Shortly after his arrival he had a large volume approximately mL of nonbilious projectile vomit. He described general weakness and fatigue the previous night and on waking, with no history of headaches, diarrhea, fevers, or other symptoms of infection.
In the past 4 months he had experienced intermittent generalized abdominal pain, nausea, anorexia, vomiting, and mild weight loss 3 kg. He had presented 2 months earlier with vomiting. Investigations including a complete blood count, electrolytes, liver function tests, albumin-corrected calcium, magnesium, and phosphate were within reference intervals at that time.
An abdominal ultrasonography was unremarkable. The episodes of vomiting had become increasingly more frequent and forceful. His past medical history was otherwise unremarkable. He was intermittently drowsy but easily rousable. He had no focal neurological signs, and his power and reflexes were essentially normal.
There were no cardiac murmurs, and his respiratory examination was unremarkable. His abdomen was soft and nontender, with normal bowel sounds. Biochemical testing on presentation showed hypokalemia, hypochloremia, and hyperbicarbonatemia Table 1. He had evidence of dehydration and prerenal azotemia increased urea, creatinine, and urate and normal total protein and albumin.
His liver function tests, lipase, thyroid function tests, albumin-corrected calcium, phosphate, and magnesium were normal. An electrocardiogram revealed a prolonged corrected QT interval QTc ms. Despite the normal albumin-corrected calcium, the presence of carpopedal spasms and the prolonged QTc interval prompted the collection of a venous blood gas, which revealed hypocalcemia [ionized calcium of 0. In the setting of metabolic alkalosis, the respiratory drive is typically reduced as part of the process of respiratory compensation, with the rise in PCO 2 blunting the rise in pH.
The presence of tachypnea in this patient was thought to be due to hyperventilation related to anxiety and distress and potentially may have further worsened the alkalosis and ionized hypocalcemia, leading to acute symptoms. What are some of the common causes of metabolic alkalosis in pediatric populations? What is the clinical significance of urinary chloride concentration in distinguishing among the causes of metabolic acidosis?
What is the effect of pH change on the total and ionized calcium concentrations? The patient was managed acutely with intravenous calcium gluconate, fluid resuscitation and rehydration with normal saline, and intravenous potassium chloride replacement. He was then commenced on maintenance oral calcium carbonate.
Following the normalization of the ionized calcium, correction of the metabolic alkalosis, and cessation of the oral calcium replacement for 24 h, the parathyroid hormone also normalized. Over the proceeding days, he continued to experience nausea, limited oral intake, and vomiting. Magnetic resonance imaging of the brain excluded an intracranial lesion as a cause of his chronic vomiting.
An abdominal ultrasound demonstrated a diffusely thickened and irregular pylorus with no evidence of external compression. Gastric outlet obstruction was confirmed with a fluoroscopic barium meal study Fig. It was thought that the potential contribution of hypocalcemia-related pyloric spasm to the severity and chronicity of the vomiting was not significant owing to the absence of alkalosis, hypocalcemia, or abnormalities on the abdominal ultrasonography performed when he presented 2 months earlier.
Gastric outlet obstruction at the pylorus of the stomach is indicated by the arrows. Contrast agent within the stomach is observed to reflux back from the body of the stomach as a peristaltic wave arrives at the gastric outlet obstruction. Endoscopy revealed ulcerative esophagitis and antral gastritis. Antral biopsy was strongly positive on the rapid urease test; Helicobacter pylori infection was confirmed on culture. The patient was managed with antibiotic therapy amoxicillin and clarithromycin and a proton pump inhibitor.
His nausea and vomiting settled over the subsequent few days and his appetite markedly improved. In the pediatric population, hypokalemic, hypochloremic metabolic alkalosis is seen in the neonatal period as a result of idiopathic hypertrophic pyloric stenosis leading to chronic gastric outlet obstruction.
