Emergency Treatment in Pediatric: 2016

Vaginal problems

Vulvitis

Prepubertal girls have a relative lack of estrogen and are thus prone to vulvitis. It is characterised by an inflamed, irritated vaginal orifice, often with a foul itchy discharge.

There can be pain or discomfort on micturition. It can be caused by:

• poor hygiene

• threadworms

• excessive inappropriate washing

• atopic or seborrheic eczema

• specific infections, e.g. streptococcal infection

• rarely candida, only after a course of antibiotics

• sexual abuse

A full history and investigations often provide a few clues to the etiology of the condition. Threadworms are fairly common as a cause of vulval itching, especially at night. Any specific conditions should be treated appropriately and the child and parent should be given advice on appropriate bathing and clothing.

Vulvovaginitis

A girl who has a discharge associated with the vulvitis has vulvovaginitis. The commonest causes vary with the age of the child. Infectious vaginitis is more common in sexually active adolescents and fungal infections are also more common owing to the more acid pH at this age. Children can also acquire infections such as Chlamydia trachomatis, gonorrhea and trichomonas via the birth passage or from sexual abuse. Non-specific vulvovaginitis is most common between the ages of 2 and 6 years, especially in the overweight girl. This has several causes, including:

• infection such as Staphylococcus aureus, Hemophilus influenzae, Gardnerella vaginalis

• sexually transmitted disease

• foreign body (rare)

• non-specific

Child sexual abuse should be borne in mind and excluded if possible. Specific infections are treated and general advice given as for vulvitis.

Acute enlargement or pain in the scrotal area is an important clinical sign as it may signal a surgical emergency. Boys with either of these symptoms need to be seen promptly because of the risk of testicular torsion. Testicular torsion may result in infarction of the testis in 6–12 hours if there is progressive obstruction to the blood supply.

The key questions that direct and inform the management are:

• whether this is a painless or painful problem

• whether it is associated with localized or generalized swelling.

Scrotal pain

a. Spermatic cord torsion

Torsion is the most important cause of scrotal pain. It is most common in early puberty, but can occur at any age. An unusual attachment of the testis within the tunica vaginalis results in the testis lying transversely and this predisposes to twisting. Clinically there is an abrupt onset of pain in the testicle often after trauma or exercise.

The pain is sharp and is often accompanied by systemic symptoms such as nausea and vomiting. On examination there is a high riding, tender testicle which is made more uncomfortable by elevation. There is a knot of blood vessels at the upper margin, which may be confused with epididymitis. Classically, there is an absent cremasteric reflex on the affected side. If the torsion is allowed to continue, there is increasing scrotal edema and inflammation, which obscure the landmarks.

If there are strong clinical signs of torsion then surgical exploration is indicated. The purpose of surgery is to untwist the affected testicle and anchor the opposite testicle (orchidopexy). Imaging studies are done only when the clinician is sure that torsion does not exist and is seeking supporting evidence. Imaging investigations can be either a nuclear testicular scan or color Doppler sonography. Either is acceptable though sonography is less sensitive.

b. Torsion of the testicular appendage

There are five vestigial appendages associated with the testis. Torsion can occur of any of them, usually in boys aged 7–12 years. The onset of pain is slow and milder than torsion of the spermatic cord. There are no systemic symptoms but usually only slight swelling of the testis. There may be a bluish discoloration in the upper scrotum (‘blue dot sign’). A nuclear scan will show increased blood flow in the upper region, which can be confused with epididymitis. The treatment is usually analgesia, bed rest and scrotal elevation.

c. Epididymo-orchitis

This condition occurs more commonly in adults and adolescents and is generally rare in children. Inflammation of the epididymi can be viral (adenovirus, mumps or Epstein-Barr virus) or occasionally bacterial in association with anatomical problems of the urinary tract. The possibility of spermatic cord torsion must be considered. Urinalysis may show mild pyuria. A nuclear scan will show increased blood flow to the epididymis. Treatment is supportive. Antibiotics directed to common urinary pathogens are used when bacterial infection is suspected.

d. Trauma

Trauma to the scrotum is usually a precisely remembered event in a boy’s life. If there is no history, another cause should be sought for scrotal pain. The mechanism of injury is often straddle type such as falling astride a bicycle bar. It is generally rare in prepubertal children because of the small size and mobility of the testes. There is often overlying bruising and, if severe enough, a traumatic hematocele. Surgical evacuation may be required if there is a significant collection of blood. In milder cases, cold compresses and analgesics suffice.

e. Other causes

The vasculitic process of Henoch-Schönlein purpura can involve the spermatic cord and testicle causing acute pain and swelling. Children typically have a purpuric rash on the buttocks and legs, which is diagnostic. Treatment in most circumstances consists of rest and pain relief, although severe testicular swelling may be an indication for steroid treatment.

An incarcerated inguinal hernia can also cause acute scrotal pain. There is often a history of intermittent groin swelling, which improves spontaneously. On examination a hernia is detected and cannot be reduced manually. If allowed to persist it can look very much like an acute torsion of the testis with systemic symptoms. Imaging with Doppler sonography or testicular scan can help clarify the cause. Surgical exploration and treatment is required.

Painless scrotal swelling

a. Hydrocele

Hydrocele is a collection of fluid between the tunica vaginalis and the testicle. In the first year of life the process vaginalis often closes and the hydrocele resolves. It often presents as a clear, bluish swelling in the region of the testicle. If it shrinks with gentle pressure, then there is a hernia component. Surgery is not usually advised before 1 year of age since many spontaneously resolve. If the hydrocele persists, or if there is a hernia component present, then surgery is recommended.

b. Varicocele

This is a collection of enlarged spermatic cord veins. It is more common in adolescents and on the left side. It is most obvious in the standing position and occasionally causes pain, especially with exertion. In most cases surgery is not required unless there are symptoms of atrophy of the testes (which is rare).

c. Other causes

An uncomplicated reducible inguinal hernia can cause intermittent testicular swelling. This often requires elective surgical repair because of the risk of incarceration. Acute scrotal edema is a form of urticaria. It starts in the scrotal area and can extend posteriorly. The cause of this is unknown but may include an insect bite allergic reaction, cellulitis or contact dermatitis. Almost all children with this condition are prepubertal. Treatment is symptomatic.

Phimosis

Phimosis is a tightness of the foreskin so that it cannot be drawn over the glans. It is most logically defined as either physiological or pathological. Physiological phimosis occurs because of the inability to retract infantile foreskin, owing to congenital adhesions between the glans and foreskin. By age 2–3 years, these adhesions break down and retraction becomes possible. However, around 6% of boys still have physiological phimosis at age of 10–11 years.

