority of polyunsaturated fatty acids accumulate in the third trimester. This renders lipid less available as a potential fuel source in the young child.
The most dramatic difference between adult and pediatric patients is in the relative quantity of stored protein. The protein reserve per kilogram of ideal body weight in the adult is nearly twofold that of the neonate. Thus, infants cannot afford to lose significant amounts of protein during the course of a protracted illness or injury.
An important feature of the metabolic stress response, unlike in starvation, is that the provision of dietary glucose does not halt gluconeogenesis. Consequently, the catabolism of muscle protein to produce glucose continues unabated.
Neonates and children also share much higher baseline energy requirements than adults.
In addition, among preterm infants with low birth weight, the birth weight inversely correlates with resting energy expenditure (REE).
Clearly, the child’s need for rapid growth and development is a large component of this increase in energy requirement.
Moreover, increased heat loss via the relatively large body surface area of the young child and immature thermoregulation in preterm infants further contribute to elevations in energy expenditure.
As illustrated, the recommended protein needs for the infant are two to three times those of the adult.
In premature infants, a minimum protein allotment of 2.8 g/kg/day is required to maintain in utero growth rates.
The increased metabolic demand and limited nutrient reserves of the infant mandates early nutritional support in times of injury and critical illness to avoid negative nutritional consequences.
An accurate assessment of body composition is necessary for planning nutritional intake, monitoring dynamic changes in the body compartments (such as the loss of lean body mass), and assessing the adequacy of nutritional supportive regimens during critical illness.
Ongoing loss of lean body mass is an indicator of inadequate dietary supplementation and may have clinical implications in the hospitalized child. However, current methods of body composition analysis (e.g., anthropometry, weight and biochemical parameters) are either impractical for clinical use or inaccurate in a subgroup of hospitalized children with critical illness.
One of the principal problems in critically ill children is the presence of capillary leak, manifesting as edema and large fluid shifts.
These make anthropometric measurements invalid, and other bedside techniques have not been adequately validated.
How is REE measured?
REE can be measured using direct or indirect methods.
The direct calorimetric method measures the heat released by a subject at rest and is based on the principle that all energy is eventually converted to heat. In practice, the patient is placed in a thermally isolated chamber, and the heat dissipated is measured for a given period.
This method is the true gold standard for measured energy expenditure.
Direct calorimetry is not practical for most hospitalized children, and REE is often estimated using standard equations. Unfortunately, REE estimates using standardized World Health Organization (WHO) predictive equations are unreliable, particularly in critically ill children. REE estimation is difficult in critically ill or postoperative children. Their energy requirements show individual variation and depend on severity of injury, sedation, and environmental factors.
Indirect calorimetry measures VO2 (the volume of oxygen consumed) and VCO2 (the volume of CO 2 produced) and uses a correlation factor based on urinary nitrogen excretion to calculate the overall rate of energy production.
The measurement of energy needs is “indirect” because it does not use direct temperature changes to determine energy needs.
Indirect calorimetry provides a measurement of the overall respiratory quotient (RQ), defined as the ratio of CO2 produced to O2 consumed (VCO2/ VO2) for a given patient.
Oxidation of carbohydrate yields an RQ of 1.0, whereas fatty acid oxidation gives an RQ of 0.7.
However, the role of the RQ as a marker of substrate use and an indicator of underfeeding or overfeeding is limited.
The body’s ability to metabolize substrate may be impaired during illness, making assumptions about RQ values and substrate oxidation invalid.
Although RQ is not a sensitive marker for adequacy of feeding in individual cases, RQ values greater than 1.0 can be associated with lipogenesis secondary to overfeeding.
However, numerous factors, related and unrelated to feeding, can alter the value of a measured RQ in critically ill patients, for example, hyperventilation, acidosis, effects of cardiotonic agents and neuromuscular blocking, and an individual response to a given substrate load, injury, or disease.
Furthermore, in the setting of wide diurnal and day-to-day variability of REE in critically ill individuals, the extrapolation of short-term calorimetric REE measurements to 24-hour REE may introduce errors.
The use of steady-state measurements may decrease these errors. Steady state is defined by change in VO2 and VCO2 of <10% over a period of 5 consecutive minutes.
The values for the mean REE from this steady-state period may be used as an accurate representation of the 24-hour TEE in patients with low levels of PA.
In a patient who fails to achieve steady state and is metabolically unstable, prolonged testing is required (minimum of 60 minutes) and 24-hour indirect calorimetry should be considered.
Indirect calorimetry is not accurate in the setting of air leaks around the endotracheal tube, in the ventilator circuit or through a chest tube, or in patients on ECMO.
