suctioning, and corticosteroid therapy– Chloride resistant: hyperaldosterone state, Severe K depletion
• Metabolic acidosis– pH 7.10, PCO2 12, PO2 96, HCO3 10– Compensation is by hyperventilation-exhibited by low CO2– Bicarbonate losses occur as buffer system is imbalanced and other cations
must accompany loss in the kidneys subsequently causing a loss in these electrolytes-usually potassium and sodium.
• An electrolyte abnormality is often the first sign of an acid base disorder. The anion gap is the sum of routinely measured cations minus the routinely measured anions.
• Because of electrochemical balance, the concentrations of serum cations and anions are the same.
• In routine measurement of electrolytes, however, more anions are unmeasured than are cations; this leads to an expectedanion gap.
– Chem: Na 182, K 1.8, Cl 114, CO2 49, BUN 46, Creat 0.8, gluc 125, Ca 5.7, PO4 5.9, Mg 2.5, Tbili 0.6, AST 113, ALT 63, alk phos 335, Tpr 5.3, alb 3.3
– VBG: 7.42/79.6/26.0/49.9/20.2; Na >170, K 2.01, Cl 121, gluc 129, iCa 0.92
– EEG showed multiple seizures originating mainly from the right hemisphere, and at times from the left hemisphere, clusters of 10-30 seconds long electrographic seizures, some of which were associated with stiffening and changes in vital signs
• Loaded with keppra 20mg/kg, followed by maintenance dosing (100mg IV) q12h
• Also started on vitamin B6, 50mg IV BID (supports the GABAergic inhibitory interneuron system)
• Gained seizure control on scheduled keppra and phenobarbitol
• Extubated HD #7
• Started PO feeding HD #9; swallow study done after discharge showing aspiration of thin liquids; requires feeds with thickener and outpatient speech therapy
• Removed from mother’s care and placed in CPS custody in a foster home
• In severe hypernatremia (Na > 160 mEq/L)– Altered mental status
– Lethargy
– Coma
– Seizures
**in severe cases such as salt poisoning with a rapid rise in Na level, the rapid rise leads to acute brain shrinkage, which then results in vascular rupture with cerebral and subarachnoid hemorrhage, demyelination, and irreversible neurologic injury
• Associated with dysnatremias, both hypo and hyper (as well as aggressive correction of hyponatremia)
• Caused by severe damage of the myelin sheath of neurons in the brainstem
• In a literature review of 76 patients with CPM (worldwide over 5 decades), the majority (58/76) had moderate to severe neurological symptoms at time of diagnosis– 36/72 died but 7/72 had moderate to severe neurologic deficits and 26/72 had
mild deficits or were neurologically asymptomatic
• Imaging studies and increased awareness have likely improved the diagnosis of this disorder while also improving management and prevention of severe sequelae
• C. R. is a 5 month old male admitted from OSH ER near Mexican border after approximately 1 week history of cough and rhinorrhea without fever. Initially diagnosed with viral URI by an ER in Mexico, but when when symptoms persisted 3 days later with diarrhea and increased respiratory rate, mother went to PCP who sent her to the ER on US side.
• Social History: Lives with mother and 2 year-old brother with mother’s cousin and her husband in border town. Father lives in Mexico with paternal GM and 2 older siblings. Father smokes outside, no pets.
• Family History: Brother - Leukemia, Maternal GM - diabetes
• Vitals: Temp 97.9, HR 118, RR 45, B/P 94/42, 100% sats• General: Thin, non-toxic• Neuro: Alert, cries with exam, tracks and makes eye contact• CV: RRR, no murmur, pulses 2+ to bilateral upper and lower extremities• Resp: Clear bilateral breath sounds, no distress or accessory muscle use• FEN/GI: Soft, non-tender, non-distended, normal bowel sounds, no
hepatosplenomegaly, no palpable masses• Extremities: Full ROM, no edema or joint swelling• GU: Normal uncircumcised male• Integ: No rashes, warm and dry, pink, brisk refill• HEENT: Normocephalic, atraumatic, AFOSF, dry mucous membranes and tongue
• Babygram- Symmetric hyperinflation with a left retro-cardiac opacity consistent with atelectasis or infiltrate. Left femoral CVL present.
• RUS-Right kidney with mild fullness of pelvis. Left kidney with mild dilatation of renal pelvis. Diffuse patchy echogenicity consistent with medullary nephrocalcinosis.
Fluids and Electrolyte Problems:Which Kids are at Risk?
• Shock - Endothelial leak stimulates body to release ADH as osmolality rises; fluid repletion is required for correction; stress response occurs and cortisol is released
• Surgery - Causes non-osmotic stimuli for ADH release leads to hyponatremia; higher risk during neurosurgical and renal cases
• Disruption of the endothelial glycolax and loss of pre-capillary vasoconstriction causes a leak from the intravascular space which creates increase in interstitial volume, tissue edema and impairs organ function.