Phimosis

Pathological phimosis occurs when the foreskin cannot be retracted after it has previously been retractable. Clinically this results in ballooning of the foreskin during urination. There may be mild obstruction to urinary flow or recurrent balanitis. Circumcision may be recommended if any of these pathological conditions are present.

Paraphimosis

Paraphimosis is a clinical condition that occurs when the foreskin is retracted and remains proximal to the glans penis. In this position the foreskin becomes progressively swollen due to vascular obstruction and may actually strangulate the glans. This situation will occur after forced retraction of the foreskin (e.g. for catheterization) or vigorous cleaning. If allowed to persist, increasing edema makes reduction progressively more difficult. The usual treatment is manual reduction. A local anesthetic block of the dorsal nerve of the penis is inserted. The foreskin is compressed to reduce the edema and then the foreskin is reduced by pressure on the glans.

Paraphimosis

Treatment depends on the age and degree of discomfort that the child is experiencing. If the swelling has been present for a prolonged period, then reduction may need to be under conscious sedation. Rarely reduction with accompanying circumcision under general anesthetic is required.

Posthitis/balanitis

Posthitis (inflammation of the prepuce) is more common than balanitis (inflammation of the glans). It is less common in children than in adults. In most cases the cause is infectious in origin although contact irritation, allergy and trauma may also be contributing factors.

The treatment is directed towards the causative organism obtained by swabbing and culture. Mild cases usually respond to twice daily baths with gentle retraction of the foreskin along with a topical antibiotic ointment such as Polysporin. In more severe cases (inflammation involving more than a third of the shaft of the penis), treatment is usually with an oral broad spectrum antibiotic that is effective against uropathogens and staphylococcus (e.g. amoxycillin and clavulinic acid). This is in addition to cleaning and regular baths. These latter simple measures can prevent the recurrence of balanitis.

Hypertension in Pediatric Emergency

Transient hypertension can occur in a child as a result of stress, fear or pain. Blood pressure (BP) measurements repeated on several different occasions (at least three) are required to diagnose hypertension. The cuff bladder should cover at least 3/4 of the child’s arm length, and the child should be quiet and calm. In children with measured high BP, it is important to differentiate between those who have immediately dangerous hypertension and those who may have long-standing hypertension. In these patients a search for a possible underlying cause should be made. Table 9.3 shows the upper 95th centile measurements for blood pressure.

Hypertension in Pediatric Children Emergency

Causes of hypertension

The causes of hypertension break down into essential hypertension and secondary causes. Secondary causes fall into a few main groups, depending on the system of origin.

These include:

• Renal (75%): postinfectious glomerulonephritis, chronic glomerulonephritis, obstructive uropathy, reflux nephropathy, renovascular, hemolytic uremic syndrome, polycystic kidney disease

• Cardiovascular (15%): coarctation of the aorta

• Endocrine (5%): pheochromocytoma, hyperthyroidism, congenital adrenal hyperplasia, primary hyperaldosteronism, Cushing syndrome

• Other (5%): neuroblastoma, neurofibromatosis, steroid therapy, raised intracranial pressure.

History

The history essentially should contain details of the family history (e.g. pheochromocytoma) and of genitourinary symptoms.

The examination must include the height and weight, blood pressure measurements of both upper and lower limbs, and a full neurological examination. .

Causes of secondary hypertension

• Appearance: Cushingoid, obese

• Skin: café-au-lait spots, neurofibromas, hirsutism, vasculitis

• Fundoscopy: hypertensive retinopathy

• CVS examination: left ventricular hypertrophy, murmurs (particularly interscapular)

• Abdomen: renal/adrenal masses, renal bruits

Investigation

a. Initial investigations should include:

• urine analysis

• urine microscopy

• blood urea and electrolytes

• creatinine

b. Further investigations may include:

• urinary catecholamines

• chest X-ray

• ECG

• renal ultrasound

• gluconate scan

• plasma renin pre- and post-captopril

• thyroid function tests

• cortisol/aldosterone levels

• 17-hydroxyprogesterone

• renal angiography.

Management

a. Asymptomatic hypertension

No urgent treatment is required for asymptomatic hypertension. The child can be investigated and managed as an outpatient and should be referred to the general pediatric outpatient clinic.

b. Acute severe hypertension

These patients require admission to ICU for urgent treatment. Hypertensive encephalopathy presents as severe headache, visual disturbance and vomiting, progressing to focal neurological deficits, seizures and impaired conscious state, with grossly elevated BP, papilledema and retinal hemorrhages. These patients almost always have chronic renal disease and are on dialysis. The differential diagnosis includes uremic encephalopathy and metabolic disturbance. BP should be lowered in a controlled fashion, with anticonvulsants given for seizures.

Antihypertensives. The choice includes the drugs listed below, although this is not an exhaustive list:

• Intravenous labetalol: 0.2 mg kg−1 initially; later by i.v. infusion of labetalol 0.5–3 mg/Kg weight per hour. It should be avoided if there is heart failure, asthma or bradycardia.

• Intravenous hydralazine: 0.1 – 0.2 mg/Kg weight (max. 10 mg) stat, then 4–6 micro grams/Kg weight per minute (max 300 micrograms per min). It may cause tachycardia, nausea and fluid

retention.

• Oral captopril: 0.1 mg/Kg weight initially, increasing to a maximum of 1 mg/Kg weight (max. 50 mg). Thereafter 0.1–1.0 mg/Kg weight per dose 8-hourly. Captopril is usually effective within 30–60 minutes.

Hematuria in Pediatric Emergency

Hematuria is the presence of red blood cells in the urine. The presence of 10 or more RBCs per high-power field is abnormal. Urinary dipsticks are very sensitive and can be positive at less than five RBCs per high-power field. In the emergency department it is important in evaluating a child with hematuria to identify serious, treatable and

progressive conditions

Red or brown urine does not always indicate hematuria. The discoloration may be as a result of hemoglobinuria, myoglobinuria, some medications and some food. Urate crystals are commonly present in the urine of newborn babies. They can produce a red discoloration of the nappy (‘brick dust’ appearance), which is sometimes mistaken for blood. Blood in the urine can come from sources other than the urinary tract (e.g. vaginal hemorrhage, rectal fissure).

