how to properly Manage of new born with vomiting

RikzClanzo 189 views 39 slides May 07, 2024
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About This Presentation

vomiting in peads


Slide Content

MANAGEMENT OF NEWBORN VOMITING

DEFINITION Vomiting describes forceful expulsion (engaging abdominal and respiratory muscles) of the reflux out of the mouth. Recurrent or persistent vomiting warrants further investigations Persistent vomiting can be complicated by : Dehydration Hypokalemic hypochloremic metabolic alkalosis Malnutrition Constipation

Vigorous vomiting can result in: Esophageal mucosal tear (Mallory- Weis Tear) Esophageal rupture ( Boerhaave syndrome) ) Vomiting is a common, but nonspecific symptom May be acute, chronic or recurrent Acute : may be due to viral infections, e.g , Rotavirus Chronic : Cyclic – ≥ 5 episodes occurring at high intensity (≥4 emesis/hr) and infrequently (≤2 episodes/week) with normalcy period in between Chronic – frequent episodes (≥2/week) at low intensity (1-2 emesis/hr)

In the first day of life, vomiting suggests upper GI tract obstruction or increased ICP A common manifestation of: Overfeeding Incorrect/ inexperienced technique of feeding Normal reflux It could rarely be due to: Pyloric stenosis Milk allergy Duodenal ulcer Stress ulcer Inborn error of metabolism Adrenal insufficiency

VOMITING SCALE Mild:  1 - 2 episodes/ day Moderate:  3 - 7 episodes/day Severe:  Vomits everything, nearly everything or 8 or more episodes/ day The main risk of vomiting is dehydration. The younger the child, the greater the risk for dehydration.

PATHOPHYSIOLOGY Violent descent of the diaphragm and constriction of the abdominal muscles with relaxation of the gastric cardia actively force gastric contents back up the esophagus. This process is coordinated in the medullary vomiting center, which is influenced directly by afferent innervation and indirectly by the chemoreceptor trigger zone and higher central nervous system (CNS) centers

COMMON PRESENTATIONS IN THE HOSPITAL

1. BOWEL OBSTRUCTION It may be due to the following: Hypertrophic pyloric stenosis – presenting with projectile non-bilious vomiting between 3 - 6 weeks of age Bowel atresia Malrotation of volvulus Meconium plug syndrome Hirschprung disease Imperforate anus

Level of obstruction determines clinical presentation: Proximal obstruction- early vomiting with minimal distention Distal obstruction – late vomiting with distention Electrolyte imbalance and dehydration are common

TREATMENT 1. Prompt resuscitation 2. Urgent review by a surgeon 3. Do not give anything orally 4. Insert NGT (esp in vomiting and abdominal distention) 5. IV fluids to use are: half strength Darrow’s solution or normal saline + 5% dextrose Shock present: correct with 20ml/kg bolus of normal saline or Ringers lactate as IV bolus No shock but dehydrated: give 10-20ml/kg half strength Darrow’s sol. or N/Saline +5 % dextrose over 20 mins Then give maintenance fluid volume + same volume that comes out of NGT + any vomit

6. Administer antibiotics: Ampicillin (50mg/kg IV q6hrly) plus Gentamicin (5mg/kg IV OD) plus Metronidazole (15mg/kg as a single loading dose, followed by 7.5mg/kg q12hrly, starting 24 hrs after loading dose)

2. PYLORIC STENOSIS Most common surgical disorder of GI tract in infants Pylorus is thickened & elongated with narrowed lumen due to hypertrophy of circular fibers of pylorus 4 – 6x more common in boys

CLINICAL PRESENTATION Non-bilious vomiting gradually increasing in frequency & severity becoming projectile in nature Most present beyond 3 weeks of birth but 20% are symptomatic at birth The following result from recurrent and persistent vomiting: Dehydration Malnutrition Hypochloremic alkalosis Constipation

On examination after feeding: A palpable olive shaped mass in the mid-epigastric region (75-80% of cases) A vigorous peristaltic wave can be seen move from the left hypochondrium to umbilicus

INVESTIGATION: Abdominal USS Diagnostic test of choice Shows muscle thickness >4mm and pylorus length >16mm When in doubt? Barium study of upper GI tract Upper GI endoscopy

TREATMENT Rapidly correct dehydration and electrolyte abnormalities Refer to surgery: - Surgical (Ramstedt pyloromyotomy) correction is the tx of choice

3. MALROTATION

Rotational abnormalities developing during maturation of gut cause recurrent obstruction, occurring as either the Ladd’s band or volvulus of gut over the narrow mesenteric pedicle. 80 -90% occurs in first year of life Characterized by abdominal pain with bilious vomiting. - Abdominal distention may not be a prominent finding

Findings can be confirmed on barium meal follow through showing: duodenojejunal junction on right side of spine (instead of left of midline of pylorus), abnormally positioned cecum, and small bowel loops on right side of abdomen If volvulus is present? > Contrast appears as cockscrew appearance at level of second portion of duodenum

The corkscrew sign describes the spiral appearance of the distal duodenum and proximal jejunum seen in midgut volvulus

TREATMENT Resuscitate Refer for surgical laporotomy. Surgical correction is done through the Ladd’s procedure, which involves the following: Derotation of volvulus Division of Ladd’s band Widening of base of mesentery Placement of bowel in state of non-rotation Appendectomy

4. DUODENAL ATRESIA

Duodenal atresia is the congenital absence of a portion of the first part of the small bowel . Symptoms typically present shortly after birth. Present with either bilious or non-bilious vomiting It typically does not present with abdominal distension. A classical x-ray finding associated with duodenal atresia is the ‘double bubble sign.’

