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Gastroenterology Features of gastrointestinal disorders in children Acute abdominal pain requires detailed evaluation to identify surgical, gastrointestinal and extra- gastrointestinal causes. Vomiting and diarrhoea are common and usually transient;...
Gastroenterology Features of gastrointestinal disorders in children Acute abdominal pain requires detailed evaluation to identify surgical, gastrointestinal and extra- gastrointestinal causes. Vomiting and diarrhoea are common and usually transient; serious causes are uncommon but important to identify. Worldwide, gastroenteritis is one of the most common causes of death in children under 5 years of age. The number of children and adolescents developing inflammatory bowel disease is increasing, but in contrast to adults, bowel cancer is extremely rare. Constipation is common and often requires long-term treatment. Acute abdominal pain The differential diagnosis of acute abdominal pain in children is extremely wide, including both surgical causes and medical conditions, not only of the gastrointestinal tract but also external to it Of the surgical causes, appendicitis is by far the most common. In children it is essential not to delay the diagnosis and treatment of acute appendicitis, as pro- gression to perforation can be rapid. It is easy to be little the clinical signs of abdominal tenderness in young children. However, in nearly half of the children admitted to hospital with acute abdominal pain, the pain resolves undiagnosed. It is noteworthy that: 1. Lower lobe pneumonia may cause pain referred to the abdomen. 2. Primary peritonitis is seen in patients with ascites from nephrotic syndrome or liver disease. 3. Diabetic ketoacidosis may cause severe abdominal pain. 4. Urinary tract infection, including acute pyelonephritis, is a relatively uncommon cause of acute abdominal pain, but must not be missed. A urine sample should be tested, in order to identify not only diabetes mellitus but also conditions affecting the urinary tract. 5. Pancreatitis may present with acute abdominal pain and serum amylase should be checked. 6. The testes in boys, hernial orifices and hip joints must always be checked. 7. Consider gynaecological problems in older females, and if testing for pregnancy is required A urine sample should be tested to identify not only diabetes mellitus but also conditions affecting the urinary tract Intra-abdominal Surgical Medical Extra-abdominal and mesenteric adenitis Constipation Acute appendicitis Intussusception Peritonitis hydronephrosis renal calculus Henoch– Trauma Schönlein purpura Hepatitis Pancreatitis Psychological Unknown 1-Acute appendicitis Acute appendicitis is the most common cause of abdomi- nal pain in childhood requiring surgical intervention Although it may occur at any age, it is very uncom- mon in children under 3 years of age. The clinical features of acute uncomplicated appendicitis are: symptoms: 1. anorexia 2. vomiting 3. abdominal pain, initially central and colicky (appendicular midgut colic), but then localizing to the right iliac fossa (from localized peritoneal inflammation) signs: 1. fever 2. abdominal pain aggravated by movement, e.g. on walking, coughing, jumping, bumps on the road during a car journey 3. persistent tenderness with guarding in the right iliac fossa (McBurney’s point); however, with a retrocaecal appendix, localized guarding may be absent, and in a pelvic appendix there may be few abdominal signs. preschool children: It is uncommon but potentially serious. The diagnosis is more difficult, particularly early in the disease. Perforation may be rapid, as the omentum is less well developed and fails to surround the appendix, and the signs are easy to underestimate at this age. Appendicitis is a progressive condition and so repeated observation and clinical review every few hours are key to making the correct diagnosis,. No laboratory investigation or imaging is consistently helpful in making the diagnosis. A raised neutrophil count is not always present on a full blood count. Although ultrasound is no substitute for regular clinical review, it may support the clinical diagnosis (thickened, non-compressible appen- dix with increased blood flow), and demonstrate associ- ated complications such as an abscess, perforation or an appendix mass, and may exclude other pathology causing the symptoms. Appendicectomy is straightforward in uncomplicated appendicitis. Complicated appendicitis includes the presence of an appendix mass, an abscess, or perforation. If there is generalized guarding consistent Appendicitis at operation showing a with perforation, fluid perforated acutely inflamed appendix resuscitation and intravenous covered in fibrin antibiotics are given prior to laparotomy. If there is a palpable mass in the right iliac fossa and there are no signs of generalized peritonitis, it may be reasonable to elect for conservative management with intra- venous antibiotics, with appendicectomy being performed after several weeks. If symptoms progress, laparotomy is indicated 2-Non-specific acute abdominal pain and mesenteric adenitis Non-specific acute abdominal pain is abdominal pain which resolves in 24–48 hours. The pain is less severe than in appendicitis, and tenderness in the right iliac fossa is variable. It often accompanies an upper respiratory tract infection with cervical lymphadenopathy. In some of these children, the abdominal signs do not resolve and laparoscopy and an appendicectomy is performed. Mesenteric adenitis is often diagnosed in those children in whom large mesenteric nodes are observed and whose appendix is normal, but there are doubts whether this condition truly exists as a diagnostic entity. Constipation is a common cause of non-specific abdominal pain, which may have an acute onset and be severe and accompanied by vomiting in extreme cases. Summary pyelonephritis. of the testis in boys. coughing, walking or jumping. 