Causes of hematuria

Common causes for microscopic hematuria include an association with viral infections, UTIs, trauma and Henoch-Schönlein purpura. Common causes for macroscopic hematuria include the above, but macroscopic hematuria is more likely to come from the bladder or urethra. Symptomless or ‘benign hematuria’ can occur frequently in children without growth failure, hypertension, edema, proteinuria, urinary casts or renal impairment.

Investigations

The investigation and management of hematuria in Pediatric

Treatment

Many children with isolated microscopic hematuria require no immediate investigation and simply need to be checked to see if the problem persists. This should be arranged with the general practitioner or through outpatient clinic if the family do not have a GP. In the setting of an acute febrile illness, exclude UTI by urine culture and arrange for the urine to be tested again after the acute illness has passed.

Nephrotic Syndrome in Pediatric Emergency

Nephrotic syndrome is a clinical disorder characterised by edema, proteinuria (>3g per day), hypoalbuminemia and hypercholesterolemia. Minimal change glomerulonephritis accounts for 80–85% of nephrotic syndrome in childhood. Complications include infections, thrombosis and renal impairment.

History

Edema is the primary feature. This may be subtle or gross and is usually noticed in the peri-orbital region, scrotum or labia. It may include, in addition, peripheral edema of the limbs and sacrum. The history is often of weight gain, poor urine output and sometimes of discomfort as a result of the edema. A history of preceding upper respiratory tract infection or diarrhea may be present.

Examination

Examination should confirm the presence of edema. Ascites and pleural effusions may be present when edema is gross. Peripheral perfusion and blood pressure should be assessed. Examination should include a search for signs suggesting the onset of complications such as infected ascites, renal vein thrombosis (e.g. enlarged renal mass, loin tenderness and marked hematuria) and cerebral vein thrombosis. Urinalysis should always be included to make the diagnosis as other causes of edema such as protein losing enteropathy or cardiac failure may occur.

Investigation

Urinalysis usually shows +++ or ++++ protein on dipstick. The degree of proteinuria is variable and is usually of the selective type. Microscopic hematuria is present in 15–20% of patients with minimal change nephrotic syndrome. Microscopy of the urine may show red blood cells or granular casts, which suggests the alternative diagnosis of chronic glomerulonephritis as the underlying cause for nephrotic syndrome.

A timed collection of urine for protein excretion is not necessary when the diagnosis is clear. Blood urea and creatinine tests are important to establish the presence or absence of renal impairment. Blood electrolytes, total protein, albumin, globulin and cholesterol should also be measured.

Treatment

All children should be admitted to hospital with their first presentation of nephrotic syndrome. With relapses, they can sometimes be managed as outpatients after consultation with their treating physician. The components of the treatment will be considered individually

a. Albumin

In nephrotic syndrome, acute renal impairment is due to renal hypoperfusion. Albumin is the treatment of choice. Intravenous albumin is indicated for:

• anuria

• hypotension

• poor skin perfusion with skin mottling

• poor capillary return.

These are all indicators of a depleted vascular space. Albumin should be given only in consultation with the treating consultant. The dose is 20% albumin 5 ml/kg weight(1 g/kg weight) over 4 hr i.v. Beware of the possibility of hypertension and pulmonary edema. Gross genital edema causing discomfort may also be an indication for albumin.

b. Furosemide

Furosemide (1 mg/kg weight i.v.) should be given only if the peripheral perfusion markedly improves following the albumin or there are signs of pulmonary edema or hypertension.

c. Steroids

Corticosteroids are usually given in the form of prednisolone. Occasionally their use may be delayed until postrenal biopsy at the discretion of the treating physician. The usual dose of prednisolone is 60 mg/m² per day as single dose up to a maximum of 80 mg per day until remission of proteinuria (to trace or negative on urinalysis) for 4 days, then in reducing doses. There are various regimens for dose reduction. One example is:

• prednisolone 45 mg/m² per day for 8 days then

• 60 mg/m² per alternate day for 8 days (four doses) then

• 45 mg/m² per alternate day for 8 days then

• 30 mg/m² per alternate day for 8 days then

• Reduce by 5 mg every 8 days until finished

d. Antibiotics

The altered immune system in patients with nephrotic syndrome is responsible for their enhanced risk of infection. Oral penicillin 12.5 mg/kg weight per dose b.d. is effective prophylaxis during the edematous phase. If the child is profoundly ill or appears to have sepsis, give cefotaxime 50 mg/kg weight per dose 6 hourly to a maximum of 2 g per dose (to cover Streptococcus pneumoniae, Hemophilus influenzae and Escherichia coli).

e. Anticoagulants

Renal, femoral, cerebral and pulmonary thrombosis can occur in nephrotic patients owing to hypovolemia, high platelet counts and loss of antithrombin III. Thus low-dose aspirin (10 mg/kg weight alternate days) is recommended in edematous nephrotic patients.

General measures

Other general measures include:

• Free fluid intake

• Diet with no added salt

• Strict fluid balance

• Daily weight

Relapses

Over 75% of patients will experience at least one relapse. A relapse is defined as proteinuria ++++ or +++ for 4 days. Management should be discussed with a physician. Prednisolone 60 mg/m² per day should be given until the urine is protein-free for 3 days and then the dose should be slowly reduced as above. If edema is absent, these relapses may not require penicillin and aspirin. Infrequent relapses (less than two relapses within a 6-month period) can be managed in the manner outlined above.

Urinary Tract Infection (UTI) in Pediatric

The urinary tract is a common site of infection in children. The annual incidence is up to 1% in girls, but less common in boys. Radiological abnormalities are present in about 40% of children with UTIs, the most common being reflux. Asymptomatic bacteriuria in schoolgirls is about 1–2%. It is often difficult to diagnose a UTI on history or examination alone in children and a high index of suspicion must be held. The consequences of missing a UTI in a child with even minor urinary tract abnormalities may be significant.

Positive dipstick for leucocytes and nitrites in a sick child does not exclude another site of serious infection (e.g. meningitis). Organisms may also spread from the urinary tract to elsewhere including the meninges. Therefore further investigations as part of a septic work-up (e.g. LP) should not be omitted in a sick child who returns a positive dipstick.

Urinary Tract Infection (UTI) in Pediatric

Source pict: http://www.tipdisease.com/2013/12/urinary-tract-infection-in-children.html

History

Symptoms of serious urinary infections are often non-specific and include fever, irritability, poor feeding and vomiting. More specific features may include loin or abdominal pain, frequency and dysuria. These localising signs are often absent in younger patients. Some children with UTIs may look quite well, while others may appear very unwell.