CLINICAL FEATURES Hallmark – bilious vomiting without abdominal distention on the first day of life Peristaltic waves may be visible early in the disease process Jaundice seen in 1/3 of infants

DIAGNOSIS “ double bubble ” appearance seen on plain abdominal xray Contrast studies are done to rule out malrotation and volvulus Diagnosis can be made prenatally by fetal USS which reveals a sonographic double bubble

TREATMENT 1. NGT and OGT decompression 2. IV fluid replacement 3. Evaluate for any associated anomalies Echocardiography Renal USS CXR X-Ray of spine Definitive treatment is usually delayed until life threatening anomalies are assessed and managed.

4. Refer for surgery – “Duodenoduodenostomy Post op: Gastrostomy tube is placed to drain stomach and protect airway IV nutritional support on transanastomotic jejunal tube is needed until an infant starts to feed orally

5. COW MILK PROTEIN ALLERGY

Most common food allergy in infants who are top fed Occasionally occurs in breastfed infants due to passage of cow milk antigen in breast milk Affects 2.5% of children with highest prevalence in 1 st year of life Family hx of atopy is common 50% outgrow the allergy by 1yr old and 95% by 5yrs old

TWO TYPES OF REACTION TO COW’S MILK Immediate – IgE Mediated Occurs within minutes of milk intake Characterized by the following: Vomiting pallor Shock like state Urticaria Angioedema Delayed – T Cell Mediated Has an indolent course Presents with GI symptoms

SYMPTOMS Diarrhea with blood and mucus Reflux symptoms (uncommon) Hematemesis (uncommon) Respiratory symptoms in 20-30% of cases Allergic rhinitis Asthma Atopic manifestations in 50-60% of cases Eczema Angioedema Iron deficiency Hypoproteinemia Eosinophilia

DIAGNOSIS Sigmoidoscopy Apthous ulcers Nodular lymphoid hyperplasia Rectal biopsy Predominant eosinophils Elimination and challenge test Gold standard diagnostic test for any food allergy Symptoms subside after removal of milk and recur within 48hrs of re-exposure

TREATMENT 1. Remove all animal milk/ milk products from diet 2. Alternatives to cow’s milk Soy milk Extensively hydrolyzed formula Elemental amino acid formula ( for those who cannot tolerate extensively hydrolyzed formula ) 3. Counsel and educate parents on diet and calcium supplements

Symptomatic relief for gastroenteritis can be achieved through the use of anti-emetic agents such as Ondansetron in infants and children 6 months of age and older. Assess and treat for dehydration and electrolyte disturbances. Mild dehydration can be treated with encouragement of oral fluids Moderate to severe dehydration should be treated with IV fluids.

Outcomes of full-term infants with bilious vomiting: observational study of a retrieved cohort Syed Mohinuddin 1, Pankaj Sakhuja 1, Benjie Bermundo 1, Nandiran Ratnavel 1, Stephen Kempley 2, Harry C Ward 3, Ajay Sinha 2 Abstract Bilious vomiting in a neonate may be a sign of intestinal obstruction often resulting in transfer requests to surgical centres . The aim of this study was to assess the use of clinical findings at referral in predicting outcomes and to determine how often such patients have a time-critical surgical condition ( eg , volvulus, where a delay in treatment is likely to compromise gut viability). Methods:  4-year data and outcomes of all term newborns aged ≤7 days with bilious vomiting transferred by a regional transfer service were analysed . Specificity, sensitivity, likelihood ratios, correlations, prior and posterior probability of clinical findings in predicting newborns with surgical diagnosis were calculated. Results:  Of 163 neonates with bilious vomiting, 75 (46%) had a surgical diagnosis and 23 (14.1%) had a time-critical surgical condition. The diagnosis of a surgical condition in neonates with bilious vomiting was significantly associated with abdominal distension (χ(2)=5.17, p=0.023), abdominal tenderness (χ(2)=5.90, p=0.015) and abnormal abdominal X-ray findings (χ(2)=5.68, p=0.017) but not with palpation findings of a soft as compared with a tense abdomen (χ(2)=3.21, p=0.073). Abnormal abdominal X-ray, abdominal distension and tenderness had 97%, 74% and 62% sensitivity, respectively, with regard to association with an underlying surgical diagnosis. Normal abdominal X-ray reduced the posterior probability of surgical diagnosis from 50% to 16%. Overall, clinical findings at referral did not differentiate between infants with or without surgical or time-critical condition. Conclusions:  We recommend that term neonates with bilious vomiting referred for transfer are prioritised as time critical.

REFERENCE Nelson’s Textbook of Pediatrics, 19 th Edition Ghai’s Essential Pediatrics, 9 th Edition WHO Pocket Book Of Hospital Care for Children, 2 nd Edition Drug Doses, Frank Shann, 17 th Edition

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