3=Intussusception Intussusception describes the invagination of proximal bowel into a distal segment. It most commonly involves ileum passing into the caecum through the ileocaecal valve (Intussusception is the most common cause of intestinal obstruction in infants after the neonatal period. Although it may occur at any age, the peak age of presentation is 3 months to 2 years of age. The most serious complication is stretching and constriction of the mesentery resulting in venous obstruc- tion, causing engorgement and bleeding from the bowel mucosa, fluid loss, and subsequently bowel perforation, peritonitis and gut necrosis. immediate fluid resuscitation and urgent reduction of the intussusception are essential to avoid complications. Presentation 1. Paroxysmal, severe colicky pain with pallor – during episodes of pain, the child becomes pale, especially around the mouth, and draws up the legs. There is recovery between the painful episodes but subsequently the child may become increasingly lethargic. 2. May refuse feeds, may vomit, which may become bile-stained depending on the site of the intussusception. 3. A sausage-shaped mass – is often palpable in the abdomen 4. Passage of a characteristic redcurrant jelly stool comprising blood-stained mucus – this is a characteristic sign but tends to occur later in the illness and may be first seen after a rectal examination. 5. Abdominal distension and shock Usually, no underlying intestinal cause for the intussus- ception is found, although there is some evidence that viral infection leading to enlargement of Peyer’s patches may form the lead point of the intussusception. An iden- tifiable lead point such as a Meckel diverticulum or polyp is more likely to be present in children over 2 years of age. Intravenous fluid resuscitation is likely to be required immediately, as there is often pooling of fluid in the gut, which may lead to hypovolemic shock An X-ray of the abdomen may show distended small bowel and absence of gas in the distal colon or rectum. Sometimes the outline of the intussusception itself can be visualized. Abdominal ultrasound is helpful both to confirm the diagnosis (the so-called target/dough- nut sign, Fig. 14.3c) and to check response to treat- ment. Unless there are signs of peritonitis, reduction of the intussusception by rectal air insufflation is usually attempted by a radiologist. This procedure should only be carried out once the child has been resuscitated and is under the supervision of a paediatric surgeon in case the procedure is unsuccessful or bowel perfora- tion occurs. The success rate of this procedure is about 75%. The remaining 25% require operative reduction (Fig. 14.3d). Recurrence of the intussusception occurs in less than 5% but is more frequent after hydrostatic reduction. Summary Intussusception age. urgent treatment. unless peritonitis is present. can be seen in the upper abdomen. The child has become shocked. 4-Meckel diverticulum Around 2% of individuals have an ileal remnant of the vitello-intestinal duct, a Meckel diverticulum, which con- tains ectopic gastric mucosa or pancreatic tissue. Most are asymptomatic but they may present with severe rectal bleeding, which is classically neither bright red nor true melaena. There is usually an acute reduction in haemoglo- bin. Other forms of presentation include intussusception, volvulus (twisting of the bowel), or diverticulitis, when inflammation of the diverticulum mimics appendicitis. A technetium scan will demonstrate increased uptake by ectopic gastric mucosa in 70% of cases (Fig. 14.4). A negative technetium scan does not exclude the possibility and a laparoscopic examination can be used to make the diagnosis. Treatment is by surgical resection Technetium scan showing uptake by ectopic gastric mucosa in a Meckel diverticulum in the right iliac fossa (arrow). The scan has also outlined gastric mucosa in the stomach and excretion into the bladder Summary intussusception or volvulus. 