Examination

This is often normal other than the presence of fever. Loin or suprapubic tenderness may be present. Urinary dipstick testing is only a screening test for a UTI. It has poor sensitivity and specificity (see below).

Initial investigations

A UTI cannot be diagnosed on symptoms alone, nor by culture of urine from a bag specimen. A definitive diagnosis can only be made by culture of urine obtained in a sterile fashion from a mid-stream urine (MSU), suprapubic aspiration (SPA), or a catheter specimen of urine (CSU). Prior antibiotic therapy may lead to negative urine culture in patients with UTI. The laboratory will test for antibacterial activity in the urine. Any child who is unwell or is under 6 months old should also have blood culture and electrolytes tested and should be considered for lumbar puncture.

a. Dipstick urine tests

Dipsticks can detect urinary protein, blood, nitrites (produced by bacterial reduction of urinary nitrate), and leucocyte esterase (an enzyme present in white blood cells). They are a screening test only. If you really suspect UTI you must send a specimen for microscopy and culture. Blood and protein are unreliable markers of UTI. Not all organisms produce nitrites and nitrites take time to develop in urine and so have poor sensitivity. Nitrites may appear in the urine in the presence of infections in other body systems.

Not all patients with UTI have pyuria. Leucocyte esterase can only be detected with relatively high WBC counts in urine, so the test has low sensitivity. Leucocytes from local sources (vagina, foreskin) may contaminate urine. Leucocytes appear in the urine in many other febrile illnesses, e.g. upper respiratory tract infection, pneumonia, etc. So the specificity is low. Overall combined sensitivity for both nitrites and leucocytes is around 50%, i.e. dipsticks may miss 50% of infections.

b. Urine specimen collection

There are several ways to collect urine specimens in children, each with its benefits and problems. Practice differs around the world. In the UK, SPA is the method of choice in

infants if a clean catch specimen is not possible. However, in North America, SPA is rarely practised. Parents are offered a choice between awaiting bag screening, confirmed

by CSU on positive specimens, or immediate catheterisation.

- Urine bag. A urine bag is useful for collecting urine for screening purposes in children who cannot void on request (approximately 0–3 years). The genitalia should be washed with water and dried before application of the bag. Urine is tested with a dipstick for leucocytes and nitrites. If it is positive for either, you should obtain a definitive specimen by SPA (or CSU if SPA fails). If clinical suspicion is high, send a definitive specimen for culture regardless of the dipstick result. A negative dipstick result does not exclude a UTI. Do not send bag specimens for culture in acute presentations. Antibiotics should not be given unless a definitive urine specimen has been obtained.

- Suprapubic aspiration (SPA). SPA remains the preferred method in the UK to collect a minimally contaminated specimen. It should be considered in children too young to obtain an MSU, and with a high probability of UTI, or who are unwell and who warrant a more invasive investigation. The child should be offered fluid to drink. Bedside ultrasound equipment, if available, can improve the success rate of SPA by detecting a full bladder. One author reports 60% success collection rate of SPA and this increases to 80% if bladder ultrasound is used. The specimen should be screened with a dipstick and then sent for culture. Any growth from SPA urine usually indicates infection (but note possible contamination by skin commensals and fecal flora may occasionally produce a mixed growth).

- Catheter specimens. These are useful if SPA fails. The first few drops of the specimen should be discarded and the remaining specimen should always be sent for culture. Any growth of over 103 organisms per ml indicates infection.

- Mid-stream urine (MSU). A mid-stream urine can be obtained from children who can void on request. The genitalia should be washed with water and dried before the specimen is taken. The first few millilitres should be voided and not collected and then a specimen is obtained. A pure growth of over 108 organisms per ml indicates infection. Apure growth of over 105 organisms per ml may indicate early infection and requires a repeat

Treatment of UTI

Antibiotics may be given orally or intravenously for a UTI. Oral medication is appropriate for those over the age of 6 months who are not systemically unwell. Cotrimoxazole (200/40 mg in 5 ml) 0.3 ml/ Kg weight b.d. orally for 1 week is a suitable antibiotic. Alternatives include cephalexin 15 mg kg−1 (500 mg) orally three times a day. Any child who is unwell, and most children under 6 months, should be admitted for i.v. antibiotics. Treatment options vary around the world but suitable regimens include cefuroxime 50 mg/Kg weight per dose (maximum 2g) or gentamicin 7.5 mg/Kg weight (maximum dose 240 mg) i.v. daily and benzylpenicillin 50 mg/Kg weight (maximum dose 3 g) i.v. 6 hourly for children over 1 month of age. Gentamicin levels should be taken to ensure appropriate time between subsequent doses. All children should have antibiotic sensitivities checked at 24–48 hours and therapy adjusted accordingly. For children who are still in nappies a prophylactic dose of antibiotic, e.g. co-trimoxazole (200/40 mg in 5 ml) 0.15 ml/Kg weight in a single daily dose, or nitrofurantoin 3 mg/Kg weight at night should be maintained until the child is seen for follow up. If the child is not settling, repeat the urine culture to determine eradication of organism. A shocked child will require fluid resuscitation. Any child with underlying urinary tract abnormalities should be discussed with the registrar or consultant.

Follow up investigations

All children with proven UTI should be referred for follow up in the general pediatric clinic, or by the child’s own pediatrician. All those with their first UTI should have a renal ultrasound. A micturating cysto-urethrogram (MCU), abdominal X-ray and DMSA (dimercapto-succinoacetic acid) scan may be necessary, but the decision needs to be considered on an individual basis. They are usually done in children under 1 year of age, and may be necessary for older children according to circumstances. For older children, discussion of the need for MCU should be deferred to the outpatient follow up visit.

Assessment

Occasionally an astute clinician makes the diagnosis of diabetes mellitus in a mildly ill child, with <3% dehydration, no acidosis and no vomiting. Baseline investigations should be carried out, as in the child with ketoacidosis. The diagnosis of diabetes mellitus brings with it a lifetime of treatment. The education and care of child and family should be taken over by a team including a pediatrician, nurses and a dietician. However, management can be initiated without admission to hospital.

Management

Initial insulin treatment. Give 0.25 units/Kg weight of quick-acting insulin s.c. stat. If the child is within 2 hours of a meal, give the meal-time dose only. Halve the dose if he or she is under 4 years old. Before breakfast and lunch (7.30 a.m., 11.30 a.m.) give 0.25 units/Kg weight of quick-acting insulin. Before the evening meal (5.30 p.m.) give 0.25 units/Kg weight of quick-acting insulin and 0.25 units/Kg weight of intermediate-acting insulin. If this is the first insulin dose, give 0.25 units/Kg weight quick-acting insulin only, followed by a further 0.25 units/Kg weight quick-acting insulin at midnight followed by a snack.