Less common causes of pediatric gastric outlet obstruction include malrotation, midgut volvulus, and antral webs in the first year of life and Crohn disease and hiatus hernia in later childhood. Neoplasia, although rare in childhood, should be considered in the differential diagnosis. In addition to primary gastric lymphoma and adenocarcinoma, external compression can result from a wide range of tumors, including hepatoblastoma, hepatocellular carcinoma, pancreatoblastomas, and soft-tissue sarcomas of the mesentery or abdominal viscera 1.
It is infrequently seen in childhood. Obstruction results from acute peptic ulcers due to inflammation-induced edema and tissue deformation, whereas chronic peptic ulcer disease leads to scarring and tissue remodeling as part of the healing process 3.
Helicobacter pylori infection is commonly associated with dyspepsia and nausea, which may exacerbate the vomiting 3. Metabolic alkalosis can also result from exogenous base from iatrogenic causes such as bicarbonate-containing intravenous fluids, antacids, and oral cation-exchange resins and is also seen in Milk-alkali syndrome 4. The typical renal response to hypovolemia and hypochloremia secondary to excessive gastric loss of hydrochloric acid observed in prolonged vomiting includes the preferential reabsorption of sodium and excessive reabsorption of bicarbonate in the absence of adequate chloride to maintain electrical neutrality and the secretion of hydrogen and potassium in exchange for sodium.
Management is aimed at ensuring that the patient is total body water replete, with water and oral or intravenous sodium-chloride replacement as the mainstay of therapy. The patient's clinical presentation was consistent with hypocalcemia, confirmed on ionized but not albumin-corrected calcium, in the context of metabolic alkalosis. The increase in calcium binding by albumin has been reported to reach clinical significance at pH 7. The pattern of discordance varied, with no consistent bias in a particular direction for any specific method.
In the case of this patient, the discrepancy between ionized calcium [ion-selective electrode measured on a Radiometer ABL series blood gas analyzer Radiometer Medical ] and albumin-corrected calcium was due specifically to the altered protein binding of calcium from the metabolic alkalosis. Other factors need to be considered when investigating potential causes of discrepancies between the albumin-corrected calcium and ionized calcium.
These causes include chelation by collection tube additives such as citrate, EDTA, and unfractionated heparin; hyperalbuminemia and hyperproteinemia; and increased fatty acids that enhance calcium binding by albumin 5.
The presence of true hypocalcemia was supported by the finding of an increased parathyroid concentration, which subsequently normalized with correction of the ionized calcium. Chronic vomiting secondary to gastric outlet obstruction can result in the biochemical syndrome of hypokalemic, hypochloremic metabolic alkalosis.
Peptic ulcer disease was previously recognized as the most common cause of gastric outlet obstruction in adults before the era of targeted Helicobacter pylori treatment.
It should still be considered a potential cause in both the adult and the pediatric populations. Changes in pH can affect the degree of calcium binding to protein both in vitro and in vivo. In the presence of disorders of acid—base balance, measurement of ionized calcium should be performed when evaluating disturbances of calcium homeostasis.
This illustrative case demonstrates the importance of ionized calcium measurements in conditions characterized by perturbations of acid—base balance.
In addition, it highlights the need to consider peptic ulcer disease, particularly in association with Helicobacter pylori infection, as a cause of gastric outlet obstruction in the pediatric population.
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He improved after treatment with racemic epinephrine and dexamethasone. The following week, his symptoms returned and he again was diagnosed with croup. His laboratory tests were significant for severe hypocalcemia serum calcium of 4. This episode was attributed to recent initiation of potassium phosphate. Hypocalcemia resolved with intravenous and enteral calcium supplementation and discontinuation of potassium phosphate. The cholecalciferol was discontinued.
About one week later he underwent lysis of intra-abdominal adhesions due to pain and abdominal distention with PD. Due to recurrence of symptoms and leakage of PD fluid, he was admitted for initiation of hemodialysis HD due to ultrafiltration failure.
His was dialyzed on a 2. Five days after discharge, he developed a hemoglobin level of 6. Two days later, during his outpatient HD treatment, he was noted to have hyperkalemia potassium of 6. He had persistent hyperkalemia at his next dialysis visit potassium level of 6. He also had persistent diarrhea. Two days after starting SPS, he had potassium of 4. Three days later the patient was noted to be hypokalemic potassium of 3.