5-Malrotation and volvulus Malrotation is a congenital abnormality of the midgut, in which the small intestine most commonly lies predominantly on the right-hand side of the abdomen, with the caecum in the right upper quadrant. This results from a failure of the intestine to ‘rotate’ into the correct position during fetal life and secure or ‘fix’ the mesentery in the correct position. The reason for this developmental failure is unknown. Fibrous bands called ‘Ladd bands’ tether the caecum to the right upper quadrant and these cause intestinal obstruction by compressing the duodenum (Fig. 14.5a,b). Figure 14.5 (a) The most common form of malrotation, with the caecum remaining high and fixed to the posterior abdominal wall. There are Ladd bands (arrow) obstructing the duodenum. Dotted lines show normal anatomy. (b) Volvulus from rotation of the bowel (arrow). This will result in ischaemia of the small and proximal large intestine. The poorly-tethered gut is able to swing and twist more readily, resulting in volvulus. There are two presentations: 1. obstruction 2. obstruction with a compromised blood supply. 3. Obstruction with bilious vomiting is the usual presenta- tion in the first few days of life but can be seen at a later age. Any child with dark green vomiting needs an urgent upper gastrointestinal contrast study to assess intestinal rotation, unless signs of vascular compromise are present, when an urgent laparotomy is needed. This is a surgical emergency as, when a volvulus occurs, the superior mesenteric arterial blood supply to the small intestine and proximal large intestine is compromised, and unless it is corrected it will lead to infarction of these areas At operation, the volvulus is untwisted, the duodenum mobilized, and the bowel placed in the non-rotated posi- tion with the duodenojejunal flexure on the right and the caecum and appendix on the left. The malrotation is not ‘corrected’, but the mesentery broadened. The appen- dix is generally removed to avoid diagnostic confusion should the child subsequently have symptoms suggestive of appendicitis Summary Malrotation bowel. Recurrent abdominal pain Recurrent abdominal pain is a common childhood problem. It is often defined as episodes of abdominal pain at least 4 times per month sufficient to interrupt normal activities and lasts for at least 2 months. It occurs in about 10% of school-age children. The pain is charac- teristically periumbilical and the children are otherwise entirely well. An organic cause needs to be identified but is present in less than 10% of cases (Fig. 14.6). This requires a full history and thorough examination. Particular attention needs to be paid to identify functional constipation, which is common and may cause abdominal pain, and coeliac disease, and inflammatory bowel disease. The perineum should be inspected for anal fissures and other perianal disease and child maltreatment needs to be considered. The child's growth should be checked. The aim is to avoid subjecting the child to unnecessary investigations. ‘Red flag’ features to help identify organic causes are listed in Box 14.1. Investigations are guided by clinical features but baseline screening tests to be considered are listed in Box 14.2. number of symptom complexes are recognized as causing ‘functional abdominal pain disorders (FAPDs)’. They are sub- classified (Fig. 14.7) as: irritable bowel syndrome (most common) abdominal migraine functional dyspepsia functional abdominal pain (not otherwise specified, i.e. do not meet above classification). Gastrointestinal Hepatobility/pancre Gynaecological atic Constipation Dysmenorrhoea Hepatitis Abdominal migraine Pancreatitis disease disorders for inflammation syndrome stool – inflammatory bowel disease infection inflammatory bowel disease Irritable bowel syndrome (IBS) A family history is often present. There is a characteristic set of symptoms, with non-specific abdominal pain, often peri-umbilical, related to one or more of: defecation alteration in stool frequency change in appearance of stool (diarrhea or constipation). Children with functional constipation also often report pain and distinguishing it from IBS can be problematic. If the abdominal pain resolves with constipation treat- ment, the child has functional constipation. If pain does not resolve after treatment, the child is likely to have IBS with constipation. Pathogenesis IBS is now considered a disorder of visceral hypersensitiv- ity and neurological hypervigilance in combination with psychosocial stressors (see Fig. 14.7). Patients are par- ticularly sensitive to low- or high-pressure stimuli in the bowel, as shown by children with IBS reporting discomfort at lower rectal distention pressure than controls. These changes appear to be secondary to insults of the gut– brain–microbiota axis and neuro-immune interactions in the gut, which alter the perception of pain. These insults may vary widely – 1. genetic (e.g. family history of irritable bowel syndrome), 2. early life events (e.g. bowel surgery), 3. environmental (e.g. cow’s milk protein allergy, post enteri- tis) 4. gastrointestinal (e.g. infections, antibiotics) 5. psychosocial triggers (e.g. stress, anxiety, maltreatment). In some children, a vicious cycle of anxiety with escalating pain leading to family distress may develop, accompanied by demands for increasingly invasive investigations Abdominal migraine In abdominal migraine there are paroxysms of intense, acute periumbilical, midline or diffuse abdominal pain, lasting at least an hour, interfering with normal activities. Additional symptoms may be 1. vomiting, 2. nausea, 3. anorexia, 4. headaches, 