Ongoing insulin treatment. Once normoglycemia is achieved and ketonuria disappears, you should change the insulin to a twice daily mixture of short and intermediate insulins usually at 1 unit/Kg weight but this may need modification. It should be given as 2/3 in morning and 1/3 at night; 2/3 of each dose should be intermediate-acting, and 1/3 short-acting. Occasionally older adolescents go onto a basal bolus regimen of 30– 40% intermediate acting insulin given at 10 p.m., with the rest given as short-acting insulin in 3 equal doses before meals.

You must inform your consultant about all admissions of children with diabetic ketoacidosis.

Mildly ill hyperglycemic diabetic patients who are already on insulin Children who have already been diagnosed as having diabetes mellitus and who are already on insulin can present to the Emergency Department with a mild illness and hyperglycemia. They are usually advised to take 10% of total daily dose of insulin as rapid-acting insulin every 2 hours until normoglycemic (in addition to usual insulin). You should notify your consultant if there are any management issues that you want to discuss.

Diabetes Melitus in Pediatric Emergency

Thirty per cent of children with diabetes present with vomiting and secondary dehydration from the development of acidosis and ketosis. Diabetic ketoacidocis is a medical emergency. The clinical presentation may vary from polydipsia and polyuria or abdominal pain and vomiting to dehydration and weight loss with rapid acidotic breathing. It is important to check the blood glucose in any child who presents with any of these signs or symptoms.

Assessment

Assessment includes the clinical assessment, particularly of the level of dehydration and the laboratory investigations. The level of dehydration is often overestimated.

Degree of dehydration

• Mild-nil (<4%): no clinical signs

• Moderate (4–7%): easily detectable dehydration, e.g. reduced skin turgor, poor capillary return

• Severe (>7%): poor perfusion, rapid pulse, reduced blood pressure, i.e. shock.

Investigations

• Blood glucose, urea, electrolytes.

• Arterial or capillary acid/base

• Urine: ketones, culture

• Check for precipitating cause, e.g. infection (urine, FBC, blood cultures; consider CXR)

• Islet cell antibodies and insulin antibodies in newly diagnosed patients.

Management

Fluid requirements

If hypoperfusion is present, give normal saline at 20 ml/kg weight stat. This should be repeated until the patient is hemodynamically stable with warm, pink extremities and rapid capillary refill time. If more than 30 ml/kg weight is needed, call for senior advice. Rehydration should continue with normal saline.

The child should be kept nil by mouth (except ice to suck) until alert and stable. A nasogastric tube should be inserted if he or she is comatose or has recurrent vomiting. It should be left on free drainage. Rehydration can be completed orally after the first 24–36 hours if the patient is metabolically stable.

Maintenance fluids

If the blood sugar falls very quickly, i.e. within the first few hours, you should change to normal saline with 5% dextrose. When the blood sugar reaches 12–15 mmol/liter, use 0.45% NaCl with 5% dextrose. You should aim to keep the blood sugar at 10–12 mmol/liter.

If the blood glucose falls below 10–12 mmol/liter and the patient is still sick and acidotic, increase the dextrose in the infusate to 7.5–10%. Do not turn down insulin infusion.

Bicarbonate

Bicarbonate is usually not necessary if shock has been adequately corrected and should not be required in most cases. You must remember that treatment of the dehydration will correct the acid-base disturbance. In extremely sick children (with pH <7.0±HCO3<5 mmol/liter), small amounts of sodium bicarbonate can be given after discussion with the consultant endocrinologist. It should be given over 30 minutes with cardiac monitoring.

The acid base status must then be reassessed.

Note:

• Remember the risk of hypokalemia.

• Continuing acidosis usually means insufficient resuscitation.

Insulin

The insulin should be prepared by adding 50 units of clear/rapid-acting insulin (Actrapid HM or Humulin R) to 49.5 ml 0.9% NaCl (1 unit per ml solution). The insulin infusion may be run as a sideline with the rehydrating fluid via a 3-way tap, provided a syringe

pump is used. Ensure that the insulin is clearly labelled.

You should start at 0.1 units/Kg weight per hour in newly diagnosed children, and in those already on insulin who have glucose levels >15 mmol/liter. Children who have had their usual insulin and whose blood sugars are <15 mmol/liter should receive 0.05 units/kg weight per hour. Adjust the concentration of dextrose to keep the blood glucose at 10–12 mmol/liter.

Adequate insulin must be continued to clear acidosis (ketonemia).

The insulin infusion can be discontinued when the child is alert and metabolically stable (blood glucose <10–12 mmol/liter, pH>7.30 and HCO3>15). The best time to change to subcutaneous insulin is just before meal time. The insulin infusion should only be stopped 30 minutes after the first subcutaneous injection of insulin.

Potassium

Potassium chloride should be added to each bag of i.v. fluid once the patient has urinated. Add this at a rate of 40 mmol/liter if the body weight <30 kg, or 60 mmol/liter if >30 kg. You should measure the levels 2 hours after starting therapy and 2–4 hourly thereafter.

Specimens should in general be arterial or venous. Give no potassium if the serum level is >5.5 mmol/liter or if the patient is anuric.

Admission to ICU

Consider admission to the ICU if the patient is under 2 years of age at onset or if in coma, cardiovascular compromise or is having seizures. Strict monitoring must continue while the child is transferred to ward or to the ICU .

Monitoring during transport to ICU

• Strict fluid balance; check all urine for ketones

• Hourly observations: pulse, BP, respiratory rate, level of consciousness and pupils

• Hourly glucose (Glucometer) during insulin infusion; other biochemistry as clinically indicated

• 4 hourly temperature measurements

Added hazards during the management of ketoacidosis include:

1. Hypernatremia.

Measured serum sodium is depressed by the dilutional effect of the hyperglycemia. To ‘adjust’ sodium concentration, use the following formula:

i.e. 3 mmol/liter of sodium to be added to the measured result for every 10 mmol/liter of glucose above 5.5 mmol/liter. If Na is >160 mmol/liter, the case should be discussed with the consultant. The sodium should rise as the glucose falls during treatment. If this does not happen or if hyponatremia develops, it usually indicates overzealous volume correction and insufficient electrolyte replacement. This may place the patient at risk of cerebral edema.

