Learn — GI, renal & endocrine conditions

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Regurgitation vs vomiting

Regurgitation, also called posseting, is the effortless return of a small amount of milk with a burp in a comfortable, thriving baby, whereas vomiting is the forceful, coordinated expulsion of gastric contents driven by the vomiting centre and preceded by nausea and retching. The distinction is the whole of the assessment: regurgitation is a normal developmental finding that needs teaching and reassurance, while vomiting is a symptom whose colour, force and timing point at pyloric stenosis, intestinal obstruction, raised intracranial pressure or sepsis.

Regurgitation is small in volume, effortless, unaccompanied by distress and occurs in a baby who is gaining weight normally; it is caused by a lax lower oesophageal sphincter, a short intra-abdominal oesophagus, a wholly liquid diet and lying flat.
Physiological reflux peaks at about 4 months and settles in the great majority of infants by 12 months as the sphincter matures and the child sits and takes solids.
Reflux becomes gastro-oesophageal reflux disease when it causes harm — poor weight gain, feed refusal, back-arching with irritability, recurrent aspiration pneumonia, apnoea or haematemesis from oesophagitis.
Projectile, non-bilious vomiting beginning at 3 to 6 weeks in a baby who is hungry immediately afterwards, with visible left-to-right gastric peristalsis and a palpable olive-shaped mass in the right upper abdomen, is infantile hypertrophic pyloric stenosis, commonest in first-born males.
Pyloric stenosis produces a hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria; ultrasound confirms it by pyloric muscle thickness and channel length, and the treatment is Ramstedt pyloromyotomy.
Pyloromyotomy is never an emergency operation — the emergency is the electrolyte derangement, and the child is not taken to theatre until the chloride, potassium and alkalosis are corrected, because anaesthesia in an alkalotic infant causes apnoea.
Bilious, green vomiting at any age means intestinal obstruction distal to the ampulla of Vater until proved otherwise; in the first weeks of life it is malrotation with midgut volvulus, which kills bowel within hours.
Vomiting with a bulging fontanel, an early-morning headache, a rising head circumference or altered consciousness is raised intracranial pressure, and with fever and neck stiffness it is meningitis.
A newborn vomiting with weight loss, dehydration, hyponatraemia and hyperkalaemia, especially with ambiguous genitalia or hyperpigmentation, is in a salt-losing crisis of congenital adrenal hyperplasia rather than having simple feed intolerance.
Management of simple regurgitation is positional and behavioural: smaller and more frequent feeds, correct attachment to reduce air swallowing, careful burping, and holding the baby upright for 20 to 30 minutes after a feed — but the baby is still put down on the back to sleep, because prone sleeping raises the risk of sudden infant death.

Pyloric stenosis

Infantile hypertrophic pyloric stenosis is progressive hypertrophy of the circular smooth muscle of the pylorus that narrows the gastric outlet until nothing leaves the stomach, and it is the commonest surgical cause of vomiting in infancy. The trap for the nurse is that it is a metabolic emergency and a surgical elective: the baby is dying of dehydration and hypochloraemic alkalosis, not of the pylorus, so the operation waits until the biochemistry is corrected.