5. photophobia 6. pallor. In between episodes, there are long periods (often weeks) of no symptoms interspersed with episodes following a characteristic pattern for the child, with abdominal pain the main symptom. There is often a personal or family history of migraine, and similar triggers to classic migraine (stress, fatigue, travel), similar associated symptoms (e.g. anorexia, nausea and vomiting), similar relieving factors (e.g. rest and sleep), and can evolve into migraine headaches in adult life. Functional dyspepsia This may present with postprandial fullness or early satiety, with or without upper abdominal bloating, nausea or excessive belching, or severe pain or burning in the epigastric area. The pain is not relieved by defecation but may be induced or relieved by eating. There is some evidence for delayed gastric emptying as a result of gastric dysmotility. There is no evidence in children that Helicobacter pylori gastritis causes dyspeptic symptoms in the absence of duodenal ulcer. Peptic ulcer disease Duodenal ulcers are uncommon in children but should be considered in those with epigastric pain, particularly if it wakes them at night, if the pain radiates through to the back, or when there is a history of peptic ulceration in a first-degree relative. These can be caused by H. pylori infection. Initial diagnosis of H. pylori infection is generally made with gastric biopsy on endoscopy. Non- invasive tests such as 13C breath test, which detects urease produced by the organism following the administration of 13C-labelled urea by mouth, or stool antigen tests for H. pylori are used to confirm successful eradication of H. pylori infection. In children, non-invasive tests are not recommended for initial diagnosis and treatment. Children in whom peptic ulceration is suspected or diagnosed on endoscopy should be treated with proton- pump inhibitors, e.g. omeprazole, and eradication therapy with antibiotics should be given Vomiting Posseting and regurgitation are terms used to describe the non-forceful return of milk, but differ in degree. Posseting describes the small amounts of milk that often accompany the return of swallowed air (wind), whereas regurgitation describes larger, more frequent losses. Posseting occurs in nearly all babies from time to time. Vomiting is the forceful ejection of gastric contents. It is a common problem in infancy and childhood (Fig. 14.8). It is usually benign and is often caused by feeding dis- orders or mild gastro-oesophageal reflux or gastroenteritis. Potentially serious disorders need to be excluded, as listed as ‘red flag’ clinical features in Box 14.3. When assessing the clinical features of vomiting: 1. Figures of speech such as ‘bringing everything up’ need to be picked apart: mild viral vomiting may result in a temporary inability to tolerate solids, but sips of liquids are ‘kept down 2. The word ‘bile’ may be used by parents or older children to mean ‘clear acidic stomach contents’. The presence of green bile in vomit is an emergency, as it suggests that the bowel is obstructed and the flow of bile is reversed. 3. In intestinal obstruction, the more proximal the obstruction, the more prominent the vomiting and the sooner it becomes bile- stained, unless the obstruction is proximal to the ampulla of Vater. 1. Small quantity of blood in vomit may be swallowed blood, from a cracked nipple in a breastfed baby or nose bleeds in older children. True haematemesis is a ‘red flag’ clinical feature. 2. Abdominal distension in intestinal obstruction becomes increasingly pronounced the more distal the obstruction 3. When accompanying bouts of coughing it needs to be distinguished from spontaneous, unprovoked, vomiting. 4. The child who is systemically unwell needs to be identified, as it may be a feature of systemic infection, which may be outside the Vomiting preschool School age and Infants children Gastroenteritis Feeding problems Infection: Infection: Infection – including pyelonephritis, septicaemia, meningitis Gastroenteritis media Peptic ulceration and H. pylori infection media Meningitis Appendicitis Whooping Whooping cough cough (pertussis)Appendicitis Migraine (pertussis) Raised intracranial pressure Meningitis Intussusception Coeliac disease Eosinophilic Malrotation oesophagitis Renal failure Volvulus Diabetic ketoacidosis Adhesions Foreign body – Alcohol/drug ingestion or medications Cyclical bezoar vomiting syndrome Bulimia/anorexia nervosa Coeliac disease Pregnancy Intussusception Malrotation Torsion of the testis Volvulus hernia Hirschsprung disease Figure 14.8 Causes of vomiting. gastrointestinal tract, especially urinary tract and central nervous system, and other serious illness Box 14.3 ‘Red flag’ clinical features in the vomiting child Bile-stained vomit Intestinal obstruction (see Ch. 11, Neonatal medicine) Haematemesis Oesophagitis, peptic ulceration, oral/nasal bleeding, and oesophageal variceal bleeding Projectile vomiting, in first few weeks of life Pyloric stenosis Vomiting at the end of paroxysmal coughing Whooping cough (pertussis) Abdominal tenderness/abdominal pain on movement Surgical abdomen Abdominal distension Intestinal obstruction, including strangulated inguinal