Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

@xirurgi_2025 - 795 - файл

.pdf

Скачиваний:

Добавлен:

29.08.2026

Размер:

12 Мб

Скачать

☆

<<< < Предыдущая 2 3 4 5 6 7 8 9 10 11 12 1314 / 3514 15 16 17 18 19 20 21 22 23 24 25 26 > Следующая >>>

CHAPTER17

https://t.me/med1917

The Umbilicus

CASE 1

A few weeks after birth, the mother noticed an intermittent swelling at her baby’s umbilicus, covered with skin. It became quite large on crying, making her concerned about rupture. The lump often gurgled if compressed, but did not particularly upset the neonate.

1.1 Is this lesion dangerous, and what is its natural history?

1.2 Is an operation needed?

1.3 Why is there a hole in the abdominal wall?

CASE 2

A week or two after separation of the cord stump, the umbilicus remained slightly red and damp. Despite careful drying, the

Embryology

The umbilicus is first formed by folding of the embryonic disc to form a three-dimensional embryo, with fusion or zippering in the ventral midline towards the umbilical ring. The ring remains necessarily widely open during early fetal life, allowing physiological midgut herniation. Abnormalities in either folding or midgut herniation may produce the more serious but rare conditionsof exomphalos and gastroschisis (see Chapter8). Theopen umbilical ring is also a conduit for connections between the midgut and yolk sac (termed vitello-intestinal or omphalo-mesenteric duct) and between the bladder and allantois (urachus). These vestigial connections may persist after birth producing clinical features in accordance with the nature of persistence.

The umbilicus at birth

At birth, two umbilical arteries (branches of the internal iliac arteries) and one umbilical vein (via the falciform ligament and ductus venosus) form the umbilical cord. Routine assessment of umbilical cord vascular anatomy

dampness persisted, and by 6 weeks, there was a cherry-red mass protruding from the umbilical scar.

2.1 Why has this occurred and how is it treated?

CASE 3

A 6-year-old boy presented with a small, mildly tender lump

cm above the umbilicus. He has a history of recurrent epigastric

5 pains, particularly after meals. His mother rst noticed the lump in infancy but did not seek attention as it appeared to be harmless.

Q 3.1 What are the contents of the lump?

3.2 Is it dangerous?

Q Q

3.3 Does it need treatment?

is an important element of the postnatal examination as abnormalities can be associated with other important congenital conditions. In the hours and days after birth, the cord vessels are obliterated, becoming the medial arcuate ligaments (umbilical arteries) and ligamentum teres (umbilical vein). Also after birth, the cord desiccates and separates. The umbilical ring closes. However, delayed contraction of this fibromuscular ring may allow the peritoneum and abdominal contents to bulge through the defect. Colonisation of the residual necrotic cord stump tissue bacteria may produce a low-grade infection resulting in granulation tissue formation.

The range of umbilical abnormalities is summarised in

Table17.1.

Umbilical hernia

Some degree of umbilical herniation is present in almost20% of newborn babies: the incidence is higher in premature neonates or in conditions in which intraabdominal pressure is increased, for example, ascites,

Jones’ Clinical Paediatric Surgery, Seventh Edition. Edited by John M. Hutson, Michael O’Brien, Spencer W. Beasley, Warwick J. Teague and Sebastian K. King. © 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.

117

118 Part IV: Abdomen

https://t.me/med1917

Table 17.1 Abnormalities of the umbilicus

Skin-covered swelling Umbilical hernia Large membrane-covered

swelling

Uncovered bowel protruding

atbirth Infection of cord stump Omphalitis Mucous discharge Umbilical granuloma

Air and faecal discharge Patent vitello-intestinal

Urine discharge Patent urachus

Exomphalos (or omphalocele)

Gastroschisis

heterotopic bowel mucosa

(omphalo-mesenteric) tract

Figure 17.1 Umbilical hernia in a baby.

Down syndrome or congenital hypothyroidism. Because the anomaly occurs after involution of the umbilical cord, associated anomalies are rare, and the hernia is covered by skin.