Telemetry showed appropriate sinus bradycardia overnight without evidence of heart block. Calcium levels improved to 8. Most recently, he has maintained a stable calcium of about 8. Within a week after initiation of the medication, both developed hypocalcemia on routine labs without overt clinical manifestations. Potassium exchange resins are used to treat hyperkalemia in CKD frequently. It removes potassium by exchanging sodium ions for potassium ions in the intestine before the resin is excreted.
Hypokalemia, hypocalcemia, and even tetany have been described after SPS therapy [ 1 , 2 ]. A study done by Greenman et al. The affinity of ion-exchangers for cations of bivalent elements such as calcium is greater than that for univalent ions such as potassium.
Among the univalent ions, the affinity for hydrogen ions exceeds most others [ 5 ]. There is a steady loss of calcium in the gut which leads to a risk of gradual demineralization of bone when patients are maintained on cation exchangers for months to years. These studies noted that when patients developed hypocalcemia, the serum calcium levels increased only temporarily with supplementation.
The rapid removal of calcium is likely due to deposition in the bones [ 2 , 5 ]. Our patients however, were noted to have an acute drop in their serum calcium levels within a week of initiation of SPS therapy. Their hypocalcemia responded rapidly to calcium supplementation. Multiple studies have been done measuring the calcium and potassium content in formulas pretreated with SPS.
In , Starbuck showed a decrease in potassium and calcium ion content and an increase in sodium content of milk treated with SPS [ 7 ].
A more recent study by Bunchman et al. Human testing in five patients did not show any clinical symptoms of hypocalcemia [ 8 ]. Hobbs et al. There are case reports of metabolic alkalosis occurring in patients receiving alkali therapy along with SPS [ 1 , 10 ]. This occurs because, in the presence of an ion exchange resin, the salt formed by interaction of the antacid with hydrochloric acid in the stomach does not neutralize the bicarbonate in the small bowel.
The bicarbonate that is reabsorbed by the gut cannot be excreted in the presence of poor renal function, leading to metabolic alkalosis. Newer agents, including sodium zirconium cyclosilicate and patiromer have been studied for the use management of chronic hyperkalemia in patients with CKD [ 3 , 11 , 12 ].
Details comparing currently available drugs used for hyperkalemia are shown in Table 1. Metabolic acidosis of chronic renal failure usually protects patients from overt symptoms of hypocalcemia. Tetany or seizures may occur when acidosis is corrected rapidly without correcting hypocalcemia at the same time.
This report illustrates the necessity of very close monitoring of electrolytes, calcium, and phosphorus balance in pediatric patients on dialysis. Newer agents including patiromer and sodium zirconium cyclosilicate are potentially safer medications for management of hyperkalemia in patients with CKD.
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Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Aadil Kakajiwala , 1,2 Kevin T. Academic Editor: Salih Kavukcu. Received 24 Apr Accepted 03 Jul Published 01 Aug Abstract Background. Introduction Sodium polystyrene sulfonate SPS is a cross-linked polymer, used in the treatment of hyperkalemia. Case Presentation 2.
Case 1 An month-old male child with steroid resistant nephrotic syndrome due to diffuse mesangial sclerosis rapidly progressed to end stage renal disease. Figure 1. Sodium polystyrene sulfonate SPS Sodium zirconium cyclosilicate Patiromer FDA approval Approved Still pending Approved in adults Mechanism of action Nonspecific sodium-cation exchange resin Selective potassium cation binding agent Calcium based cation exchange resin Adverse effects Colon necrosis , GI disturbances, hypokalemia, hypomagnesemia, hypocalcemia, metabolic alkalosis GI disturbances, hypokalemia GI disturbances, hypokalemia, hypercalcemia, hypomagnesemia.
Table 1. Potassium sparing agents for management of hyperkalemia [ 3 ]. References H. Macaulay and G. Chaitman, D. Dixit, and M. View at: Google Scholar L. Greenman, J. Shaler, and T. Dock and N.
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