hernia, ascites Hepatosplenomegaly Chronic liver disease, inborn error of metabolism Blood in the stool Intussusception, bacterial gastroenteritis, inflammatory bowel disease Severe dehydration, shock Severe gastroenteritis, systemic infection (urinary tract infection, meningitis), diabetic ketoacidosis Bulging fontanelle or seizures Raised intracranial pressure, meningitis Faltering growth Gastro-oesophageal reflux disease, coeliac disease and other chronic gastrointestinal conditions Summary stenosis. Gastro-esophageal reflux Gastro-oesophageal reflux is the involuntary passage of gastric contents into the oesophagus. It is extremely common in infancy. It is caused by functional immaturity of the lower oesophageal sphincter which is inappro- priately relaxed. The predominantly fluid diet, a mainly horizontal posture and the short intra-abdominal length of oesophagus in infants all contribute. Most infants with gastro-oesophageal reflux have recurrent regurgitation or vomiting but are putting on weight normally and they are well While common in the first year of life, nearly all sympto- matic reflux resolves spontaneously by 12 months of age. This is probably due to a combination of maturation of the lower oesophageal sphincter, an upright posture and more solids in the diet. Whilst gastro-oesophageal reflux is usually a benign, self-limited condition, if complications are present (Box 14.4), it is called gastro-oesophageal reflux disease. This is more common in: 1. children with cerebral palsy or other neurodevelopmental disorders 2. preterm infants 3. following surgery for oesophageal atresia or diaphragmatic hernia 4. obesity 5. hiatus hernia Investigation Gastro-oesophageal reflux is usually diagnosed clinically and no investigations are required. However, they may be indi- cated if the history is atypical, complications are present, or there is failure to respond to treatment (see Case history 14.1). Investigations include: 1. 24-hour oesophageal pH monitoring to quantify the degree of acid reflux, with a pH probe passed through the nose into the lower oesophagus 2. wireless pH monitoring, when the probe is placed in the distal oesophagus endoscopically and pH is monitored remotely, which is particularly helpful in children with neurodevelopmental or behavioural problems 3. 24-hour impedance monitoring, with a probe in the lower oesophagus, is available in some centres. Weakly acidic or non-acid reflux, which may cause disease, is also measured 4. endoscopy including oesophageal biopsies to identify oesophagitis and exclude other causes of vomiting. A contrast study of the upper gastrointestinal tract is not recommended to diagnose or assess the severity of gastro-oesophageal reflux disease in infants, children and young people. Management Uncomplicated gastro-oesophageal reflux has an excel- lent prognosis and can be managed by parental reassur- ance, feeding assessment, smaller, more frequent feeds or adding inert thickening agents to feeds (e.g. Carobel). A 1–2-week trial of alginate therapy, which forms a protec- tive gel above stomach contents, may be considered, if these other methods are ineffective. Gastro-oesophageal reflux disease is managed with stomach acid suppression with either hydrogen receptor antagonists or proton-pump inhibitors (e.g. omeprazole). Surgical management is reserved for children with complications unresponsive to intensive medical treatment or oesophageal stricture. A Nissen fundoplication, is performed Summary unresponsive to treatment. rarely, fundoplication. Gastro-oesophageal reflux disease Katie, aged 11 months, presented with a history of frequent symptoms. A 24-hour oesophageal pH study (off treatment) regurgitation of feeds from a few weeks of life. She had showed severe ongoing gastro-oesophageal reflux disease two chest infections which required short hospital admis- (Fig. 14.9a,b). An upper gastro-intestinal endoscopy showed sions. Her parents reported that recent vomit contained oesophagitis on histology. Symptoms resolved with a higher small amounts of altered blood. A short trial of feed thick- dose of omeprazole. Her parents also commented on how eners, alginate and omeprazole had not improved her much better she slept at night. Severe gastroesophageal reflux Normal 8 8 6 6 pH pH 4 4 2 2 0 0 10:00 13:00 16:00 19:00 22:00 01:00 10:00 13:00 16:00 19:00 22:00 01:00 04:00 04:00 Figure 14.9 (a) Section of an oesophageal pH (b) Normal pH study for comparison, with pH study showing severe gastro-oesophageal reflux, above 4 for most of the time. with frequent drops inpH below 4. Pyloric stenosis In pyloric stenosis, there is hypertrophy of the pyloric muscle causing gastric outlet obstruction. It presents at 2–8 weeks of age, irrespective of gestational age. It is more common in boys (4:1), particularly first-born, and there may be a family history, especially on the maternal side. Clinical features are: non-bilious vomiting, which increases in frequency and forcefulness over time, ultimately becoming projectile feeds normally after vomiting until dehydration leads to loss of interest in feeding weight loss if presentation is delayed. A hypochloraemic hypokalaemic metabolic alkalo- sis