While the infant lies quietly, the umbilical skin

merely looks redundant, but on crying or straining, bowel fills the hernia and the lesion enlarges to become tense and bluish beneath the thin shiny skin [Fig.17.1]. The bowel may be reduced easily, often with an audible gurgle.

While most umbilical herniae close spontaneously,

there are several practical points that must be explained to the parents:

1 The time of natural closure: in the first 3–4 months

oflife, the bulge may actually increase a little before getting smaller. Resolution usually occurs in the first 12months, but may take up to 3 years.

2 Importance of defect size: even defects that appear

very large at birth may close spontaneously. A defect diameter less than 1 cm at 12 months of age is considered an indicator of likely closure, although spontaneous closure of larger defects may still occur.

3 The skin never ruptures, and the thin skin evident in

the first 4 weeks gradually becomes thicker.

4 Strangulation is remarkably uncommon and it is safe

to wait. The size and tenseness of the hernia when the infant cries is often interpreted incorrectly as causing pain: umbilical herniae probably are symptomless.

Treatment

For the majority, no treatment is required. Strapping is contraindicated because it is ineffective and may cause complications. Umbilical hernia repair is reserved for

defects that fail to close spontaneously and is normally deferred until after 3 years of age.

Para-umbilical (or supra-umbilical) hernia

This is a defect in the linea alba separate from, but adjacent to, the umbilical cicatrix. Most are just above the umbilicus. The defect is a transverse elliptical slit with sharp edges, in contrast to the rounded shape and blunt edges of a central umbilical hernia. This morphological distinction imparts two key differences compared with umbilical herniae. First, there is an increased risk of strangulation. Second, spontaneous closure is less likely. For these reasons, operative repair is more often required, usually as an elective procedure after the third year of life.

Epigastric hernia

Extraperitoneal fat from within the falciform ligament may protrude through a tiny defect in the decussating fibres of the linea alba. It produces a lump in the epigastrium, which may be noticed incidentally. Typically, an epigastric hernia is otherwise asymptomatic, but some cause recurrent, vague epigastric tenderness or abdominal pain, particularly after eating and during exercise. Afirm fatty swelling is palpable in the midline of the epigastrium, usually midway between the xiphisternum and umbilicus. Treatment is by excision or reduction of the protruding fat and closure of the defect in the linea alba.

Chapter17: The Umbilicus 119

https://t.me/med1917

Umbilical sepsis

Umbilical sepsis (omphalitis) is a potentially dangerous infection of the exposed cord stump occurring in the neonatal period. The most common causative organisms are Staphylococci, Escherichia coli and Streptococci. Consequently, an important aspect of preventive medicine is to keep the umbilical stump clean and dry. In minor infections, the umbilical region is red and swollen with a seropurulent discharge, but usually responds well to local and/or systemic antibiotics.

Proactive treatment of omphalitis is important as there may be little superficial evidence that infection has spread further via the lymphatics or the umbilical vessels. Infecting organisms may exploit superficial vessels or the recently patent umbilical arteries and vein to gain access to the bloodstream, with resultant septicaemia. Dissemination of infection via the umbilical arteries may cause abscesses in the distribution of the internal iliac arteries. Ascent of infection along the umbilical vein may involve the portal vein and via the ductus venosus to the vena cava. Clinically, overt infections in these venous structures are rare but serious, and latent infection may lead to thrombophlebitis and portal vein thrombosis. Portal hypertension may ensue, ensues with recanalisation and the opening of collaterals vessels, leading to a cavernomatous malformation of the portal vein (see Chapter26).

The infant with a discharge fromtheumbilicus

Heterotopic mucosa

Sometimes, a small focus of ectopic bowel mucosa at thebase of the umbilicus masquerades as a granuloma with mucous or seropurulent discharge. This typically spherical lesion can be recognised by its deeper, cherryred colour and location in the depths of the umbilical cicatrix. Presence of a small opening on its surface suggests a persistent vitello-intestinal duct and a sinugram is indicated (see below). In the absence of any such opening, distinction from a granuloma is a moot point as both are effectively treated by silver nitrate. One or two applications are usually all that are needed to remove the gut epithelium, which is replaced rapidly by normal skin. Very occasionally, operative excision is required.