2. Hypoglycemia.

Hypoglycemia can occur during correction of the hyperglycemia. If the blood glucose is <2.2 mol/liter give i.v. 10% dextrose 5 ml/kg weight. Do not discontinue the insulin infusion. Continue with a 10% dextrose infusion until stable. Cerebral edema. Some degree of subclinical brain swelling is present during most episodes of diabetic ketoacidosis. Clinical cerebral edema occurs suddenly, usually between 6 and 12 hours after starting therapy (range 2–24 hours). Mortality or severe morbidity is very high without early treatment.

3. Cerebral edema

Occurrence of cerebral edema is reduced by slow correction of the fluid and biochemical abnormalities. Optimally, the rate of fall of blood glucose and serum osmolality should not exceed 5 mmol/liter per hour, but in children there is often a quicker initial fall in glucose. Patients should be nursed head up. The warning signs are :

Warning signs of cerebral edema

• First presentation, long history of poor control, young age (<5 years)

• No sodium rise as glucose falls, hyponatremia during therapy, initial adjusted hypernatremia

• Headache, irritability, lethargy, depressed consciousness, incontinence, thermal instability

• Very late—bradycardia, increased BP and respiratory impairment

Treatment consists of:

• Mannitol 20% 0.5 g/kg weight i.v. stat if hemodynamically stable. Give immediately when the clinical diagnosis is made—do not delay for confirmatory brain scan.

• Reduce fluid input to 2/3 and replace deficit over 72 hours rather than 24 hours.

• Nurse head up.

• Transfer immediately to ICU.

Hypoglycemia in Pediatric Emergency

There should be a low threshold for performing a Dextrostix test in the acutely unwell child in the Emergency Department. Beyond the neonatal period, hypoglycemia is defined as a blood glucose less than 2.5 mmol/liter. In children who have had a seizure, hypoglycemia can be the cause of the seizure, or the result of a prolonged seizure.

Effects of hypoglycemia

The effects of the hypoglycemia itself, from whatever cause, are mainly effects on the central nervous system and those of adrenergic overdrive as Table below. Other clinical signs will depend on the cause of the hypoglycemia and a thorough clinical examination is required, including height and weight.

Hypoglycemia Effects in pediatric

Investigation

Blood and urine must be taken off for metabolic investigation as soon as the child presents, before treatment is commenced. Investigations are listed in Box A.

Note that:

• Hyperinsulinism is the commonest cause of hypoglycemia in children under 2 years old, This diagnosis is excluded by ketonuria.

• ‘Accelerated starvation’ (idiopathic ketotic hypoglycemia) is the commonest cause of hypoglycemia after the age of 2 years, but may present earlier. The diagnosis can be established when fasting-induced hypoglycemia is accompanied by elevated urinary ketones, in the absence of other pathology. It is treated by frequent high protein and carbohydrate meals.

Urine and blood Investigations in Hypoglycemia in pediatric emergency

Management

Symptomatic hypoglycemia should be treated with an i.v. bolus of 5 ml/kg weight of 10% dextrose (0.25–0.5 mg/kg weight). The expected maintenance infusion rate is 3–5 ml/kg weight per hour of 10% dextrose (6–8 mg/kg weight per minut). A required infusion rate of 10–20 mg/kg weight per minute is consistent with hyper-insulinism.

Adrenal Crisis in Pediatric Emergency

An adrenal crisis is a physiological event caused by an acute relative insufficiency of adrenal hormones. It may be precipitated by physiological stress, such as infection or surgery in a susceptible patient. It should be considered in patients with:

• congenital adrenal hyperplasia

• hypopituitarism with replacement therapy

• previous or current prolonged steroid therapy

• a history of central nervous system pathology or neurosurgical procedures.

Assessment

Signs of both glucocorticoid deficiency and mineralocorticoid deficiency should be looked for if adrenal insufficiency is suspected. In the history and examination, you should look for the following:

• glucocorticoid deficiency presenting with weakness, anorexia, nausea and/or vomiting, hypoglycemia, hypotension (particularly postural) and shock

• mineralocorticoid deficiency presenting with dehydration, hyperkalemia, hyponatremia, acidosis and prerenal renal failure.

Investigations

Prompt treatment is essential and should be based on the following investigations:

• immediate blood glucose using a Dextrostix

• serum glucose, urea, sodium and potassium

• arterial or capillary acid base

Where the underlying diagnosis of adrenal insufficiency is suspected, you should collect at least 2 ml of clotted blood for later analysis (cortisol and 17-hydroxyprogesterone). The results are unlikely to be available to help in the emergency management of the patient.

Management

Susceptible patients who present with vomiting

Susceptible patients who present with vomiting but who are not other-wise unwell should be considered to have incipient adrenal crisis. To prevent this from possibly developing further:

• Administer i.v. or i.m. hydrocortisone 2 mg /kg weight

• Give oral fluids and observe for 4–6 hours before considering discharge.

• Discuss with appropriate consultant.

For all other children

For all other children where adrenal insufficiency is suspected, the various abnormalities should be considered, namely, fluid requirements, hydrocortisone requirements, hypoglycemia, hyperkalemia and precipitating causes such as sepsis.

1. Give intravenous fluids

The level of dehydration should be assessed and intravenous fluids given accordingly. For management of various levels of dehydration,

Management of dehydration in adrenal insufficiency

a. For shock and severe dehydration

Normal saline 20 ml/kg weight i.v. bolus. Repeat until circulation is restored.
Administer remaining deficit plus maintenance fluid volume as normal saline in 5% dextrose evenly over 24 hours.
Check electrolytes and glucose frequently.
After the first few hours, if serum sodium is >130 mmol/liter, change to half normal saline.
10% dextrose may be needed to maintain normoglycemia.

b. For moderate dehydration in adrenal insufficiency

Normal saline 10 ml/kg i.v. bolus. Repeat until circulation is restored.
Administer remaining deficit plus maintenance fluid volume as normal saline in 5% dextrose evenly over 24 hours.

c. For mild dehydration in adrenal insufficiency

No bolus.
1.5 times maintenance fluid volume administered evenly over 24 hours.