develops as a result of vomiting stomach contents. Hyponatraemia may also be present. Diagnosis Gastric peristalsis may be seen as a wave moving from left to right across the abdomen (Fig. 14.10a). Classically, pyloric stenosis has been confirmed by per- Fig. 14.10a forming a test feed, where the baby is given a milk feed which initially calms the hungry infant, and allows for examination. The diagnosis is made if the pyloric mass, which feels like an olive, is palpable in the right upper quadrant (Fig. 14.10b). As the stomach is usually overdistended with air, Fig. 14.10b This has been replaced by ultrasound, which has become the standard diagnostic procedure by visualizing the hypertrophied pylorus (Fig. 14.10c). Fig. 14.10c Management the definitive treatment is surgical (pyloro- myotomy), this performed safely after acid-base electrolyte imbalances have been corrected, which may take more than 24 hours of intravenous fluid rehydration. (Fig. 14.10d) Fig. 14.10d Pyloric stenosis at operation showing pale, thick pyloric muscle, and pyloromyotomy Summary history. possible dehydration. GASTROENTRITIS Gastroenteritis In low- and middle-income countries, gastroenteritis remains a major cause of child mortality. it remains a common reason for hospital admission in young children. The most frequent cause of gastroenteritis in children in high- income countries are viruses. Rotavirus was by far the commonest pathogen causing severe gastroenteritis, But following inclusion of the rotavirus vaccine into the standard immunization schedule, its incidence has fallen markedly and is now very low. Norovirus is now the commonest cause, but results in less severe disease. Other viruses include sapo- virus and enteric adenovirus, and astrovirus. Bacterial causes are less common in high-income coun- tries but may be suggested by the presence of blood in the stools. Clinical features are a poor guide to the patho- gen, but Campylobacter jejuni infection, Shigella and some salmonellae species produce a dysenteric type of infec- tion, with blood and pus in the stool, abdominal pain and tenesmus. Shigella infection may also be accompanied by high fever. Clostridium difficile causes diarrhoea in chil- dren with chronic diseases. Cholera and enterotoxigenic Escherichia coli infection are associated with profuse, rapidly dehydrating diarrhoea. The third cause of gastroenteritis is protozoan parasite infection such as Giardia and Cryptosporidium, but these rarely cause acute gastroenteritis. In gastroenteritis there is a 1. sudden change to loose or watery stools of increased frequency 2. often accom- panied by vomiting. 3. There may be contact with a person with diarrhoea and/or vomiting or recent travel abroad. Dehydration leading to shock is the most serious compli- cation and its prevention or correction is the main aim of treatment. The following children are at increased risk of dehydration: 1. infants, particularly those under 6 months of age or those born with low birthweight 2. if they have passed five or more diarrhoeal stools in the previous 24 hours 3. if they have vomited more than twice in the previous 24 hours 4. if unable to tolerate supplementary fluids 5. if they have malnutrition or immune deficiency. Infants are at particular risk of dehydration compared to older children or adults as they have a high turnover of fluids (100–120 ml/kg per day, i.e. 10% to 12% of bodyweight) as they have: a) a high body water content b) high metabolic rate c) a greater surface area-to-weight ratio, leading to greater insensible water losses (15–17 ml/kg per day) d) immature renal tubular reabsorption e) cannot communicate their need for extra fluids. Assessment Clinical assessment of dehydration is difficult. The most accurate measure of dehydration is the degree of weight loss during the period of illness. The history and examination are used to clas- sify the degree of dehydration a) no clinically detectable dehydration (usually 10% loss of body weight). Shock must be identified without delay. The clinical features also vary according to the serum sodium, i.e. if the dehydration is isonatraemic, hyponatraemic or hypernatraemic. Isonatraemic and hyponatraemic dehydration In dehydration, there is a total body deficit of sodium and water. In most instances, the losses of sodium and water are proportional and plasma sodium remains within the normal range (isonatraemic dehydration). When children with diar- rhoea drink large quantities of water or other hypotonic solu- tions, there is a greater net loss of sodium than water, leading to a fall in plasma sodium (hyponatraemic dehydration). This leads to a shift of water from extracellular to intracellular compartments to equilibrate their osmolality. The increase in intracellular volume leads to an increase in brain volume, which may result in seizures, whereas the marked extracellu- lar depletion leads to early and exaggerated peripheral signs of dehydration and increased susceptibility of shock. Hypernatraemic dehydration Infrequently, water loss exceeds the relative sodium loss and plasma sodium concentration increases (hypernatraemic dehydration). This usually results from high insensible water losses (high fever or hot, dry environment) or from profuse, low-sodium diarrhoea. The extracellular fluid becomes hypertonic with respect to the intracellular fluid, which leads to a shift of water into the extracellular space from the intracellular compartment. Signs of extracellular fluid deple- tion are therefore less per unit of fluid loss, and depression of the fontanelle, reduced tissue elasticity, and sunken eyes and other peripheral signs of dehydration are reduced. This makes this form of dehydration more difficult to recognize clinically, particularly in an obese infant. It is a dangerous form of dehydration as water is drawn out of the brain and cerebral shrinkage within a rigid skull may lead to irritability and abnormal neurological signs. Management This is shown in Fig. 14.12. Where clinical dehydration is not present on clinical assessment, the aim is to avoid its devel- opment. Breastfeeding or other milks should be contin- ued, fluid intake encouraged, and oral rehydration solution offered. If there is clinical dehydration, oral rehydration solu- tion is the mainstay of therapy. Intravenous fluids are only indicated for shock or deterioration or persistent vomiting. Oral rehydration therapy This is a key component of the management of gastro- enteritis . It contains both sodium and glucose, which increases active sodium and passive water absorption. This works effectively even in the presence of inflammation of the gut, and is therefore effective in diarrhoeal illness. The oral rehydration solution does not ‘stop’ the diarrhoea, which often continues, But the absorption of water and solutes exceeds secretion and keeps the child hydrated until the infective organism is eradicated. It should be offered in small amounts given frequently, by nasogastric tube if necessary. Hypernatraemic dehydration If intravenous fluids are required, a rapid reduction in plasma sodium concentration and osmolality will lead to a shift of water into cerebral cells and may result in seizures and cerebral oedema. The reduction in plasma sodium should therefore be slow, over at least 48 hours (with 0.9% saline or 0.9% saline with 5% glucose, tailored to response) the plasma sodium measured regularly, aiming to reduce it at less than 0.5 mmol/l per hour. Antidiarrhoeal drugs (e.g. loperamide, Lomotil) and antiemetics Medications are not indicated for the vomiting or diar- rhoea of gastroenteritis in children as it usually resolves in a few days without treatment. Antibiotics Antibiotics are not routinely required to treat gastroen- teritis, even if there is a bacterial cause. They are only indi- cated for suspected or confirmed sepsis, extra- intestinal spread of bacterial infection 1. salmonella gastroenteritis if aged under 6 months 2. in malnourished or immunocom- promised children 3. for specific bacterial infections (e.g. Clostridium difficile associated with pseudomembranous colitis, cholera, shigellosis Outcome After diarrhoea has improved, if breastfeeding, continue if possible. Reintroduce solid food and milk. Avoid fruit juices and carbonated drinks. multiple episodes of diarrhoea are a major contributing factor to the devel- opment of malnutrition. Following diarrhoea, nutritional intake should be increased. Zinc supplementation is rec- ommended Postgastroenteritis syndrome Infrequently, following an episode of gastroenteritis, the introduction of a normal diet results in a return of watery diarrhoea. In such cases, oral rehydration therapy should be restarted. Inflammation can damage the gut’s microvilli, reducing the expression of lactase enzymes. Post-infective lactose. Summary Gastroenteritis organisms. clinical deterioration. Management of gastoenteritis Shock Prevent dehydration Oral rehydration solution Continue Give fluid deficit replacement breastfeeding and (based on 5% body weight) as other milk feeds well as maintenance fluid Encourage fluid intake requirement (See Appendix to compensate for A.7). Give ORS often and in increased small amounts Continue gastrointestinal losses breastfeeding Figure 14.12 Initial Discourage fruit juices management of Consider supplementing ORS and carbonated drinks dehydration due to with usual fluids if inadequate Oral rehydration intake of ORS gastroenteritis. solution (ORS) as If inadequate fluid intake or supplemental fluid if at vomits persistently, consider increased risk of giving ORS via nasogastric dehydration tube Oral rehydration solution In gastroenteritis, death is from shock from has saved and continues to dehydration; its prevention or correction is save millions of lives the mainstay of management worldwide. Lactose intolerance Lactose intolerance is a form of malabsorption, where lactase enzyme is not expressed on the microvilli of the intestine. Lactose is not broken down into glucose and galactose, this results in recurrent bloating, abdominal pain and foul-smelling ‘yeasty’ stool whenever dairy prod- ucts are consumed. Some experience nausea and vomiting. Lactose intolerance is often secondary to viral gastroen eteritis it resolves after several months of dairy-free exclusion diet, during which lactase starts to be expressed again In rare cases, lactose intolerance can be