Typically presents between 2 and 8 weeks of age, peaking at 3 to 6 weeks, in a firstborn male, with a male to female ratio of about 4 to 1 and a strong family history, especially on the mother's side. Exposure to erythromycin or azithromycin in the first two weeks of life increases the risk.
The vomiting is NON-BILIOUS and projectile, comes shortly after a feed, and the baby is immediately hungry again and feeds avidly - the hungry vomiter. Bilious (green) vomiting is never pyloric stenosis and means malrotation with midgut volvulus until proved otherwise, which is a true surgical emergency.
Examination signs: visible gastric peristaltic waves running from left to right across the epigastrium after a test feed, and a firm, mobile, olive-shaped mass in the right upper quadrant felt best from the baby's left side while she sucks on a dextrose-dipped finger with the stomach emptied by a nasogastric tube.
The classic biochemistry is a HYPOCHLORAEMIC, HYPOKALAEMIC METABOLIC ALKALOSIS from losing hydrochloric acid in the vomit, with a paradoxical aciduria appearing late when the volume-depleted kidney starts exchanging hydrogen ions to hold on to sodium.
Other findings: weight loss or a flat weight curve, dehydration with a sunken fontanelle and reduced urine output, constipation, and an unconjugated hyperbilirubinaemia in a small proportion of babies from reduced glucuronyl transferase activity, which resolves after the operation.
Ultrasound is diagnostic and has replaced the barium string sign: a pyloric muscle wall thickness of about 3 mm or more with a channel length of about 15 mm or more that fails to open during the study.
Pre-operative management is resuscitation: keep nil by mouth, pass a nasogastric tube on free drainage, and rehydrate with intravenous 0.9% sodium chloride (or 0.45% saline with dextrose as prescribed) with potassium chloride added once the baby is passing urine, continuing until the chloride is above 100 mmol/L, the bicarbonate is below 30 mmol/L, the potassium is normal and the baby is well hydrated.
The operation is a Ramstedt pyloromyotomy, open or laparoscopic, in which the hypertrophied muscle is split longitudinally down to but not through the mucosa. Feeds are restarted a few hours afterwards and built up; some vomiting in the first day or two after surgery is expected and settles.
Post-operatively watch for continued vomiting beyond 48 hours (suggesting an incomplete myotomy), fever or abdominal distension with peritonism (suggesting a mucosal perforation), and wound infection; check the blood sugar, because a starved infant becomes hypoglycaemic.

Hirschsprung disease

Hirschsprung disease is congenital absence of the ganglion cells of the Meissner submucosal and Auerbach myenteric plexuses in the distal bowel, caused by failure of neural crest cells to complete their craniocaudal migration during fetal life. The aganglionic segment cannot relax, so it is the NARROW distal segment that obstructs and the normally innervated bowel above it that dilates - the opposite of what the older name congenital megacolon suggests - and the disease kills through enterocolitis rather than through obstruction.

It occurs in about 1 in 5000 live births, is about four times commoner in boys, and always begins at the anus and extends proximally for a variable distance: rectosigmoid short-segment disease in roughly three quarters, long-segment disease in the rest, and total colonic aganglionosis in a small minority. It is associated with Down syndrome and with mutations of the RET proto-oncogene.
In the newborn it presents as failure to pass meconium within 48 hours with abdominal distension, bilious vomiting and refusal of feeds. About 90% of normal term babies pass meconium within 24 hours and 99% within 48 hours, which is what makes the delay significant.
In the older infant or child it presents as constipation dating FROM BIRTH, ribbon-like or pellet stools, a grossly distended abdomen with visible bowel loops, poor weight gain and anaemia.
The discriminator from functional constipation is the digital rectal examination: in Hirschsprung disease the rectum is EMPTY and tight and there is an explosive gush of gas and liquid stool as the finger is withdrawn, there is no soiling, and the child fails to thrive. In functional constipation the rectum is loaded with hard stool, the problem starts after infancy at around toilet training, soiling and stool withholding are common, and growth is normal.
Investigations: an unprepared contrast enema shows a narrow distal segment with a cone-shaped transition zone into dilated proximal bowel and retention of contrast beyond 24 hours; anorectal manometry shows absence of the rectoanal inhibitory reflex, the internal sphincter failing to relax when the rectum is distended.
Rectal suction biopsy is the gold standard and shows absent ganglion cells with hypertrophied nerve trunks and increased acetylcholinesterase staining. It must be taken at least 2 cm above the dentate line, because there is a normal zone of physiological hypoganglionosis immediately above the dentate line that would give a false positive result.
Initial management is decompression and resuscitation: nil by mouth, nasogastric tube on drainage, intravenous fluids and correction of electrolytes, and rectal washouts with NORMAL SALINE - never with plain water, which is absorbed across the bowel wall and causes water intoxication, hyponatraemia and seizures.
Definitive treatment removes the aganglionic segment and brings normally innervated bowel down to the anus, usually as a single-stage transanal pull-through (Swenson, Duhamel or Soave procedures), with a levelling colostomy first if the child is septic, malnourished or has a long segment.
Hirschsprung-associated enterocolitis is the leading cause of death and can occur before AND after the pull-through: fever, abdominal distension and tenderness, explosive foul-smelling diarrhoea, vomiting, lethargy and shock. Treatment is nil by mouth, aggressive intravenous fluids, broad-spectrum antibiotics including metronidazole, and rectal decompression with washouts.
After the pull-through, parents are taught anal dilatation as prescribed, perineal skin care because frequent stools excoriate the skin quickly, and the warning signs of enterocolitis, which they must be able to recite before discharge.