A high inspired oxygen fraction (FiO 2 >0.6) will also affect indirect calorimetry.
Indirect calorimetry is difficult to use in babies on ECMO because a large proportion of the patient’s oxygenation and ventilation is performed through the membrane oxygenator.
The use of indirect calorimetry for assessment and monitoring of nutrition intake requires attention to its limitations and expertise in the interpretation, as well as specialized equipment and personnel.
Nonetheless, its application in children at high risk for underfeeding and overfeeding can be helpful.
What is the definition of steady state for REE?
In the setting of wide diurnal and day-to-day variability of REE in critically ill individuals, the extrapolation of short-term calorimetric REE measurements to 24-hour REE may introduce errors.
The use of steady-state measurements may decrease these errors.
Steady state is defined by change in VO2 and VCO2 of <10% over a period of 5 consecutive minutes.
The values for the mean REE from this steady-state period may be used as an accurate representation of the 24-hour TEE in patients with low levels of PA.
In a patient who fails to achieve steady state and is metabolically unstable, prolonged testing is required (minimum of 60 minutes) and 24-hour indirect calorimetry should be considered.
What are the recommended protein requirements for hospitalized children?
The ASPEN and SCCM guidelines recommend a minimum protein intake of 1.5 g/kg/day for critically ill children between 1 month and 18 years of age.
However, it should be noted that toxicity from excessive protein administration can occur, particularly in children with impaired renal and hepatic function.
While higher protein provision may improve protein balance, the provision of protein at levels greater than 3 g/kg/day is rarely indicated and can be associated with azotemia.
In premature neonates, the possible benefits of early high protein allotments, up to approximately 4 g/kg/day, to replicate intrauterine protein accretion and growth rates have recently been extensively studied.
There is much variability among these studies, but it appears that providing 3.5 g/kg/day is reasonable.
Higher amounts, at least given enterally, may be tolerated with associated increased protein balance, though benefits to long-term growth and/or neurodevelopment have yet to be proven.
Feeding excess glucose to critically Ill neonates is recommended. True or false?
When designing a nutritional regimen for the critically ill child, excessive carbohydrate calories should be avoided.
A mixed fuel system, with both glucose and lipid substrates, should be used to meet the child’s nonprotein caloric requirements.
When the postoperative neonate is fed a high-glucose diet, the corresponding RQ is approximately 1.0 and may be higher than 1.0 in selected patients, signifying increased lipogenesis.
A mixed dietary regimen of glucose and lipid (at 2–4 g/kg/day) provides the infant with full nutritional supplementation while alleviating an increased ventilatory burden and difficulties with hyperglycemia.
Administration of high caloric (glucose load) diets in the early phase of critical illness may exacerbate hyperglycemia, increase CO2 generation with an increased load on the respiratory system, promote hyperlipidemia resulting from increased lipogenesis, and result in a hyperosmolar state.
Several reports have linked hyperglycemia with increased mortality in both critically ill children and adults.
Overall, multicenter trials in critically ill adults have established that excessive hyperglycemia (>180 mg/dL) should be avoided, though insulin-assisted strict glycemic control (<110 mg/dL) is associated with increased risk of hypoglycemia and possibly decreased survival.
Randomized multicenter trials examining tight glucose control in critically ill children have shown no differences in ventilator days, mortality, or ICU stay, and tight glucose control was associated with higher rates of hypoglycemia.
What is essential fatty acid deficiency?
RQ values may decline during illness, reflecting an increased utilization of fat as an energy source. This suggests that fatty acids are a prime source of energy in metabolically stressed infants and children.
In addition to the rich energy supply from lipid substrate, the glycerol moiety released from triglycerides can be converted to pyruvate and used to manufacture glucose. As seen with the other catabolic changes associated with illness and trauma, the provision of dietary glucose does not decrease fatty acid turnover in times of illness. The increased demand for lipid utilization in critical illness coupled with the limited lipid stores in the neonate puts the metabolically stressed infant or child at high risk for the development of essential fatty acid deficiency.
Parenterally fed children receiving inadequate lipid provision develop essential fatty acid deficiency much sooner than adults. Also, preterm infants have been shown to develop biochemical evidence of essential fatty acid deficiency 2 days after the initiation of a fat-free nutritional regimen.
In humans the polyunsaturated fatty acids linoleic and linolenic acid are considered essential fatty acids because the body cannot manufacture them by desaturating other fatty acids.
Linoleic acid is used by the body to synthesize arachidonic acid, an important intermediary in prostaglandin synthesis.
