An infant with hypertrophic pyloric stenosis presents with severe vomiting after one week of onset of symptoms. What is the most likely metabolic abnormality in this patient?
Ref : 1 .Sabisum Textbook of Surgery, 19th Edition, Pg: 1841.2. Bailey A Love's Short Practice of Surgery, 25th Edition, 1066.Explanation:The vomiting of hydrochloric acid results in hypochloraemic alkalosis but, initially, sodium and potassium levels may be relatively normal.As dehydration progresses, more profound metabolic abnormalities arise, partly related to renal dysfunction.Initially, the urine has a low chloride and high bicarbonate content, reflecting the primary metabolic abnormality.This bicarbonate is excreted along with sodium and so, with time, the patient becomes progressively hyponatraemic and more profoundly dehydrated.Because of the dehydration, a phase of sodium retention follows and potassium and hydrogen are excreted in preference.This results in the urine becoming paradoxically acidic and hypokalaemia ensues.Loss of HCI in vomiting|Hypochloremic alkalosis|Renal excretion of bicarbanote along with sodium(Base HCO3 excretion to compensate for less of acid Hcl)|Dehydration|Renal retention of sodium|Potassium and Hydrogen excreted in exchange of Sodium|Hypokalemic hypochloremic metabolic alkalosiswith paradoxical aciduriaHypertrophic pyloric stenosisAetio PathologyMost common GI surgical disorder in early infancyMost common between the ages of 2 and 8 weeks. (Does not present immediately afterbirth)Male: Female - 4:1First-born male infants being at highest risk.Hypertrophy of the circular muscle of the pylorus results in constriction and obstruction of the gastric outlet, leading to nonbilious & projectile emesisEmesis leads to Loss of hydrochloric acid with the onset of hypokalemic hypochloremic metabolic alkalosis, and dehydration.Exact cause for HPS remains unknown; a lack of nitric oxide synthase in pyloric tissue has been implicated.Clinical PresentationProgressively worsening nonbilious emesis.With time, the emesis becomes more frequent, forceful, and projectile in nature.Visible gastric peristalsis - A wave of contractions from the left upper quadrant to the epigastrium.Shortly after emesis, infants usually crave additional feedings.Palpation of the pyloric tumor (olive-shaped) in the epigastrium or right upper quadrant by an experienced examiner is pathognomonic for the diagnosis. .If the olive is palpated, no additional diagnostic testing is necessary.InvestigationsAbdominal RadiographUpper abdominal gas bubble in the stomach.UltrasoundA persistent pyloric muscle thickness more than 3 to 4 mm or a pyloric length more than 15 to18 mm in the presence of functional gastric outlet obstruction is diagnostic.When the olive is nonpalpable. the diagnosis of HPS can be made by ultrasoundUpper GI Contrast:With equivocal clinical history, an upper GI contrast study is useful to evaluate for other causes of vomiting.Treatment:Surgical ManagementThe treatment of HPS is py loro myotomy,Incising through thickened pyloric musculature while preserving the underlying mucosaRight upper quadrant or periumbilical incision is usedLaparoscopic pyloromyotomy has better cosmesis, with similar outcomes to those of the open technique.Preop and Post op management:Before surgery, it is important that the infant be fully rehydrated with IV fluids to establish an adequate urine output and correct electrolyte disturbances such as metabolic alkalosis.Because the infant with underlying metabolic alkalosis will compensate with respiratory acidosis, postoperative apnea may occur. Thus, the serum HC03 level needs to be normalized before surgery.Postoperative ly, infants are usually allowed to resume enteral feedings.Complications include incomplete myotomy, mucosal perforation, and wound infection
Hypokalemic hypochloremic metabolic alkalosis
Hypokalemic hypochloremic metabolic acidosis
Hyperkalemic hyperchloremic metabolic alkalosis
Hypokalemic hyperchloremic metabolic acidosis
Benign Gastric Disease