Glomerulonephritis — PSGN

Post-streptococcal glomerulonephritis is an immune-complex nephritis that follows infection with a nephritogenic strain of group A beta-haemolytic streptococcus and presents as the acute nephritic syndrome - haematuria, hypertension, oedema and oliguria with modest proteinuria. It is the commonest cause of acute glomerulonephritis in Indian children, usually between 5 and 12 years of age, and although more than 95% recover completely, a child can die in the first week from hypertensive encephalopathy or pulmonary oedema, so the first week is a blood pressure and fluid balance problem rather than a kidney problem.

The latent period is diagnostic: 1 to 2 weeks after streptococcal pharyngitis and 3 to 6 weeks after streptococcal pyoderma or impetigo. IgA nephropathy is the mimic and has NO latent period - the haematuria appears within a day or two of the sore throat, which is why it is called synpharyngitic.
Presentation: smoky, tea-coloured or cola-coloured urine, periorbital puffiness that is worst on waking, reduced urine output, hypertension, headache and malaise, and in severe cases breathlessness from circulatory congestion.
Urine microscopy shows dysmorphic red blood cells and RED CELL CASTS, which are the hallmark of bleeding from the glomerulus rather than from the lower tract; proteinuria is present but usually below the nephrotic range.
Complement C3 is LOW at presentation and returns to normal within 6 to 8 weeks, while C4 is usually normal because the alternative pathway is activated. A C3 that is still low after 8 to 12 weeks means the diagnosis is not post-streptococcal disease and a biopsy is needed to look for membranoproliferative glomerulonephritis or C3 glomerulopathy.
Evidence of the preceding streptococcal infection: a raised antistreptolysin O titre, which rises well after pharyngitis but poorly after skin infection because skin lipids inhibit the response, and anti-DNase B, which is the better marker after pyoderma; a throat or skin swab may still grow the organism.
Treatment is supportive. Restrict salt and fluid (fluid allowance calculated as insensible loss plus the previous day's urine output), weigh the child daily on the same scale, chart intake and output strictly, and record blood pressure four to six hourly. Give a loop diuretic such as furosemide 1 to 2 mg/kg for oedema and volume-dependent hypertension, and an oral calcium channel blocker for persistent hypertension.
A 10-day course of penicillin is given to eradicate the organism and stop its spread to contacts, but it does NOT alter the course of the nephritis once it has started. Corticosteroids have no place in uncomplicated post-streptococcal disease.
Dialysis is needed only for refractory fluid overload, severe hyperkalaemia, severe acidosis or uraemic complications; protein is restricted only while the child is uraemic, and normal diet is resumed as the urine output recovers.
Prognosis is excellent in children: gross haematuria clears in days to weeks, oedema and hypertension in one to two weeks, microscopic haematuria may persist for up to a year and low-grade proteinuria for some months. Recurrence is rare, unlike rheumatic fever, and unlike rheumatic fever it is NOT prevented by treating the sore throat with antibiotics - a discriminator worth memorising.