Persistent vitello-intestinal remnants

The vitello-intestinal duct is a communication between the midgut and yolk sac, which normally obliterates and then disappears around the sixth week of gestation. Persistence of all or part of the vitello-intestinal duct results in various pathologies. These may present in early infancy, but on occasions are not recognised until some years later, for example, haemorrhage from a Meckel’s diverticulum.

A true persistent vitello-intestinal duct indicates patency of the whole tract, from ileum to umbilical skin. Discharge of ileal contents through the small mucosal opening at the umbilicus causes inflammation, which may in turn confound clear visualisation of the duct orifice [Fig. 17.2]. Very rarely, when the duct is short and broad, the ileum may intussuscept through it

A discharge from the umbilicus may be pus, urine or faeces.

Umbilical granuloma

An umbilical granuloma is a common lesion that presents as a small mass of heaped granulation, accompanied by a seropurulent discharge. Granulation tissue is most likely produced in response to subacute bacterial infection of the cord stump. Lesions with a definite stalk may be ligated without anaesthesia. Larger or broad-based granulomas are better treated with topical application of silver nitrate. This facilitates epithelialisation of the granuloma and is usually curative.

Figure 17.2 A patent vitello-intestinal duct and patent urachus

may look similar: the diagnosis depends on whether the discharge is urinary or faecal.

120 Part IV: Abdomen

https://t.me/med1917

onto the surface of the umbilicus. The Y-shaped segment of prolapsing bowel, inside out, with two orifices is diagnostic.

A vitello-intestinal band (or Meckel’s band) is the result of a duct that has obliterated but not disappeared. Accordingly, the band runs from the ileum to the deep surface of the umbilicus. It may cause no symptoms throughout life or it may, at any age, cause intestinal obstruction when a loop of bowel becomes entangled beneath it.

Partial vitello-intestinal duct obliteration causes a sinus, cyst or Meckel’s diverticulum, according to which part of the tract persists. Sinuses indicate the persistent duct segment communicates with the skin. Cysts and sinuses may become infected, form an abscess and discharge pus at the umbilicus. Meckel’s diverticulum is a patent vitello-intestinal duct remnant with communication with the lumen of the ileum. There may be an associated Meckel’s band tethering the diverticulum and umbilicus. The presenting features and complications of Meckel’s diverticula are described in Chapter23.

All remnants of the vitello-intestinal duct are best excised, which may necessitate a laparoscopy or laparotomy to search for discontinuous segments of the tract.

Urachal remnants

The urachus, the vestigial communication between the allantois and bladder, normally obliterates and remains as the median arcuate ligament. Urinary discharge from the umbilicus indicates a rare, persistent of the urachus

[Fig.17.2]. In such infants, concomitant lower urinary tract obstruction is a recognised but rare association. Treatment is excision of the patent urachus after investigation and relief of any underlying anomalies.

More commonly, the urachus is partly obliterated and presents as a tender mass or abscess in the midline, at or below the umbilicus. The diagnosis is confirmed on ultrasonography prior to treatment by drainage and excision as a single or staged procedure.

KEY POINTS

• Umbilical hernia typically only needs treatment beyond 3 years of age.

• Infection of exposed necrotic umbilical cord stump leads to umbilical granuloma.

• Epigastric hernia contains extraperitoneal fat.

• A discharging umbilicus may indicate a patent vitello-

mesenteric duct or urachus.

Further reading

Cilley RE (2012) Disorders of the umbilicus. In: Coran AG,

Adzick NS, Krummel TM, Laberge J-M, Shamberger RC, Caldamone AA (eds) Pediatric Surgery, 7th Edn. Elsevier Saunders, Philadelphia, pp. 961–972.