The prostaglandin family includes the leukotrienes and thromboxanes, all of which serve as mediators in wide-ranging processes such as vascular permeability, smooth muscle reactivity, and platelet aggregation.
If an individual lacks dietary linoleic acid, the formation of arachidonic acid (a tetraene) cannot occur. Instead, the desaturation of oleic acid, a nonessential fatty acid, increases and eicosatrienoic acid (a triene) accumulates.
Clinically, a fatty acid profile can be performed on human serum, and an elevated triene-to-tetraene ratio greater than 0.2 is characteristic of biochemical essential fatty acid deficiency, though this cutoff is somewhat variable and depends on the specific laboratory assay utilized.
Signs of fatty acid deficiencies include dermatitis, alopecia, thrombocytopenia, increased susceptibility to infection, and overall failure to thrive.
To avoid essential fatty acid deficiency in infants, the allotment of linoleic and linolenic acid is recommended at concentrations of 3.0–4.5% and 0.5% of total calories, respectively.
In addition, evidence exists that the long-chain fatty acid docosahexaenoic acid (DHA), a derivative of linolenic acid important for neurodevelopment, also may be deficient in preterm and formulafed infants.
Clinical trials thus far have not reached consensus on whether supplementation with long-chain polyunsaturated fatty acids (i.e., DHA) is of clinical benefit in this population because most have shown neither benefit nor harm.
What is the clinical significance of lipid emulsions?
Parenterally delivered lipid solutions also limit the need for excessive glucose intake as lipid emulsions provide a higher quantity of energy per gram than does glucose (9 kcal/g vs 4 kcal/g).
This reduces the overall rate of CO2 production and the RQ value.
There are risks when starting a patient on intravenous lipid administration, including hypertriglyceridemia, a possible increased risk of infection, hematologic abnormalities, and decreased alveolar oxygen-diffusion capacity.
Therefore, most institutions initiate lipid provisions in children at 0.5–1.0 g/kg/day and advance over a period of days to 2–4 g/kg/day.
During this time, triglyceride levels are monitored closely.
Lipid administration is generally restricted to 30–40% of total caloric intake in ill children in an effort to obviate immune dysfunction, although this practice has not been validated in a formal clinical trial.
In settings of prolonged fasting or uncontrolled diabetes mellitus, the accelerated production of glucose depletes the hepatocyte of needed intermediaries in the citric acid cycle.
When this occurs, the acetyl-coenzyme A (CoA) generated from the breakdown of fatty acids cannot enter the citric acid cycle and instead forms ketone bodies, acetoacetate, and β-hydroxybutyrate.
These ketone bodies are released by the liver to extrahepatic tissues, particularly skeletal muscle and the brain, where they can be used for energy production instead of glucose.
During surgical illness, however, ketone body formation is relatively inhibited secondary to elevated serum insulin levels.
Thus, compared with starvation, ketone bodies do not significantly supplant the need for glucose in surgical patients and do not play a major role in the metabolic management of the pediatric stress response.
In addition to their nutritional role, fatty acids profoundly influence inflammatory and immune events by changing lipid mediators as well as inflammatory protein and coagulation protein expression.
After ingestion, n-6 and n-3 fats are metabolized by an alternating series of desaturase and elongase enzymes, transforming them into the membrane-associated lipids arachidonic acid, eicosapentaenoic acid (EPA), and DHA.
In PN, substitution of conventional soybean oil–based lipid emulsion (Intralipid), which is rich in proinflammatory omega-6 fatty acids, with a fish oil–based lipid emulsion (Omegaven), which has anti-inflammatory omega-3 fatty acids, has been successful at reversing cholestasis in pediatric intestinal failure–associated liver disease (IFALD) across several studies.
More recently, a lipid emulsion containing soybean oil, medium-chain triglycerides, olive oil, and fish oil (Smoflipid) was approved by the U.S. Food and Drug Administration for adult patients. Pediatric trials of Smoflipid thus far have shown promise in treating and preventing IFALD compared with Intralipid.
What are the required vitamins for the neonate and child?
In the neonate and child, required vitamins include the fat-soluble vitamins (A, D, E, and K) and the water-soluble vitamins ascorbic acid, thiamine, riboflavin, pyridoxine, niacin, pantothenate, biotin, folate, and vitamin B12.
Because vitamins are not consumed stoichiometrically in biochemical reactions but instead act as catalysts, the administration of large amounts of vitamin supplements in metabolically stressed states is not logical from a nutritional standpoint.
The trace elements required for normal growth and development include zinc, iron, copper, selenium, manganese, iodide, molybdenum, and chromium.