2. Give hydrocortisone

Hydrocortisone must be given intravenously. If intravenous access is difficult, hydrocortisone should be given intramuscularly while you are establishing the intravenous line, in the following doses:

Neonate: hydrocortisone 25 mg stat and then 50 mg/m² per 24 hours by continuous infusion

1 month–1 year: hydrocortisone 25 mg stat, then 50 mg/m² body surface per 24 hours by continuous infusion
Toddlers (1–3 years): hydrocortisone 25–50 mg stat then 50 mg/m² per 24 hours by continuous infusion
Children (4–12years): hydrocortisone 50–75 mg stat, then 50 mg/m² per 24 hours by continuous infusion
Adolescents and adults: hydrocortisone 100–150 mg stat, then 50 mg/m² per 24 hours by continuous infusion

When the patient is stable, you should reduce the intravenous hydrocortisone dose, and then switch to triple dose oral hydrocortisone therapy, gradually reducing to maintenance levels (10–15 mg/m² per day).

In patients with mineralocorticoid deficiency, start fludrocortisone at maintenance doses (usually 0.1mg daily) as soon as the patient is able to tolerate oral fluids.

3. Treat hypoglycemia

Hypoglycemia is common in infants and small children. Treat with an intravenous bolus of 5 ml/kg weight 10% dextrose in a neonate or infant and 2 ml/kg weight of 25% dextrose in an older child or adolescent. Maintenance fluids should contain 5–10% dextrose.

4. Treat hyperkalemia

Hyperkalemia usually normalises with fluid and electrolyte replacement.

If potassium is above 6 mmol/liter, perform an ECG and apply a cardiac monitor as arrhythmias and cardiac arrest can occur.
If potassium is above 7 mmol/liter and hyperkalemic ECG changes are present (e.g. peaked T waves, wide QRS complex), give 10% calcium gluconate 0.5 ml/kg weight i.v. over 3–5 minutes. Commence an infusion of insulin 0.1 units/kg weight per hour i.v. together with an infusion of 50% dextrose 2 ml/kg weight per hour.
If the potassium is above 7 mmol/liter with a normal ECG, give sodium bicarbonate 1–2 mmol/kg weight i.v. over 20 minutes, with an infusion of 10% dextrose at 5 ml/kg weight per hour.

5. Identify and treat potential precipitating causes such as sepsis.

6. Admit to appropriate inpatient facility.

Prevention

The prevention of a crisis is usually possible in susceptible individuals. Situations likely to precipitate a crisis should be anticipated and the patient given:

• triple normal oral maintenance steroid dose for 2–3 days during stress (e.g. fever, fracture, laceration requiring suture)

• intramuscular hydrocortisone when absorption of oral medication is doubtful (e.g. in vomiting or severe diarrhea)

• increased parenteral hydrocortisone (1–2 mg/kg weight) before anesthesia, with or without an increased dose postoperatively.

Jaundice in early infancy

There are many causes of jaundice in early infancy. It is clinically defined as the yellow colouration of the skin and sclera. The best approach is to define it, if it is unconjugated or a conjugated jaundice, as this will dictate the approach to investigation and treatment.

Physiological jaundice

Jaundice is very commonly noted in the first 2 weeks of life. It is part of a normal physiological process and affects 50–70% of babies. Mild jaun-dice with onset after 24 hours of life and which is fading by 14 days needs no investigation or treatment.

Causes of neonatal jaundice

Unconjugated

Breast milk jaundice: 3–5% of breastfed babies
Prematurity: exaggerated physiological pattern; may last 4 weeks
Bruising or cephalohematoma: breakdown of heme
Hemolysis (Rhesus, ABO, G6PD or pyruvate kinase (PK) deficiency, spherocytosis): early onset for ABO, Rhesus
Sepsis: rarely presents with jaundice alone (occasional for UTI); usually unwell
Metabolic (e.g. hypothyroidism): prolonged jaundice, can be mixed conjugated/unconjugated
Polycythemia: delayed cord clamping, twin-to-twin transfusion
Gilbert or Crigler—Najjar: rare, usually presents as prolonged jaundice
GI obstruction (e.g. pyloric stenosis)

Conjugated—pale stools/dark urine, raised conjugated bilirubin (>25% total or >25 µ mol/Liter)

Biliary atresia
Choledochal cyst
Neonatal hepatitis (congenital infection, alpha-1 antitrypsin deficiency,often idiopathic)
Metabolic (galactosemia, fructose intolerance—ask about sucrose/fructose in food/medication)
Complication of total parenteral nutrition (TPN)

Breast milk jaundice

This is the most common cause of prolonged jaundice beyond 14 days but other causes should be eliminated before this diagnosis is made. A breastfed baby with prolonged unconjugated jaundice, normal stool and urine colour, normal FBC, blood film and Coombs test who is well and thriving probably has breast-milk jaundice. Do not stop breastfeeding. The child should have a review in a general pediatric clinic if not improving or if there are any changes—especially in stool colour.

Conjugated hyperbilirubinemia

This must be excluded as the causes of this pattern need urgent evaluation and treatment. Surgery for biliary atresia is most successful when the condition is diagnosed and treated early. Don’t forget to ask about the color of urine and stools. View a dirty nappy yourself if possible.

Phototherapy or rarely exchange transfusion

This may be necessary in a baby with severe unconjugated jaundice associated with prematurity, hemolytic disease, or rare disorders such as Crigler—Najjar. Outside of these conditions, unconjugated jaundice is unlikely to lead to CNS or hearing problems, and no treatment is usually necessary

Diarrhea and Vomiting in Pediatric Emergency

Most diarrhea and vomiting in children is due to infective gastroenteritis ) but not all. It may be the presentation of a urinary tract infection (UTI), meningitis, appendicitis, intussusception or systemic illness. In the unwell child, especially if anuric, consider hemolytic uremic syndrome (hemolytic anemia, acute renal failure and thrombocytopenia).

Assessment

There are essentially two aspects to the assessment of a child with gastroenteritis:

• Diagnosis: Does the child have a cause other than infective gastroenteritis?

• Degree of dehydration: Does the child need admission to hospital? Is there any reason why oral rehydration is not appropriate?

An initial weight measurement should form part of the initial assessment of any child who presents with diarrhea and vomiting. Any child who is toxic, vomiting blood or bile or has severe abdominal pain or abdominal signs needs immediate consultant referral. Be especially careful of those children with chronic illnesses and poor growth, and of the very young.

You must assess degree of dehydration on clinical signs and change in body weight (if recent weight available).

• With mild dehydration (<4%) there are no clinical signs.

• Moderate dehydration (4–6%) tends to be accompanied by dry mucous membranes and sunken eyes.