Hutson JM, Beasley SW (2013) The umbilicus. In: The Surgical

Examination of Children, 2nd Edn. Springer, Heidelberg, pp. 75–82.

Wong KKY, Tam PKH (2011) Omphalomesenteric duct rem-

nants. In: Puri P (ed) Newborn Surgery, 3rd Edn. Hodder Arnold, London, pp. 661–664.

CHAPTER18

https://t.me/med1917

Vomiting in the First Months of Life

Q 2.1

CASE 1

A 4-week-old breastfed boy was completely well until a few days earlier, when he began vomiting all feeds. He was otherwise well and keen to feed despite the non-bile-stained vomiting. He had lost weight and had few wet nappies.

Q 1.1

What physical sign would conrm the diagnosis you suspect?

If you were unable to demonstrate this sign, what would

Q 1.2

you do if you still suspected the diagnosis?

Q 1.3

What initial investigation would you perform to assist you

in resuscitation?

CASE 2

A 9-day-old girl who had been completely well suddenly began vomiting bile-stained uid. There were no groin swellings. She would not feed.

What diagnosis would you wish to exclude urgently? How would you do this?

Q 2.2

If this diagnosis was conrmed, how urgent is the

Q 2.3

treatment?

CASE 3

A 3-month-old boy was always vomiting, irrespective of how frequently he fed. Initially, he had been breastfed, but he was now on the bottle, and his grandmother assisted with night feeds. He was vomiting small volumes of milk. He was not distressed by the vomiting, weighed 6 kg and was growing well.

What is the most likely diagnosis?

Q 3.1 Q 3.2

What measures could be suggested to reduce the

vomiting?

Vomiting is common in the first months of life, when the evaluation of its significance is particularly important. The temptation to disregard it must be resisted: it is a symptom, not a diagnosis, and its cause must be established [Table18.1].

Vomiting is significant when it is:

1 Bile stained 2 Persistent 3 Projectile 4 Blood stained, that is, coffee grounds, flecked with

altered blood

5 Accompanied by weight loss or failure to gain weight 6 In a child who is unwell, lethargic or listless and/or

disinterested in feeding Most vomiting is due to non-surgical conditions or feeding difficulties. Neonatal infections (e.g. septicaemia, meningitis or urinary tract infection) may present with a variety of clinical features, including vomiting, convulsions, diarrhoea, pallor, lethargy, listlessness,

cyanosis, and pyrexia or hypothermia. Gastroenteritis may be seen in bottle-fed babies but is uncommon in fully breastfed infants. In approximately 25% of those with the rare syndrome of congenital adrenal hyperplasia, there is a salt-losing metabolic disturbance that produces severe vomiting and genital abnormalities in females (Chapter10).

Malrotation with volvulus usually presents in the first week or so of life with bile-stained vomiting, but may occur at any age. The possibility of malrotation with volvulus must be entertained in any child with sudden onset of green vomiting for which there is no other obvious cause. An urgent upper gastrointestinal contrast study will diagnose malrotation if it shows that the duodenojejunal flexure is to the right of normal and below the level of the pylorus. It may also be diagnosed on ultrasonography, if there is sufficient radiological experience. If volvulus goes unrecognised, the entire midgut may be lost from ischaemia when blood flow

121

122 Part IV: Abdomen

https://t.me/med1917

Table 18.1 Causes of vomiting at 1 month of age

Septic Urinary tract infection

Meningitis Septicaemia

Mechanical Gastro-oesophageal reflux

Pyloric stenosis Strangulated inguinal hernia Malrotation with volvulus (bile-stained vomitus)

Other Congenital adrenal hyperplasia

Overfeeding

through the superior mesenteric artery is compromised. Untreated, the child will die: consequently, a child with volvulus needs an urgent operation.

Strangulated inguinal herniae may occur in infants and are easily diagnosed on examination. A hard, tender irreducible swelling at the external inguinal ring will confirm the diagnosis.

Liver

Figure 18.1

pyloric tumour.