• Extubated and vasopressors weaned off HD on hospital day #2
• Significant evidence of pancreatitis identified
– Elevated lipase and amylase
– Necrotizing pancreatitis – pancreatic insufficiency as evidenced by low fecal elastase – prescribed creon 24000 2 tablets before each meal and one tablet with snacks
Fluid and electrolyte replacement - Bicarb is BAD!!
• Bicarbonate is not indicated
– No evidence that it supports metabolic recovery
– By restoring the circulatory volume, renal function and tissue perfusion will improve which will then reverse acidosis
– Rapid correction of acidosis can cause hypokalemia, the additional Na can increase hyperosmolality and alkali therapy can increase hepatic ketone production – all of which can slow recovery
• As the incidence of obesity and type 2 diabetes diagnoses increase in children, there is another diagnosis to be concerned with/aware of for hyperglycemia differentials
• DKA – characterized by severe depletion of water and electrolytes from both intra and extracellular fluid as well as absolute or relative insulin deficiency
• HHS – characterized by extreme elevations in blood glucose concentrations and hyperosmolality without significant ketosis as well as absolute or relative insulin deficiency
• How to calculate fluid correction in DKA • For moderate to severe DKA
– Initial bolus of NS or LR 10 ml/kg (max 1L) over 1 hr, may repeat x1 if needed; no more than 20 ml/kg unless hemodynamic compromise is present
• Once HDS, goal to replace remaining fluid deficit over 24-72 hours• 2500 ml/m2 or ~1.5x maintenance• Rate of fluid administration should not exceed 3000 ml/m2 in 24
hrs – increases risk of cerebral edema • After first 48 hrs, fluids can be liberalized to as much as 3500 ml/m2
• http://www.freepik.com/free-icon/question-mark_731610.htm• Carvounis, C. P, Nisar, S., Guro-Razunan, S. (2002). Significance of the Fractional Excretion of Urea in the
Differential Diagnosis of Acute Renal Failure. Kidney Int:62(6) p. 2223-2229.• Ranger, Adrianna M, Chaudhary, Navjot, Avery, Michael, and Fraser, Douglas (2012). Central Pontine and
Extrapontine Myelinolysis in Children: A Review of 76 Patients. Journal of Child Neurology: 27(8) p. 1027-1037. • Raman,S. & Peters, M. (2014). Fluid management in the critically ill child. Pediatr Nephrol (2014) 29:23–34 DOI
10.1007/s00467-013-2412-0• Dellinger RP, Levy MM, Rhodes A, et al: Surviving Sepsis Campaign: International guidelines for management of
severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637 • Weitz, J. Fluid management in paediatric shock. (2016). PAEDIATRICS AND CHILD HEALTH 27:1 • Moritz, Michael L. and Ayus, J. Carlos. (2005). Preventing neurological complications from dysnatremias in
children. Pediatric Nephrology 20: 1687-1700. • Somers, Michael J. and Traum, Avram Z. (2017). Hypernatremia in children. Downloaded from
www.uptodate.com on October 18, 2017. • Alobaidi, R., Morgan, C. & Basu, R. (2018). Association Between Fluid Balance and Outcomes in Critically Ill
Children: A Systematic Review and Meta-Analysis. JAMA pedatr. Published online Jan 22, 2018. doi:10.1001/jamapediatrics.2017.4540
• RAAS.png courtesy of Wikipedia. Retrieved from world wide web on November 28, 2017• Stress Response courtesy of VIBE_stressresponse_091913.png• What the endothelium does courtesy of med_hr.png• Fernando Santos, F., Flor A. Ordóñez, D.,Claramunt-Taberner, D. & Gil-Peña, H. (2015). Clinical and laboratory approaches in the
diagnosis of renal tubular acidosis. Pediatr Nephrol 30:2099–2107 DOI 10.1007/s00467-015-3083-9 • Bagga, A. & Sinha, A. Evaluation of Renal Tubular Acidosis. (2007). Indian J Pediatr 2007; 74 (7) : 679-686] • Madkaikar, M., Shabrish, S. & Desai, M. Current Updates on Classification, Diagnosis and Treatment of Hemophagocytic
Lymphohistiocytosis (HLH) Indian J Pediatr (May 2016) 83(5):434–443 DOI 10.1007/s12098-016-2037-y • Oh, G. & Sutherland, S. (2016). Perioperative fluid management and postoperative hyponatremia in children. Pediatr Nephrol (2016)
31:53–60 DOI 10.1007/s00467-015-3081y• Rosenbloom, Arlan I. The management of Diabetic Ketoacidosis in Children. Diabetes Therapy (2010) 1(2):103-120. • Orlowski, James P., Cramer, Cheryl L., and Fiallos, Mariano R. Diabetic Ketoacidosis in the Pediatric ICU. Pediatric Clinics of North
Diabetic ketoacidosis and hyperglycemic hyperosmolar state. ISPAD Clinical Practice Concensus Guidelines 2014 Compendium. • Agus, Michael S. D. and Wolfsdorf, Joseph I. (2005). Diabetic Ketoacidosis in Children. Pediatric Clinics of North America. (52) 1147-
1163. • Jeha, George S. and Haymond, Morey W. Treatment and complications of diabetic ketoacidosis in children and adolescents.
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