• With increasing severity to 7–9%, the signs of dehydration are more pronounced with cool peripheries, decreased skin turgor, impaired peripheral circulation and acidotic breathing.

• A shocked child needs immediate intravenous resuscitation.

Fecal samples should be collected for microbiological culture if the child has significant associated abdominal pain or blood in the motions, as a bacterial cause of gastroenteritis is more likely.

Management

The child with diarrhea should continue to be fed unless severely dehydrated. Most children can be rehydrated with oral or nasogastric feeds unless shocked. Do not give medications to reduce the vomiting or diarrhea. They do not work and may be harmful.

Oral rehydration

There is no evidence that milk, or other foods, should be diluted or excluded during the diarrheal illness, unless there is documented lactose intolerance, although a short period without food will not harm children. Breastfeeding should continue.

For mildly dehydrated children, increased frequency of normal drinks, giving small amounts often, will be adequate. Do not give fizzy drinks or fruit juice as their osmolarity is too high. For moderately dehydrated children, who are still drinking, small frequent amounts of fluids should be given according to the volumes given on the charts below. The fluids should be oral rehydrating fluids.

Commercially available preparations usually have 35–50 mmol sodium/Liter. Examples include Diorylate or Rehydrat. Clear instructions and a written information sheet should be given to the parents together with an indication of when to seek review. Indications for admission are:

• refusal to take fluid

• severe pain

• bilious vomiting

• abdominal distension

• blood in the motions

• altered level of consciousness

• increasing dehydration

• parents coping poorly

Nasogastric rehydration

Nasogastric rehydration is a safe and effective way of rehydrating most children with moderate to severe dehydration, even if the child is vomiting. There are a number of possible regimens. Current practice is to replace deficit over 6 hours and then give daily maintenance over the next 18 hours using oral rehydration solution. To calculate hourly rates see Table 7.4.

However, recent recommendations from the American Academy of Pediatrics say that rapid nasogastric rehydration over a 4-hour period is safe and effective. Using 100 ml/kg weight over 4 hours for a moderately dehydrated child or for more severe even 150 ml/kg weight over 4 hours is an appropriate replacement rate. In most cases it is not necessary to check electrolytes.

Intravenous rehydration

Any child with severe dehydration requires immediate boluses of 20 ml/kg weight normal saline until circulation restored (i.v. or i.o.). Urgent U&Es, glucose, FBC, blood gas and urinalysis. Consider whether a septic work-up and parenteral antibiotics are needed or a surgical consultation.

Always remember the ABC approach to a sick child. If serum Na+ is between 130 mmol/liter and 150 mmol/Liter, aim to replace deficit and maintenance over 24 hours after the circulation has been restored by fluid boluses. Reassess clinically and reweigh on the ward at 6 and 12 hours.

Contact a gastroenterology consultant if the child is hemodynamically unstable, has a past history of gut surgery or other significant disease. If serum Na+ is less than 130 mmol/Liter or more than 150 mmol/Liter, aim to replace deficit carefully over 48–72 hours, and consult with senior staff.

Constipation in Pediatric Emergency

Constipation is defined as hard stools that are difficult to pass. Defecation may be painful and may be less frequent than normal. There is a wide range of normal stool frequency: normal breastfed infants may have a stool following each feed or only one every 7–10 days; bottle-fed infants and older children will usually have a bowel action at least every 2–3 days. Constipation occurs more commonly in older children when they have been switched from breast milk or formula to cow’s milk. Constipation may be associated with abdominal pain, reduced appetite and irritability. Vomiting is rarely a sign of constipation alone.

Children may develop constipation as a result of:

• a natural tendency related to reduced gut motility

• a poor diet

• a toddler behavior pattern

• inadequate fluid intake (sometimes after acute illness)

• reduced activity

• painful anal conditions, e.g. fissures

• sometimes following sexual abuse.

Organic causes are rare after early infancy.

Assessment

All infants under 3 months should be discussed with the registrar or consultant. They may require referral for exclusion of Hirschsprung disease. Suggestive symptoms and signs include delayed passage of meconium, vomiting, failure to thrive, abdominal distension and a positive family history.

Do not perform a rectal examination—it is rarely helpful and usually traumatic to the child. An inspection of the anus is important to exclude painful conditions. Acute anal fissures are generally posterior and may occur after passage of a large stool or may complicate inflammation of the perianal skin, e.g. in pinworm (or threadworm) infestation. Perianal cellulitis is caused by group A streptococcal infection and is characterised by induration and marked erythema of the perianal skin with mucopurulent exudate. An abdominal X-ray is not helpful in the initial assessment and should not be ordered. Remember that urine infections are more common in constipated children and should be sought if symptoms are suggestive.

Assesment Constipation in Pediatric Emergency

Management

Carers need to be reassured about the safety of laxatives in children. Rectal medications should be avoided in the first instance and not prescribed without discussion with a consultant. Management can be divided into three main steps

Step 1

Initially give a high fibre diet with adequate fluid intake, adequate exercise and regular toileting.

Step 2

The child will need laxatives, including a stool softener and an aperient.

A suggested regime is: Parachoc or Lactulose; plus sennakot

• Liquid paraffin (<5 years: 10 ml daily; 6–12 years: 15 ml daily). Parachoc should be avoided if there is an increased risk of aspiration, e.g. in cerebral

palsy with bulbar involvement. Children may be given up to 25 ml of Parachoc per dose.

• Lactulose (<5 years: 5 ml b.i.d.; >5 years: 10 ml b.i.d.). Children may be given up to 25 ml of Lactulose per dose.

• Senna granules: (2–6 years: 1/2 teaspoon nocte; 6–12 years: 1 teaspoon nocte). The maximum daily dose of Sennakot granules should be 3 teaspoons per day

Abdominal pain may occur as a side effect. Increased doses may be required in some children with chronic constipation. The dose should be titrated to achieve at least one soft stool per day.

If overflow incontinence is present, warn families that it may worsen initially with treatment.

Step 3

Rarely patients may require admission to achieve bowel emptying. Treatment will involve a bowel preparation agent either Picoprep (Picolax in the UK) sachets (sodium picosulphate 10 mg, magnesium oxide 3.5 mg, citric acid 12.0 g, aspartame 36 mg): <2 years—1/4 sachet; 2–4 years—1/2 sachet; 4–9 years—3/4 sachet, repeating in 6 hours if no response; or colonic lavage solution (e.g. Golytely: orally or via a nasogastric tube).

Disposition

All patients should be referred for follow up in a general pediatric clinic within 7 to 10 days.