Surgical Problems in Children

Surgical conditions in children encompass a broad spectrum of congenital anomalies, acquired pathology, and surgical emergencies. Congenital anomalies remain a leading cause of morbidity and mortality in Australian paediatrics, accounting for approximately 25% of paediatric hospital admissions. Timely recognition by primary care clinicians, appropriate investigation, and early referral to paediatric surgical specialists are critical to optimising outcomes.

In Australia, paediatric surgical services are concentrated in tertiary children's hospitals in each state and territory. The Australian Institute of Health and Welfare (AIHW) reports that congenital heart defects, musculoskeletal anomalies, and gastrointestinal malformations are among the most common surgical conditions in the neonatal and infant period. The Royal Australasian College of Surgeons (RACS) maintains paediatric surgery as a distinct specialty, with fellowship training programmes across Australian and New Zealand centres.

This article addresses four key areas of paediatric surgical problems relevant to primary care: head and facial deformities, neck lumps, congenital heart disorders (specifically VSD and PDA), and inguinoscrotal conditions including undescended testis and hernias. Each section outlines the pathology, clinical features, initial assessment, investigation, and management principles, with reference to Australian guidelines and PBS-listed therapies.

Australian Burden of Disease

• Congenital anomalies affect ~3–5% of all Australian live births (Birth Defects Registry data).
• Congenital heart defects occur in ~8 per 1,000 live births; VSD is the single most common lesion.
• Cleft lip and/or palate occurs in ~1 in 700 live births, with higher prevalence among Aboriginal and Torres Strait Islander populations.
• Cryptorchidism (undescended testis) is found in ~3% of full-term and up to 30% of preterm male neonates.
• Inguinal hernia occurs in ~1–5% of all children and up to 10–30% of preterm infants.
• AIHW data show that surgical access in rural and remote Australia is significantly delayed compared with metropolitan centres, contributing to higher complication rates.

Cleft Lip and Palate

Orofacial clefts are among the most common congenital anomalies, with an incidence of approximately 1 in 700 live births in Australia. Clefts may involve the lip alone (CL), the palate alone (CP), or both (CLP). The aetiology is multifactorial, involving genetic susceptibility and environmental factors (maternal smoking, folate deficiency, anticonvulsant exposure).

Classification

Key Management Principles

• Antenatal detection: Cleft lip may be detected on 20-week morphology ultrasound; palate clefts are often missed antenatally.
• Feeding support: Babies with cleft palate cannot generate negative intraoral pressure; require specialised bottles (e.g., Haberman feeder, Pigeon cleft palate teat) and positioning (upright). Refer to lactation consultant/cleft dietitian urgently.
• Hearing: >90% of children with cleft palate have otitis media with effusion (OME); regular audiology review from infancy and consideration of ventilation tubes (grommets).
• Speech: Assess by 18–24 months; velopharyngeal insufficiency (VPI) may require speech therapy or secondary surgery (pharyngoplasty).
• Orthodontic/dental: Alveolar bone grafting at ~8–10 years (mixed dentition); ongoing orthodontic management.
• Genetic counselling: Offer to all families; recurrence risk ~3–5% for non-syndromic CLP; higher if syndrome identified.

Ear Deformities

Prominent Ears (Lop Ears)

Prominent ears affect ~5% of the population and result from underdevelopment of the antihelical fold and/or conchal hypertrophy. While primarily a cosmetic concern, the psychosocial impact on children can be significant, particularly from school age.

• Non-surgical correction: Ear splinting/moulding in the neonatal period (first 6 weeks of life) is highly effective when the cartilage is malleable. Early referral to paediatric plastic surgery is recommended.
• Surgical correction (otoplasty): Recommended at age 5–6 years (before school entry) when the ear has reached ~85% of adult size. Involves cartilage scoring/repositioning ± conchal setback. Bilateral procedure under general anaesthesia; day surgery in most cases.
• Microtia: Severe underdevelopment of the pinna; may be isolated or associated with hemifacial microsomia/Goldenhar syndrome. Reconstruction using autologous rib cartilage (age ~8–10 years) or Medpor implant. Refer to specialist craniofacial centre.

Preauricular Sinus/Pit

Present in ~1% of children; usually unilateral and asymptomatic. Located anterior to the helical root. Excision is indicated only if recurrent infection occurs. Screen for associated hearing impairment (renal tract ultrasound is no longer recommended for isolated preauricular pits).

Dermoid Cysts

Dermoid cysts are benign congenital inclusion cysts lined by keratinising epithelium, containing hair, sebaceous material, and sometimes teeth. They grow slowly and present at characteristic sites in children.