Nephrotic syndrome — paediatric

Nephrotic syndrome is the combination of heavy proteinuria, hypoalbuminaemia, oedema and hyperlipidaemia caused by increased permeability of the glomerular filtration barrier to protein. In a child between 1 and 10 years with no atypical features, about 90% of cases are minimal change disease, so treatment is started with corticosteroids WITHOUT a renal biopsy, and the danger to the child comes not from the kidney but from the infections and thromboses that follow the loss of protein in the urine.

Diagnostic thresholds: proteinuria above 40 mg per square metre per hour, or a urine protein-to-creatinine ratio above 2 mg/mg, or 3+ to 4+ on the dipstick on three consecutive days, with a serum albumin below 2.5 g/dL, oedema and raised cholesterol.
The oedema is pitting and gravity-dependent: it starts as puffiness around the eyes on waking and moves to the legs, scrotum or labia and the abdomen as ascites by evening. Puffy eyes in a child are far more often nephrotic syndrome than allergy, and the urine must be dipsticked before any antihistamine is given.
Definitions that examiners test: remission is urine protein nil or trace for 3 consecutive days; relapse is 3+ or 4+ for 3 consecutive days; frequent relapse is 2 or more relapses within 6 months of the first remission or 4 or more in any 12 months; steroid dependence is 2 consecutive relapses while on alternate-day steroid or within 14 days of stopping it.
First episode treatment per the Indian Society of Paediatric Nephrology: prednisolone 2 mg/kg per day (maximum 60 mg) daily for 6 weeks, then 1.5 mg/kg (maximum 40 mg) on alternate days for 6 weeks, then stopped - a 12-week course. A relapse is treated with daily prednisolone until remission, then alternate-day treatment for 4 weeks. Steroid resistance is defined as failure to achieve remission after 6 weeks of daily prednisolone, and it is that child who is biopsied.
Atypical features that call for a biopsy BEFORE steroids: age under 1 year or over about 12 years, gross or persistent microscopic haematuria, hypertension, a raised creatinine, a low C3, or extrarenal features such as a rash or arthritis.
Infection is the commonest complication and the commonest cause of death, because immunoglobulin G and complement factor B are lost in the urine. Spontaneous bacterial peritonitis is the classic one, most often caused by Streptococcus pneumoniae, followed by cellulitis of the oedematous skin, pneumonia and urinary infection.
Thrombosis is the second great danger: loss of antithrombin III with haemoconcentration causes renal vein, deep vein and cerebral sinus thrombosis, so these children are kept mobile, are not left with unnecessary central or femoral lines, and are kept adequately hydrated.
Hypovolaemia can coexist with gross oedema - abdominal pain, cold peripheries, tachycardia, a narrow pulse pressure, poor urine output and a high haematocrit - and it is treated with albumin or saline as prescribed, NOT with more diuretic, which will make it worse.
Nursing care: weigh at the same time daily on the same scale, measure abdominal girth, chart intake and output strictly, record blood pressure, teach the parent to dipstick the first morning urine at home and keep a diary, give no added salt while oedematous and on steroids, provide adequate protein and calories, elevate and meticulously care for oedematous scrotal and periorbital skin, and avoid intramuscular injections into oedematous tissue.
Immunisation and infection prevention: keep inactivated vaccines up to date including pneumococcal and annual influenza, give LIVE vaccines only when the child is off steroids or on low-dose alternate-day treatment, avoid contact with chickenpox and measles, and report any exposure so that prophylaxis can be considered.
For frequent relapsers and steroid-dependent disease, steroid-sparing agents are levamisole, cyclophosphamide, mycophenolate mofetil, calcineurin inhibitors such as tacrolimus, and rituximab; steroid-resistant disease is usually focal segmental glomerulosclerosis and is treated with a calcineurin inhibitor and an angiotensin-converting enzyme inhibitor.

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