Schema showing the two places to palpate a

Rectus abdominus

muscles

Pyloric stenosis

Congenital hypertrophic pyloric stenosis is the most common cause of vomiting that requires an operation in infants and affects 1:300 children, of whom 80% are boys.

Pyloric stenosis is important because it is common, there is a risk to life and permanent relief is obtained by a relatively simple operation. The aetiology remains obscure and is partly genetic, as almost 20% of those affected have a family history.

Symptoms

The usual presentation is with severe vomiting that commences between 3 and 6 weeks of age in an otherwise well baby. Pyloric stenosis is exceptionally rare inneonates younger than 10 days, or infants older than 11 weeks.

Copious vomiting occurs after all feeds; the vomitus contains curdled milk and is practically never bile stained. It may contain some brown coffee-ground flecks of altered blood, reflecting the gastritis secondary to the gastric outlet obstruction. Often, the vomiting is forceful or projectile and may occur well after the last feed. Initially, the child is active and hungry, and a key feature is his readiness and ability to feed again immediately after vomiting. Later, with increasing dehydration and electrolyte imbalance, he becomes weak, listless

and lethargic, not unlike the clinical picture seen in a child with sepsis. He loses weight and looks scrawny. If untreated, he may ultimately die from dehydration and metabolic alkalosis.

Signs

Peristaltic waves of gastric contraction indicate hypertrophy of the gastric muscle secondary to progressive outlet obstruction: their observation makes pyloric stenosis likely. Palpation of the thickened pylorus in the epigastrium, however, is pathognomonic and confirms the diagnosis. The hypertrophic and thickened pylorus is traditionally called a pyloric tumour: it feels like an olive, a small pebble or the terminal segment of the little finger. It is relatively mobile. It is palpable most easily in the angle between the liver and the lateral margin of the right rectus abdominis muscle or in the gap between the two recti midway between the umbilicus and the xiphisternum [Fig.18.1]. It is felt most easily when the baby is relaxed and not crying and when the stomach is empty. When difficulty is experienced feeling the tumour, a nasogastric tube may be passed to empty the stomach.

Failure to palpate the pyloric tumour

If the initial palpation is not conclusive, further observation is necessary and a second examination is made a few hours later. Other manoeuvres that may assist in pal-

Chapter18: Vomiting in the First Months of Life 123

https://t.me/med1917

pating an elusive pyloric tumour are summarised in Table18.2. When symptoms suggest pyloric stenosis but no tumour may be palpated, and septic causes of vomiting have been excluded, a paediatric surgeon should be consulted, and imaging of the pylorus may be required. Realtime ultrasonography may identify the hypertrophied

Table 18.2 Tips for palpating a pyloric tumour

1. Ensure the baby is relaxed

2. Empty overfull stomach

Is the diagnosis

3. wrong?

4. Pyloric stenosis suspected but not proven

Be patient Palpate gently; avoid hurting the infant Flex the hips Wait until crying stops or infant is asleep Allow infant to feed or suck dummy Palpate at start of feed Repeat examination Pass NG tube to empty stomach

Check for sepsis/inguinal hernia if

peristaltic waves absent and pylorus

not palpable Ultrasonography Upper gastrointestinal contrast study

pylorus [Fig. 18.2]. A contrast meal performed under fluoroscopic control will reveal gastric outlet obstruction [Fig. 18.3] and may show other pathologies, including gastro-oesophageal reflux, but is not often needed. These investigations are required in a minority of cases only.

Initially, the diagnosis may be attributed to pre-existing gastro-oesophageal reflux (which is present in many infants) or feeding problems. Often, there is a history of several changes in feeding patterns before the diagnosis is made. However, palpating a tumour is the sine qua non of diagnosis and excludes all other causes. Other features, such as visible gastric peristalsis and projectile vomiting, are supporting evidences, but not in themselves diagnostic.