Overview of Paediatric Neck Masses

The differential diagnosis of paediatric neck lumps varies significantly from adults. In children, inflammatory and congenital causes predominate, while malignancy (lymphoma, thyroid carcinoma) is uncommon but must be considered. A systematic approach based on location, character, and age is essential.

Thyroglossal Duct Cyst

The thyroglossal duct cyst (TGDC) is the most common congenital anomaly of the neck, accounting for ~70% of congenital neck masses. It results from incomplete obliteration of the thyroglossal duct, the embryological tract connecting the foramen caecum of the tongue to the thyroid gland. The cyst is lined by columnar or squamous epithelium and contains mucoid material.

Clinical Features

• Midline or paramidline neck mass, classically at or just below the level of the hyoid bone.
• Moves upward with tongue protrusion and with swallowing (due to attachment to the hyoid).
• Usually asymptomatic; may present with acute swelling and erythema if infected (preceding URTI).
• Typically presents in childhood (50% before age 5); can present at any age.
• A pit (sinus) may be present in the skin of the neck if prior infection has drained spontaneously.

Investigations

• Ultrasound: First-line imaging; confirms cystic nature and confirms the presence of orthotopic thyroid tissue (critical before surgery).
• Thyroid function tests: Usually normal; check if thyroid tissue not clearly identified on ultrasound.
• CT/MRI: Not routinely required; may be useful for recurrent or ectopic cases.
• Thyroid scintigraphy: Reserved for cases where orthotopic thyroid cannot be confirmed on ultrasound.

Management

• Sistrunk operation: The standard procedure involves excision of the cyst, the central portion of the hyoid bone, and a core of tissue extending to the foramen caecum. This approach reduces recurrence from ~50% (simple cyst excision) to ~3–5%.
• Treatment of infected cysts: Antibiotics (flucloxacillin 12.5 mg/kg PO QID or cefazolin 25 mg/kg IV TDS) ± incision and drainage if abscess forms. Definitive surgery is delayed until inflammation resolves (usually 6–8 weeks).
• Thyroid carcinoma in TGDC: Rare (~1%); usually papillary thyroid carcinoma. Managed with Sistrunk operation ± total thyroidectomy ± radioiodine depending on staging.

Lymphangioma (Cystic Hygroma)

Lymphangiomas are benign malformations of the lymphatic system. Cystic hygromas are the most common subtype, composed of macrocystic lymphatic channels. They are typically diagnosed antenatally on ultrasound or present in the first two years of life.

Clinical Features

• Soft, compressible, transilluminable mass most commonly in the posterior triangle of the neck.
• May extend into the floor of mouth, parapharyngeal space, or mediastinum.
• Can enlarge dramatically with URTI or haemorrhage into the cyst (acute presentation with airway compromise).
• Antenatally detected cystic hygromas in the first trimester are associated with chromosomal abnormalities (Turner syndrome, trisomy 21).

Management

• Observation: Small, asymptomatic lesions may be observed as ~15–20% regress spontaneously.
• Sclerotherapy: First-line for macrocystic lesions. OK-432 (picibanil) or bleomycin sclerotherapy performed under ultrasound guidance by interventional radiologist. Multiple sessions may be required.
• Surgical excision: Indicated for microcystic disease, failed sclerotherapy, or lesions causing airway compromise. Complete excision can be challenging due to infiltration of surrounding structures; recurrence rates 10–25%.
• Sirolimus: Emerging therapy for complex or refractory lymphatic malformations; used off-label under specialist guidance (paediatric surgeon/oncologist). Dose: 0.8 mg/m² PO BD, titrated to trough 10–15 ng/mL.

Overview

Congenital heart defects (CHD) affect approximately 8 per 1,000 live births in Australia, making them the most common group of major congenital anomalies. Ventricular septal defect (VSD) and patent ductus arteriosus (PDA) are the two most common individual lesions, together comprising approximately 40–50% of all CHD. The majority of children with CHD in Australia are now diagnosed antenatally (morphology scan at 18–20 weeks) or in the newborn period, thanks to universal pulse oximetry screening and antenatal ultrasound programmes.

Ventricular Septal Defect (VSD)

A VSD is a defect in the interventricular septum, allowing left-to-right shunting of blood. It is the most common congenital heart defect (~30% of all CHD). Classification is by location: perimembranous (~70%), muscular (~20%), inlet (5%), and outlet (supracristal, ~5%).

Clinical Presentation

Natural History & Spontaneous Closure

• Small muscular VSDs: ~80% close spontaneously by age 5 years.
• Perimembranous VSDs: ~35–40% close spontaneously, often with aneurysmal tissue of the tricuspid valve.
• Inlet and outlet VSDs: Rarely close spontaneously.
• Supracristal (outlet) VSDs: Associated with aortic regurgitation from prolapse of the right coronary cleft; early closure recommended even if small.