congenital, in which case it is caused by a genetic inability to produce lactase. Lactase supplements are available, but they are easily denatured by stomach acid, so are not always effective. Chronic non-specific diarrhea This condition, previously known as toddler diarrhoea, It is the most common cause of persistent loose stools in preschool children. Characteristically, the stools are of varying consistency, sometimes well formed, sometimes explosive and loose. The presence of undigested veg- etables in the stools is common. Affected children are well and thriving. In a proportion of children the diar- rhoea may result from undiagnosed coeliac disease or excessive ingestion of fruit juice, especially apple juice. Summary Occasionally the cause is temporary cow’s milk allergy following gastroenteritis, when a trial of a cow’s milk protein free diet may be helpful. Once possible underly- ing causes have been excluded, malabsorption. in the majority of cases the loose stools probably result from dysmotility of the gut (a form of irritable bowel diarrhoea. syndrome) and fast-transit diarrhoea; it almost always improves with age malabsorption’) obstruction lymphangiectasia congenital anomalies or malabsorption Constipation Constipation is an extremely common reason for consultation in children, most often between 2 and 4 years of age (Fig. 14.18). Parents may use the term to describe decreased frequency of defecation, the degree of hard- ness of the stool or painful defecation. The ‘normal’ fre- quency of defecation is highly variable and varies with age. Breastfed infants usually have a stool frequency of 4 or more times a day, but may not pass stools for several days and be entirely healthy. It is usually twice a day by 1 year of age. Thereafter, most children have a daily bowel action. Constipation is defined as the presence of two or more of the clinical features: 1. the infrequent passage (fewer than three complete stools per week) 2. hard, large stool 3. ‘rabbit dropping’ 4. overflow soiling. There may be straining or pain and bleeding associated with hard stools or abdominal pain and reduced appe- tite, which waxes and wanes with passage of stool. Faecal impaction is when there are severe symptoms overflow soiling and a faecal mass on abdominal examination. The constipation may have been precipitated by dehydra- tion or reduced fluid intake or change in diet or an anal fissure causing pain. It may relate to the child withholding stool (may be accompanied by ‘retentive posturing’ with straight legs, tip- toes with arched back) to avoid distrac- tion from play, or problems with toilet training. Examination usually reveals a well child whose growth is normal, the abdomen is soft and any abdominal disten- sion is normal for age. The back and perianal area are normal in appearance and position and lower limb neu- rological examination is normal. A soft faecal mass may sometimes be palpable in the lower abdomen, but is not necessary for the diagnosis. Digital rectal examination should not be performed A primary underlying cause for constipation is rare, but a number of underlying conditions should be consid- ered: ‘red and amber flag’ symptoms and signs indicative of more significant pathology are detailed in Box 14.6. Investigations are not required to diagnose idiopathic constipation, . If there is growth faltering or intractable constipation, investigations for hypothyroidism, coeliac disease and hypercalcaemia may be indicated. Hirschsprung disease The absence of ganglion cells from the myenteric and sub- mucosal plexuses of part of the large bowel results in a narrow, contracted segment. The abnormal bowel extends from the rectum for a variable distance proximally, ending in a normally innervated, dilated colon. In 75% of cases, the lesion is confined to the rectosigmoid, but in 10% the entire colon is involved. Presentation is usually in the neonatal period with intestinal obstruction heralded by failure to pass meconium within the first 24 hours of life. Abdominal dis- tension and later bile- stained vomiting develop (Fig. 14.21). Rectal examination may reveal a narrowed segment and withdrawal of the examining finger often releases a gush of liquid stool and flatus. Figure 14.21 Abdominal Temporary improvement in the distension from obstruction following the dilatation Hirschsprung disease. caused by the rectal examination can lead to a delay in diagnosis. Occasionally, infants present with severe, life-threaten- ing Hirschsprung enterocolitis during the first few weeks of life. In later childhood, presentation is with chronic constipation, usually profound, and associated with abdominal distension but usually without soiling. Growth faltering may also be present. Diagnosis is made by demonstrating the absence of ganglion cells, together with the presence of large, acetylcholinesterase-positive nerve trunks on a suction rectal biopsy. Anorectal manometry or barium studies may be useful in giving the surgeon an idea of the length of the aganglionic segment but are unreliable for diagnos- tic purposes. Management is surgical and usually involves an initial colostomy followed by anastomosis of normally innervated bowel to the anus.
