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Neonates—fluid requirement is 65 mL/kg over 24 hours.
By the end of the first week of life—fluid requirements increase to 100 mL/kg over 24 hours.
To calculate based on weight:
[100 mL/kg per 24 hours (4 mL/kg per hour) for first 10 kg] + [50 mL/kg per 24 hours (2 mL/kg per hour) for each kg 11–20] + 25 mL/kg per 24 hours (1 mL/kg per hour) for each additional kilogram over 20]
Maintenance fluid—dextrose 5% in 1/4 normal saline
Crystalloid: lactated Ringer or 0.9% normal saline
Ten to 20 mL/kg bolus
For ongoing fluid loss (high nasogastric output, protracted vomiting or diarrhea), replace 1 mL fluid loss with 1 mL replacement every 4 hours using D5 1/2 normal saline + 20 mEq KCl/L
Blood product replacement
Packed red blood cells (pRBCs): 10–15 mL/kg
Fresh frozen plasma (FFP): 10–15 mL/kg
Platelets: 1 unit/5 kg body weight
Clinical signs of dehydration
Lethargy, decreased feeding
Tachycardia, reduced urine output, depressed fontanelle
Clinical signs of fluid overload
New/increased oxygen requirement, respiratory distress
Tachypnea, tachycardia
Metabolic acidosis—inadequate tissue perfusion
Causes
Intestinal ischemia (necrotizing enterocolitis, midgut volvulus, incarcerated hernia)
Bicarbonate loss from gastrointestinal (GI) tract (diarrhea)
Chronic renal failure with acid accumulation
Diabetic ketoacidosis
Ingestion (methanol, ethylene glycol, salicylates, paraldehyde, formaldehyde)
Treatment—treat underlying cause
Sodium bicarbonate indicated if pH less than 7.1, bicarbonate less than 10
Replacement = base deficit × weight (kg) × 0.3
Administer half of calculated replacement amount over several hours then recheck pH
Metabolic alkalosis—gastric acid loss (pyloric stenosis: hypokalemic, hypochloremic), overaggressive diuresis
Respiratory acidosis—hypoventilation
Respiratory alkalosis—hyperventilation
Indications: prolonged ileus, GI fistulas, gastroschisis/omphalocele, intestinal atresia, necrotizing enterocolitis, supplementation of enteral feeds in short bowel syndrome and malabsorption states, prematurity/very low birth weight
Enteral nutrition preferred whenever possible to promote growth and function of GI tract
Complications
Parenteral nutrition–associated liver disease (PNALD)
Cholestasis, can progress to end-stage hepatic fibrosis and cirrhosis
Treatment: decrease dose, modify/restrict lipids, or stop treatment; may require transplantation
Sepsis—central line–related infections; prevent with meticulous care and aggressive treatment of all infections
Most common midline congenital cervical anomaly
Cause
Thyroglossal tract arises from base of tongue (foramen cecum); residual thyroid tissue from descent may persist in midline.
Pockets can fill with fluid and mucus, enlarging when infected, presenting as a nodule.
Symptoms
Most present in first 5 years of life.
Rounded, cystic mass of varying size in midline of neck; 60% adjacent to hyoid bone
Moves cephalad with swallowing and tongue protrusion
Often asymptomatic; may cause dysphagia, pain; drainage if infected
Work-up: thyroid-stimulating hormone (TSH) level, ultrasound; if hypothyroid or concern for lack of normal thyroid gland, obtain thyroid scan
Treatment
Resection to avoid recurrent infection and rule out underlying malignancy
Sistrunk procedure: complete resection of cyst and its tract in continuity with the central hyoid bone
Recurrence (10%) from incomplete excision or intraoperative rupture
Incision and drainage of abscess, antibiotic administration; definitive resection after resolution of inflammation
Most arise from second cleft/pouch
Cause: incomplete obliteration of paired branchial clefts and arches during development
Symptoms: usually discovered in first decade, present as fistulae, sinus tract, cartilaginous remnants
Second branchial cleft sinus presents with clear fluid draining from anterior border of lower 1/3 of sternocleidomastoid muscle (SCM).
Cysts are nontender soft tissue masses beneath SCM; may become infected; risk of in situ carcinoma in adults
Work-up: ultrasound to identify cystic nature of mass if not apparent on physical examination
Treatment
Complete excision of cyst and tract
Use lacrimal probe to identify tract; may dip in methylene blue to stain tract
Multiple small transverse “stepladder” incisions used if tract is long
Aspiration and systemic antibiotics if infected, resect when inflammation resolves
Nonfunctioning lung tissue, has anomalous arterial supply (systemic artery, not pulmonary artery) and absent or abnormal bronchial communication
Male predominance (3:1), left lower side more common
Associated with congenital diaphragmatic hernia (CDH), vertebral anomalies, and congenital heart disease
Two forms
Extralobar: completely separate from normal lung, separate pleural covering
Often asymptomatic and found incidentally
May become infected by hematogenous spread of bacteria
Intralobar: Incorporated into normal surrounding lung
Present with recurrent pneumonia and abscess formation in same bronchopulmonary segment
Diagnosis:
Prenatal: ultrasound with Doppler flow, magnetic resonance imaging (MRI)
Chest radiograph, ultrasound with Doppler flow, computed tomography (CT) chest
Surgical treatment
Symptomatic sequestrations require resection
Extralobar—simple excision
Intralobar—lobectomy
Must find and ligate feeding systemic arterial vessel, usually in inferior pulmonary ligament
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