Medical Management

• Diuretics for heart failure: Frusemide 1–2 mg/kg PO/IV BD–TDS + spironolactone 1–2 mg/kg PO OD (PBS: General Benefit).
• ACE inhibitors: Captopril 0.1–0.5 mg/kg PO TDS or enalapril 0.1 mg/kg PO OD, titrate up. May reduce afterload and improve cardiac output (PBS: Restricted Benefit).
• Nutritional support: Calorie-dense feeds (breast milk fortifier or high-calorie formula), nasogastric supplementation if needed. Dietitian involvement essential.
• Endocarditis prophylaxis: No longer routinely recommended for VSD per current AHA/ESC guidelines; only for unrepaired cyanotic CHD or prosthetic material within 6 months of procedure.

Interventional Management

• Surgical closure: Indicated for large VSDs with heart failure refractory to medical management (typically by 3–6 months), VSD with pulmonary hypertension, or progressive aortic regurgitation. Performed via median sternotomy with cardiopulmonary bypass; patch closure. Operative mortality <1% in experienced centres.
• Catheter device closure: Available for selected muscular and perimembranous VSDs (typically >2 years, >10 kg). Performed by paediatric interventional cardiologist. Amplatzer VSD occluder devices are TGA-approved. Avoids sternotomy but not suitable for all defects.

Patent Ductus Arteriosus (PDA)

The ductus arteriosus is a fetal vascular connection between the aorta and pulmonary artery that normally closes within 24–72 hours of birth. Failure to close results in a PDA, which allows left-to-right shunting from the higher-pressure aorta into the pulmonary artery. PDA is particularly common in premature neonates (up to 60% of infants <28 weeks gestation).

Clinical Significance by Age

Medical Closure in Preterm Neonates

Interventional Closure

• Surgical ligation: Via left thoracotomy (minimally invasive or open). Indicated when medical closure fails, contraindicated, or in infants with large PDA causing significant symptoms. Day-case or 1-night stay in experienced centres.
• Catheter-based closure: For children >6 kg (typically >1 year). Amplatzer Duct Occluder (ADO) or coils deployed via femoral vein approach. Performed by paediatric interventional cardiologist. >95% success rate. Now the preferred method for most non-neonatal PDAs in Australia.

Referral Pathways

• Suspected CHD detected on antenatal scan: Referral to foetal cardiology (available at all tertiary children's hospitals) for foetal echocardiography. Delivery planning at a cardiac centre if critical CHD suspected.
• Suspected CHD in infancy/childhood: Urgent referral to paediatric cardiology via local children's hospital. Do not delay if signs of heart failure or cyanosis.
• Positive newborn pulse oximetry screen: Echocardiography within 24 hours at a paediatric cardiac centre.

Undescended Testis (Cryptorchidism)

Cryptorchidism is the failure of one or both testes to descend into the scrotum. It is the most common congenital anomaly of the genitourinary tract in males. The undescended testis may be located anywhere along the normal path of descent (abdominal, inguinal) or ectopic (perineal, femoral). Retractile testes (normal variant) must be distinguished from truly undescended testes.

Epidemiology & Natural History

• Prevalence: ~3% in full-term neonates, ~30% in preterm neonates (<32 weeks gestation).
• Most testes that will descend spontaneously do so by 6 months of age. After 6 months, spontaneous descent is rare (<1%).
• By 1 year, ~1% of boys have a persistent undescended testis.
• Bilateral in ~10–25% of cases; associated with disorders of sex development (DSD) if bilateral and non-palpable.

Consequences of Untreated Cryptorchidism

Clinical Assessment

• Examination: Warm room, warm hands. The child should be examined cross-legged and standing. A retractile testis can be brought to the bottom of the scrotum and will remain there briefly; a truly undescended testis retracts immediately or cannot be brought to the scrotum.
• Non-palpable testis: If the testis cannot be palpated on examination, the differential is intra-abdominal testis, absent testis (vanishing testis), or ectopic testis. Imaging (ultrasound) has limited sensitivity for intra-abdominal testes; diagnostic laparoscopy is the gold standard.
• Hormonal testing: Bilateral non-palpable testes require hCG stimulation test or AMH/INSL3 levels to confirm presence of testicular tissue, plus karyotype to exclude DSD.

Management

• Watchful waiting until 6 months: Re-examine at each well-child visit. No intervention before 6 months as spontaneous descent is common.
• Hormonal therapy: hCG injections (historical) and GnRH analogues have limited efficacy (~20% success) and are no longer recommended in Australian/eTG guidelines.
• Orchidopexy: Definitive treatment. Current recommendation: surgery by 6–12 months of age (ideally by 6 months per the European Association of Urology 2023 guideline, acknowledging variation in Australian practice where 12 months remains common). Inguinal orchidopexy for palpable testes; laparoscopic orchidopexy (Fowler-Stephens if needed) for non-palpable testes.
• Orchidectomy: Considered for a severely dysplastic, non-viable testis, particularly if contralateral testis is normal. Always preserve if viable.