Trace elements are needed for the synthesis of a ubiquitous and extraordinarily important class of enzymes called metalloenzymes.
More than 200 zinc metalloenzymes alone exist, and both DNA and RNA polymerase are included in this group. As with vitamins, these metalloenzymes act as catalytic agents.
What are the micronutrient deficiencies among Pediatric patients?
What is the recommendation regarding the use of Enteral Nutrition (EN) for critically Ill pediatric patients?
Based on adult critical care literature, the European Society of Intensive Care Medicine and the ASPEN guidelines recommend the use of early enteral feeding in critical illness (within 24–48 hours after ICU admission), except in patients with bowel ischemia or hemodynamic instability requiring significant vasopressor support.
The ASPEN and SCCM joint guidelines for critically ill children also recommend EN as the preferred mode of nutrient delivery, starting within 24–48 hours after PICU admission if able and aiming to achieve up to two-thirds of nutrient goal in the first week.
Traditionally, enteral feeding after intestinal surgery would be delayed due to expected postoperative ileus and the presence of a fresh intestinal anastomosis. However, recent experimental data suggest that early enteral feeding (within 24 hours) after intestinal surgery, proximal to an anastomosis, does not negatively affect mortality or anastomotic integrity and instead could decrease length of hospitalization.
In addition, early EN may promote more collagen deposition at the anastomosis.
Nevertheless, the timing of starting EN initiation should be tailored to each patient based on clinical judgment.
In current practice, PN is used to supplement or replace EN in those patients in whom EN alone is unable to meet the nutritional goals.
Although oral nutrition is preferred when possible, its safety needs to be ensured. Particularly pertinent to neonates or in the setting of neurologic impairment, prolonged intubation, or airway and/or upper gastrointestinal malformations, attention must be paid to identifying swallowing difficulties when providing EN.
If impaired swallowing with aspiration is suspected, formal bedside swallowing evaluation and/or radiographic contrast studies are warranted.
If aspiration is suspected or at high risk of occurring, EN should be delivered through alternative enteral access or the food consistencies modified based on recommendations from a feeding therapist.
Critically ill neonates are often deprived of oral nutrition due to a series of interacting factors including impaired feeding skills, prolonged hospitalization, multiple operative procedures, and prolonged intubation.
As a result, critical oromotor skills, which have a key window of development during the first 6 months of life, may fail to develop normally and the child may develop oral aversion. Data on prevention and
treatment of oral aversion are lacking, though conventional practice involves introduction of oral stimulation as early in life as safely possible through nonnutritive sucking or oral feeding. 153 Including feeding therapists in multidisciplinary nutritional support teams seems beneficial.
What are currently recommended strategies when EN is not tolerated for brief periods?
Use of transpyloric feeding tubes and changing from bolus to continuous feeds during brief periods of intolerance are strategies that may help achieve nutrition goals in this population.
Currently, there is not enough evidence to recommend the routine use of prokinetic medications, motility agents (for feeding intolerance or to facilitate enteral tube placement), probiotics, or prebiotics in critically ill children.
What are the current recommendations for the use of parenteral nutrition?
PN provides intravenous administration of macronutrients and micronutrients to meet the nutritional requirements when EN is not possible.
Although PN is a potentially lifesaving therapy, it is also associated with mechanical, infectious, and metabolic complications. In the setting of intact intestinal function, PN is not indicated if enteral feeds alone can maintain nutritional balance.
The decision to initiate PN is based on the anticipated length of fasting, the underlying nutritional status of the individual, and a careful examination of the risks associated with PN use in relation to the consequences of poor nutritional intake.
If the expected period during which minimal or no EN will be provided to the child is longer than 5 days, the use of PN is prudent and probably beneficial.
In children with underlying malnutrition, prematurity, or conditions associated with hypermetabolism, earlier initiation of PN can be considered.
The recent Early versus Late Parenteral Nutrition in the Pediatric Intensive Care Unit (PEPaNIC) trial randomized 1440 PICU patients to PN initiation within 24 hours of PICU admission or withheld PN until 8 days. Decreased new infections, ventilator days, and odds of renal replacement therapy were seen in the late PN group. However, a high percentage of the late PN group were discharged from the PICU before day 8, and estimations of energy expenditure were made using equations rather than actual measurement. Although the evidence is against immediate (within 24 hours) initiation of PN on PICU admission, further studies are required regarding optimal timing of initiating PN in critically ill children.
The main limiting factor for provision of full nutritional support in the form of PN is the availability of central access.