Investigation

The history (duration of vomiting, amount of vomiting, reduction in wet nappies) and clinical findings (anterior fontanelle and skin turgor) reveal the degree of dehydration. The extent of electrolyte and acid–base imbalance must be determined to guide resuscitation before operation. These infants often have an

Figure 18.2 Ultrasonographic diagnosis of pyloric stenosis shows the thickened circular pyloric muscle in (a) longitudinal and

(b)transverse plane.

(a) (b)

124 Part IV: Abdomen

https://t.me/med1917

Figure 18.3 Pyloric stenosis demonstrated using an upper

gastrointestinal contrast study, showing the string sign. The markedly narrowed pyloric canal (arrows) causes gastric outlet obstruction.

Gastro-oesophageal reflux

An incompetent sphincter at the oesophago-gastric junction allows vomiting in the neonatal period and tends to improve as the infant gets older. Vomiting occurs at any time during or between feeds and usually is neither projectile nor bile stained. If oesophagitis is present, bleeding may produce bright blood or coffee- ground flecks of altered blood in the vomitus or be revealed as anaemia, but more commonly, the infant seems unsettled and irritable. In some infants, severe gastro-oesophageal reflux leads to repeated episodes of aspiration pneumonia, failure to thrive or an oesophageal stricture.

hypochloraemic, hyponatraemic, hypokalaemic metabolic alkalosis. Further estimations of the serum electrolytes and acid–base parameters after resuscitation should confirm complete correction of the disturbance prior to an operation.

Treatment

Treatment involves correcting the fluid and electrolyte abnormality followed by pyloromyotomy, the Ramstedt operation. There are numerous resuscitation protocols available, such as intravenous administration of 0.45% sodium chloride in 5% dextrose and supplementary potassium chloride. The infusion rate is determined after estimating the percentage dehydration, the infant’s weight and maintenance requirements.

The Ramstedt operation may be done via a supraumbilical incision, via a right transverse incision or laparoscopically. The hypertrophied pyloric muscle is split longitudinally allowing the pyloric mucosa to bulge through the gap, thus providing a wider channel into the duodenum. Oral feeds may be commenced within 24 h of surgery, and babies rapidly regain their lost weight.

Figure 18.4 Severe gastro-oesophageal reflux with an

oesophageal stricture secondary to reflux oesophagitis (arrow head). The contrast may be seen to flow freely up the oesophagus (arrow).

Chapter18: Vomiting in the First Months of Life 125

https://t.me/med1917

Management

Gastro-oesophageal reflux affects many infants and the diagnosis is made on clinical grounds. There is a natural tendency towards spontaneous improvement with age, so initial treatment should be conservative, with the head of the cot elevated on blocks. Thickening of feeds and the use of mild antacids, may also be helpful. Increasingly, proton pump inhibitors are employed to decrease the acidity of the reflux, reducing the discomfort of oesophagitis.

Where there is oesophagitis, anaemia, respiratory symptoms or failure to thrive, an upper gastrointestinal contrast study is advisable to document the severity of gastro-oesophageal reflux and to demonstrate any hiatus hernia or oesophageal stricture [Fig.18.4].

Oesophagoscopy and oesophageal biopsy should be performed if haematemesis or anaemia is present, to assess the severity of the peptic oesophagitis, or when an upper gastrointestinal contrast study demonstrates oesophageal obstruction. Further information may be gained from 24 h pH monitoring and oesophageal manometry.

Surgical intervention to control the reflux is indicated if conservative treatment fails, if there is an oesophagealstricture or if a hiatus hernia is present. Operation involves plicating the gastric fundus around the lower

oesophagus [Nissen fundoplication], usually laparoscopically. The oesophageal hiatus is reinforced at the same time. Oesophageal strictures secondary to reflux normally resolve spontaneously once the reflux has been eliminated.

KEY POINTS

• Vomiting in babies is signicant when it is blood or bile stained, persistent, projectile or accompanied by weight loss.

• Bile-stained vomiting in babies without sepsis should be treated as possible malrotation with volvulus and referred as an emergency to a surgeon.

• If pyloric stenosis is suspected, the epigastrium should be observed for gastric peristalsis.