Post-Orchidopexy Surveillance

• Testicular self-examination education from puberty onwards.
• Annual follow-up to assess testicular growth and position until puberty.
• Semen analysis in adulthood if bilateral or concerned about fertility.

Inguinoscrotal Hernias in Children

Paediatric inguinal hernias result from a patent processus vaginalis (PPV) — a peritoneal outpouching that fails to obliterate after the testis descends. This is fundamentally different from adult inguinal hernias (which result from musculofascial weakness). Inguinal hernias in children are indirect in >95% of cases (through the deep inguinal ring).

Epidemiology

• Overall incidence: ~1–5% in children; up to 10–30% in preterm infants.
• Male:female ratio = 6:1 (right side most common ~60%, bilateral ~15%).
• Left-sided hernias in girls may contain ovary ± fallopian tube (sliding hernia).
• Conditions associated with increased hernia risk: prematurity, ventriculoperitoneal (VP) shunts, peritoneal dialysis, connective tissue disorders, undescended testis, ascites, cystic fibrosis.

Clinical Features

• Intermittent groin swelling that appears with crying, straining, or standing and reduces when calm.
• Palpable "silk glove" sign (rubbing of hernia sac layers over the spermatic cord) on examination.
• In boys: swelling may extend into the scrotum (inguinoscrotal hernia). In girls: inguinal or labial swelling.
• Always check the contralateral side.

Hydrocoele vs Hernia

Surgical Repair

• Timing: Paediatric inguinal hernias should be repaired as soon as reasonably possible after diagnosis. For term infants, this is usually within 1–2 weeks. For preterm neonates in the NICU, repair is performed prior to or at the time of discharge to reduce the risk of incarceration.
• Technique: Open herniotomy (high ligation of the processus vaginalis) is the standard. No mesh is required in children (unlike adults). In premature infants, the contralateral side is often explored simultaneously (patent PPV contralateral in ~40–60%).
• Laparoscopic hernia repair: Increasingly used, especially for bilateral and recurrent hernias. Allows visualisation of contralateral side.
• Risk of incarceration in preterm infants: If surgery must be delayed (e.g., medical instability), parents must be counselled on signs of incarceration and the importance of prompt ED presentation.

Drug Therapy — Perioperative Analgesia

Investigations in paediatric surgical conditions are guided by clinical presentation and the suspected pathology. The general principle is to use the least invasive investigation that will yield actionable information.

Preoperative Assessment

• Pre-anaesthetic review: All children undergoing surgery should be assessed by a paediatric anaesthetist. Risk assessment includes age, weight, comorbidities, airway assessment (Mallampati score), and fasting status.
• Fasting guidelines (ANZCA): Clear fluids: 1 hour; breast milk: 4 hours; formula/cow's milk: 6 hours; solids: 6 hours.
• Premature infants (<60 weeks post-conceptual age): Require post-operative cardiorespiratory monitoring for apnoea risk. Plan surgery at a centre with NICU/SCN capability.
• Antibiotic prophylaxis: Cefazolin 25 mg/kg IV (max 1 g) within 60 minutes before skin incision. Not routinely required for herniotomy or orchidopexy; recommended for cardiac surgery and contaminated wounds. PBS: hospital use.

Postoperative Care

• Pain management: Multimodal approach — paracetamol ± ibuprofen (age-appropriate) ± regional anaesthesia (caudal block for inguinoscrotal surgery). Avoid opioids when possible in infants. See drug cards above.
• Wound care: Most paediatric wounds are closed with absorbable subcuticular sutures; no suture removal required. Steri-strips and waterproof dressings allow bathing after 48 hours.
• Activity: Return to normal activity as tolerated. Avoid contact sport for 2–4 weeks after inguinoscrotal surgery. No specific restrictions for cardiac catheter procedures (observe femoral site for 4–6 hours).
• Follow-up: GP review at 1–2 weeks post-surgery; specialist review at 4–6 weeks. Long-term follow-up for orchidopexy (testicular growth monitoring) and cardiac defects (echocardiographic surveillance).

Procedural Sedation in Primary Care

Some minor procedures (wound closure, abscess drainage) may be performed in primary care or ED with procedural sedation. In children, this should only be performed by trained personnel with appropriate monitoring and airway equipment. Refer to the ANZCA guideline on procedural sedation. Intranasal fentanyl (1.5 µg/kg) and nitrous oxide (50–70%) are commonly used in paediatric ED settings.

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