Administration of full PN requires a central venous catheter (CVC) with its tip placed at the junction of the superior vena cava and right atrium.
If a lower extremity central line is utilized, the tip of the catheter should be placed at the junction of the inferior vena cava and right atrium.
The large vessel diameter and maximal blood flow rate at these sites allow for the safe administration of the hypertonic PN.
To avoid the complications associated with malpositioned CVC tips, the practice at our institute is to document the location of the CVC tip prior to its use.
Peripheral administration of PN in the absence of an ideally located CVC requires dilution (maximum 900 mOsm/L) to avoid the risks of phlebitis and sclerosis.
Osmolarity of the PN solution can be calculated using available online calculators or simple equations such as:
{(dextrose grams/L × 5) + (protein grams/L × 10) + (lipid grams/L × 1.5) + [(mEq/L of Na + K + Ca + Mg) × 5]}
What is a commonly used definition of severe intestinal failure?
Children with surgical conditions such as necrotizing enterocolitis, gastroschisis, and intestinal atresia may be at risk for prolonged PN dependence due to insufficient gastrointestinal absorptive function.
PN dependence of greater than 90 days is a common definition for severe intestinal failure.
Such patients have unique nutritional needs and are subject to complications intimately tied to PN.
For children with intestinal failure, PN is lifesaving, but the provision of long-term PN places them at risk for IFALD, which is multifactorial in its development, and central line–associated blood stream infections (CLABSI).
Hepatoprotective lipid strategies previously discussed and strategies to reduce CLABSI such as tunneled single-lumen catheters and ethanol lock therapy have been successful in ameliorating some of the mortality and morbidity associated with these complications.
Children with intestinal failure can have complex nutritional needs owing to impaired intestinal absorption and limitations in nutrient delivery.
Fortunately, their long-term survival (>90%) has been increasing with the advent of multidisciplinary programs that incorporate nutritionally focused care.
New therapies aimed at enhancing bowel adaptation and reducing PN dependence, such as a long-acting glucagonlike peptide-2 (GLP-2) hormonal analog (teduglutide), show promise.
How do you address acidosis and alkalosis in critically ill patients?
Acidosis (pH <7.35) and alkalosis (pH >7.45) can be generated by respiratory or metabolic causes.
When the cause is respiratory—Pa CO 2 >45 mm Hg (acidosis) or <35 mm Hg (alkalosis)—treatment is with appropriate respiratory support.
In case of metabolic causes—bicarbonate <21 mmol/L (acidosis) or > 26 mmol/L (alkalosis)—it is useful to check the anion gap [Na+ – (Cl– + HCO3-), which is normally 12 +/- 2 mEq/L] to understand the underlying cause.
Treatment should be directed toward any underlying cause, for example, metabolic acidosis caused by dehydration or sepsis.
The slow infusion of buffers such as sodium bicarbonate or tris-hydroxymethylaminomethane (THAM, a sodium-free buffer) should be used as therapeutic adjuncts. The amount of sodium bicarbonate required can be calculated using the following equation:
NaHCO 3 (mmol) = base excess x body weight (kg) X factor
Factor:
Neonates 0.5
Small children 0.4
Older children 0.3
- Dilute dose to 0.5mEq/mL.
- Give 1/2 of corrected dose, then measure serum pH.
- During CPR, give 1-2 as IV bolus, then 1/2 as slow IV infusion.
What is the current risk of anesthesia-related mortality among pediatric patients?
Recent large single-center reports have yielded a current estimate of anesthesia-related mortality of 1:250,000 in healthy children.
To put this into perspective for parents, the risk of a motor vehicle collision on the way to the hospital or surgery center is greater than the risk of death under anesthesia.
However, risks of mortality and morbidity are increased in neonates and infants <1 year of age, those who are American Society of Anesthesiologists (ASA) PS3 or greater, and those who require emergency operations.
Which of the following gives the most reliable objective measure of acute changes in nutritional status?
A retinol-binding protein
B weight to height index
C nitrogen balance
D muscle wasting
E albumin and prealbumin
A retinol-binding protein
Retinol-binding protein, prealbumin and transferrin are negative acute-phase proteins and their levels fall rapidly with acute nutritional depletion.
Albumin on the other hand reflects more chronic changes.
Weight to height index is a very crude way to assess chronic malnutrition.
SPSE 1
Which one of the following accurately approximates the protein requirements of a 28-week premature neonate?
A 1.5–2.0 g/kg/day
B 2.5–3 g/kg/day
C extremely variable but up to 7.5 g/kg/day
D 4.0–4.5 g/kg/day
E 1.0–1.5 g/kg/day
B 2.5–3 g/kg/day
Protein needs often vary widely depending on age, disease and stress status as well as developmental state.
Generally less is needed parenterally than enterally.
Adequate protein intake is essential to maintain a positive nitrogen balance to support rapid growth.
These requirements may reach 3.5 g/kg/day in premature infants or even higher in very low-birthweight infants.
This level approximates intrauterine nitrogen retention rates matched for gestational age.
Efficient protein utilisation requires about 200 non-protein calories/g of nitrogen – the nitrogen-sparing effect.
If enough non-protein calories are not supplied, protein is wasted to provide energy instead of growth.
SPSE 1
Which of the following is likely to be insufficiently provided to a preterm infant by breast milk?
A essential fatty acids
B phenylalanine and other aromatic amino acids
C cysteine and other sulphur-containing amino acids
D calcium, phosphorus and trace elements
E all of the above
D calcium, phosphorus and trace elements
The benefits of breast milk are universally known.
Breast milk is always sufficient for protein and caloric requirements, although its caloric density can be augmented to minimise volume. It also provides useful passive immunity.
However, in some infants with increased nutritional demands, breast milk may be insufficient to provide essential minerals and trace elements.
For this reason it is often appropriately fortified.
SPSE 1
When initiating peripheral parenteral nutrition, all of the following are true except:
A aim for minimal osmolar load with maximum caloric density
B observe a maximum dextrose concentration of 12.5%, but usually start at much lower levels
C eliminate lipids as a calorie source to avoid carbon dioxide retention
D use filters in a closed infusion circuit to minimise microemboli and contamination
E blood sugars should be monitored before and after initiation of total parenteral nutrition (TPN).
C eliminate lipids as a calorie source to avoid carbon dioxide retention
Lipid emulsions in parenteral nutrition are isotonic, i.e. osmotically inert.
It is essential to keep the osmolarity of TPN solutions as low as possible to minimise the incidence of peripheral vein chemical phlebitis.
Glucose and amino acids on the other hand are osmotically active particles. The higher their concentration, the higher the risk of chemical phlebitis.
Generally, glucose concentration starts at about 5% and should not exceed 12.5%.
Blood sugars should be optimised and monitored prior to initiating TPN to prevent severe hyperglycaemia.
Lipids are therefore a safe way of maximising caloric density (9 kcal/g) while minimising this complication.
SPSE 1
Which option below is not usually effective or recommended in the treatment of TPN-induced hyperglycaemia?
A decrease in rate
B add insulin to TPN
C decrease dextrose concentration in TPN
D insulin drip
E increase the concentration of linoleic acid in TPN
E increase the concentration of linoleic acid in TPN
All the other options will lead to improvement of hyperglycaemia; however, decreasing the rate or decreasing the concentration of glucose are frequently the most practical measures.
It is seldom necessary to administer insulin in any form except in the acute situation to treat glycosuria with osmotic diuresis.
Transient hyperglycaemia is common after introduction of TPN, as endogenous insulin secretion adjusts to glucose administration.
The response to administered insulin can be unpredictable and unreliable. It also tends to leach into the infusion tubing.
SPSE 1
Which of these is true with regard to fluid management in severe burns?
A Resuscitation calculations should be based on patient’s weight.
B Resuscitation calculations should be based on total body surface area (TBSA).
C Resuscitation solution should contain ample glucose to avoid hypoglycaemia.
D Target urine output should be no more than 0.25 mL/kg/hr to avoid pulmonary oedema.
E Colloid is always necessary initially to maintain intravascular volume.
B Resuscitation calculations should be based on total body surface area (TBSA).
TBSA is the most reliable way to assess fluid requirements in serious burn injuries especially in children since the TBSA in relation to weight is greater.
Because of vascular permeability the use of colloids should be discouraged, as they will leak into the tissues and defeat the aim of expanding intravascular volume.
While in the interstitium, the colloids hold on to fluid thereby prolonging the oedema phase after recovery of the capillary membrane.
Urine output should be kept between 1 and 2 ml/kg/hr as a good reflection of effective resuscitation.
Output of 0.25 ml/kg/hr is too low and is a measure of pre-renal failure.
Administration of glucose during initial resuscitation is unwise – coupled with the stress reaction, it may induce hyperglycaemia and glycosuria, which will lead to additional volume depletion.
In such a case urine output will no longer be a reliable reflection of the adequacy of resuscitation.
SPSE 1
With respect to TPN-induced liver disease, which one of the following is not applicable as a risk factor?
A relative excess of any of the major substrates, particularly amino acids
B age and prematurity
C absence of enteral feedings and consequent lack of enterohepatic circulation
D recurrent septic complications
E deficiency of fat-soluble vitamins A, D, E and K.
E deficiency of fat-soluble vitamins A, D, E and K
The fat-soluble vitamins are essential nutrients. Their deficiency, however, has not been linked to the incidence or severity of TPN-related liver disease.
All the other options have been implicated in this serious long-term complication of prolonged TPN exposure, especially prematurity.
The exact mechanism and pathophysiology of this complication is unknown.
SPSE 1
Which statement below is correct with regard to fluid compartments and proportions in fetuses and neonates?
A Total body water in a 13-week fetus is approximately 95% of body weight, of which 65% is extracellular.
B Total body water and especially extracellular water volume decreases with gestational age.
C Adult levels of extracellular water (20%–25%) are reached in the neonatal period following term birth.
D A premature infant has a relatively high total body water and extracellular water.
E All of the above.
E All of the above.
There is a relative shift of extracellular water to the intracellular compartment during all of the transformation from fetus to neonatal life.
This sequence is interrupted in the pre-term infant who at birth still has a very high total body and extracellular water.
This places an additional burden on the pre-term infant for both fetal and term diuresis.
A clear understanding of this is necessary for appropriate fluid management in the neonatal period.
After term birth, there is a pre-diuretic phase lasting about 24–36 hours in which urine output is low frequently less than 1 ml/kg/hr.
If excessive volume is given during this period in the erroneous conclusion that the patient is oliguric from hypovolaemia, volume overload may result.
The diuretic phase occurs during the second to fourth day of life, during which there is profound diuresis and natriuresis – up to 7–8 ml/kg/hr.
SPSE 1
Which of the following is incorrect about renal function in the neonate?
A Glomerular filtration rate (GFR) increases after birth as renal vascular resistance falls and renal blood flow increases.
B The GFR of neonates does not reach adult levels until about 2 years of age.
C Cord blood has a very low antidiuretic hormone (ADH) level but the neonatal kidney is extremely sensitive to it.
D The neonatal kidney has a limited ability to concentrate urine but is very efficient in excreting a water load.
E Pre-term infants have difficulty excreting a sodium load.
C Cord blood has a very low antidiuretic hormone (ADH) level but the neonatal kidney is extremely sensitive to it.
Cord blood has high levels of ADH but the neonatal kidney is resistant to its effects.
This is thought to be because of the immaturity of the countercurrent mechanism in the loop of Henle for water reabsorption.
Neonates are very efficient at excreting a water load but relatively inefficient at concentrating urine, hence the rapid and severe consequences of water deprivation.
The GFR of the term infant is only 25% of the adult and does not reach adult levels for about 2 years.
SPSE 1
An 11-year-old white male with intestinal failure has a central venous catheter (CVC) for TPN. He has developed advanced-stage liver disease and presents with acute-onset high fevers with dehydration, lethargy and leucocytosis. The liver transaminases are higher and the patient is mildly disorientated. What is the most useful and logical next step in his management?
A Immediate removal of the CVC and suspension of TPN.
B Heparin- lock the CVC and start broad- spectrum antibiotics through a peripheral line.
C Volume-resuscitate, draw blood cultures and start broad-spectrum antibiotics through the CVC.
D Proceed to liver transplantation as soon as possible.
E Repeat the blood count and liver function tests and admit to the paediatric intensive care unit for observation.
C Volume-resuscitate, draw blood cultures and start broad-spectrum antibiotics through the CVC.
This scenario is very serious and potentially life-threatening. In a patient of this description, septicaemia of some sort is the prime suspicion and will include consideration of serious line infection. Immediate removal of the catheter is not practical or necessary. These patients tend to be intravenous-access nightmares and the existing central line may be the only access available to start treatment. Certainly blood cultures should be drawn and effective antibiotics commenced. An elevation of liver transaminases may be a reflection of sepsis but can also reflect ongoing hepatocellular damage.
SPSE 1
An 11-year-old white male with intestinal failure has a central venous catheter (CVC) for TPN. He has developed advanced-stage liver disease and presents with acute-onset high fevers with dehydration, lethargy and leucocytosis. The liver transaminases are higher and the patient is mildly disorientated.
The blood culture at 48 hours is positive for Candida parapsilosis and the patient is still symptomatic.
What is the most reasonable/effective next step?
A Start appropriate antifungal antibiotics immediately through the CVC to sterilise it.
B Start appropriate intravenous antifungal antibiotics and remove the CVC as soon as possible.
C Sacrifice the CVC; insert a new one and use it to treat the candida septicaemia.
D Stop using the CVC and start oral antifungal antibiotics.
E Start appropriate intravenous antifungal antibiotics, and repeat blood cultures after another 48 hours.
B Start appropriate intravenous antifungal antibiotics and remove the CVC as soon as possible.
It is practically impossible to eradicate this organism from in situ catheters.
Appropriate antibiotics in large enough doses, given for long enough, can lead to significant salvage rates for some infections, e.g. gram-positive cocci.
While the line can be used in the meantime for treatment, plans should be made to sacrifice it as soon as possible.
Unfortunately, venous access can be a very serious problem in some of these patients and while the line is now a serious hazard, it may yet constitute the only lifeline available.
Certainly, placement of another long-term line should be deferred until the infection is eradicated.
SPSE 1
The most practical and useful method to determine the hydration and intravascular volume status of a 5-week-old baby being resuscitated for pyloric stenosis is:
A urine output/kg/hr
B blood pressure and heart rate
C skin turgor
D mental status
E serum chemistry profile.
A urine output/kg/hr
The establishment of effective urine flow of 2 ml/kg/hr or more with the appropriate intravenous solution is an indication of good volume resuscitation.
If this has been done with the right solution and in the right sequence the chemistry profile will improve but this is not usually a reliable measure of effective volume restoration.
Skin turgor, mental status and heart rate will all improve but are less precise measurements.
The author’s preference is to give repeated boluses of normal saline 20 ml/kg until urine flow is established.
Although potassium may have been low to begin with, it is improper to administer potassium until the patient is making urine.
It is rarely necessary to treat the alkalosis specifically, since it invariably improves with correction of the hypochloraemia.
SPSE 1
A 26- week-old premature baby on a ventilator is receiving TPN through a right atrial catheter inserted through the right common facial vein. On day 10 she suddenly becomes hypotensive, tachycardic and hypoxic. The pulse pressure narrows significantly and chest X-ray confirms a widened mediastinum. What is the next best diagnostic manoeuvre?
A Repeat chest X-ray to rule out barotrauma.
B Check urine output to rule out fluid overload.
C Echocardiogram to rule out pericardial effusion with tamponade.
D Abdominal X-ray to rule out pneumatosis with pneumoperitoneum.
E Arterial blood gases to determine the most appropriate ventilator changes.
C Echocardiogram to rule out pericardial effusion with tamponade.
This scenario suggests acute cardiac tamponade. The CVC tip erodes through the superior vena cava or the thin atrial wall leading to infusion of TPN into the pericardial sac.
An echocardiogram will confirm this diagnosis and ultrasound guided catheter drainage will lead to immediate resolution.
While not common, this is a well-known complication even in older children.
SPSE 1
All of the following are well- known risks with blood transfusions except:
A hypokalaemia
B hypocalcaemia
C metabolic acidosis
D hypocoagulability
E non-haemolytic febrile reactions.
A hypokalaemia
Banked blood becomes hyperkalaemic because the sodium-po pump weakens over time thereby permitting potassium to leak out of the cells.
Hypocalcaemia can result from the chelating activity of the anticoagulant used – citrate.
There is a tendency to hypocoagulability because of dilution of clotting factors and platelets.
Theses are all factors that should be borne in mind when transfusing large volumes of blood.
SPSE 1
With regard to the otherwise stable preterm neonate, which of these statements is invalid?
A Average daily water requirement may be in excess of 150 mL/kg.
B Excessive volume input has no association with intraventricular haemorrhage (IVH) but may lead to pulmonary oedema by reopening the ductus arteriosus.
C Calcium and phosphorus requirements are much higher than in the full-term neonate partly because of diminished reserves in the skeleton.
D Transepithelial water loss in a 27-week premature baby may be greater than 100 mL/kg/day and is associated with approximately 0.5 kcal/mL of heat loss.
E Taurine and cysteine may be essential amino acids.
B Excessive volume input has no association with intraventricular haemorrhage (IVH) but may lead to pulmonary oedema by reopening the ductus arteriosus.
Excessive volume input is clearly associated with a higher incidence of IVH as well as pulmonary flooding, which may follow reopening of the ductus.
Because of the immaturity of the skin, and especially in infants under radiant warmers, massive transepithelial water loss is the rule along with associated heat loss – latent heat of evaporation.
This must be accounted for in balancing the input/output equation.
Taurine and cysteine are not essential in older children and adults. They are, however, considered essential amino acids in premature neonates because of their unique requirements.
SPSE 1
