The short answer to this question is an emphatic “YES;” here is why…
A 3-day old, 2.5 kg term female presents to a local emergency department (ED) with poor feeding, loose, runny stools and respiratory distress since being discharged home the previous day. Lethargy and “breathing problems” worried the mother enough to bring her newborn daughter back to the hospital for evaluation. The ED physician took one look at this tiny patient and activated a transport team before she even began the physical examination and work-up.
Upon initial examination, the baby was ill-looking in appearance with jaundiced skin, poor turgor and an obviously sunken anterior fontanelle. She was tachypneic with intercostal retractions, and poor peripheral and central pulse quality. Per the mother’s report, the baby had no wet diapers within the past 12 hours and the last diaper change revealed copious amounts of milky white stool.
Prior to the transport team arrival, a peripheral intravenous line had been obtained in the right antecubital fossa and two (2), 10 ml/kg fluid boluses were initiated. The baby was placed under a radiant warmer. Laboratory studies were obtained with the following results:
Vital signs obtained just prior to the transport team’s arrival included a heart rate of 180-200 bpm, a respiratory rate of 60 – 70 breaths/min, a room air oxygen saturation between 95 and 98%, a blood pressure of 68/38 (MAP 48) and a rectal temperature of 35.3oC. The bedside monitor showed the following lead II rhythm:
Clinical Question
Even for neonatal experts (which I am not even close to), the primary question may be “where do you start?” You have a critically ill newborn, in shock, who is displaying dysfunction in several organ systems at 3 days of life. The answer to this question is to identify the most serious threat to this baby’s life and address it. Your role as a critical care transport provider is to stabilize and deliver this patient to expert care (in this case, a level IV nursery 20 minutes away by helicopter). Keeping this tiny patient alive relies upon how you establish your priorities and the patient’s response to your intervention for the short period of time that she is in you care.
Review of Pertinent Neonatal Electrolyte and Acid-Base Balance, and Management Principles
Total body water (TBW) changes significantly during the first year of life. In the newborn, TBW is approximately 75-80% of total body weight. This can be even higher in the newborn that is small for gestational age (SGA) (recall that the newborn in this case weighed 2.5 kg). This can explain why even the smallest loss in circulating blood volume or extracellular fluid (ECF) loss can have profound effects on a newborn’s tissue perfusion and cellular respiration. Additionally, a comparatively high metabolic and fluid turnover rate have important implications on glucose requirements and electrolyte balances. Illness can greatly exacerbate this.
Renal function and Glomerular Filtration Rate (GFR) in the developing newborn are naturally much lower compared to that of an older child or adult. This decreases the ability to regulate sodium and water. As their renal compensatory mechanisms are immature, the ability to regulate acid-base balance is also impaired. This makes the bicarbonate loss from Diarrhea and GI disturbance particularly concerning.
Diarrhea and GI loss remain as one of the primary causes of morbidity and mortality in the very young (in both developed and developing countries) with dehydration, shock and electrolyte imbalance as the primary cause of death and permanent disability. Hyponatremia, hypochloremia and hyperkalemia are primary electrolyte disturbances as a result of GI loss. Moreover, a GI disturbance can exacerbate existing issues in glucose regulation. This can make matters worse since the ability of the developing neonate to control glucose stores is naturally reduced during this developmental stage.
Potassium disorders (hyper- and hypokalemia) are common in the newborn with dehydration. This electrolyte plays a key role in electrical conduction to skeletal, smooth and cardiac muscle. If gone unregulated or untreated, this can result in cardiac arrhythmias, cardiac arrest, respiratory failure, muscle weakness and an exacerbation in GI disturbances. Hyperkalemia is common in the severely dehydrated newborn as metabolic acidosis from absolute bicarbonate loss causes a shift in potassium from intracellular to extracellular fluid.
Bicarbonate is important in the body’s buffering system and is a key component to acid-base balance. Neonates have a lower serum bicarbonate level as compared to adults and as previously noted, have immature renal compensatory mechanisms. Because of this, a natural source of bicarbonate replenishment is the base equivalents contained in mother’s milk or regulated formula. As this source of nutrition is not an option for the newborn with a feeding intolerance they are deprived of this base source.
In critical illness and acidosis, the bicarbonate level may become low because the cells are inadequately perfused and must revert to anaerobic metabolism for energy production. Logic would state that in this situation, management needs to focus on correcting the cause of the hypoperfusion rather than replacing bicarbonate. In fact, aggressive administration of bicarbonate in the neonate has been associated with deterioration in cardiac function, increases in intracellular acidosis, reduced tissue oxygenation and intraventricular hemorrhage.
In the case of severe dehydration due to diarrhea and / or absolute GI loss, the use of bicarbonate is most sincerely warranted. The typical dose is 0.5 mEq/kg of a 4.2% solution as an intermittent or continuous infusion.
Because of these key differences in anatomy and physiology, it is essential to monitor newborns for any indication of abnormalities in fluid and electrolyte balance. If oral hydration and nutrition strategies are ineffective or impractical, the newborn should receive parenteral therapy without delay. Establishing normal blood volume / TBW, tissue perfusion, electrolyte and acid-base balance is paramount. This should consist of at minimum, an isotonic crystalloid (Normal Saline or Ringers Lactate). In the above case, 5% Albumin could be considered in order to maintain the newborn’s colloid oncotic pressure (arguably, with signs of hepatic dysfunction, this would have been a reasonable choice). Bolus dosing should be 10 ml/kg per hour. Parameters to assess efficacy of therapy should be mean arterial pressure, heart rate, capillary refill time, core temperature, base deficit and blood glucose values.
Differential Diagnoses for this type of presentation may include:
- Sepsis
- Ductal-Dependent Cardiac Defect
- Biliary Atresia
- Inborn Error in Metabolism
- Congenital Adrenal Hyperplasia
Sequence of Events
Upon arrival of the transport team, the newborn’s glucose was reassessed and was found to be 89 mg/dl. Labs were reviewed and clinical examination was relatively unchanged from initial assessment. Volume resuscitation with an isotonic crystalloid was continued and a second peripheral intravenous line was established. A sodium bicarbonate infusion was ordered (this was mixed in a 10% dextrose containing solution and administered a “maintenance fluid” rate). The hyperkalemia was determined to be a priority as it was changing the morphology of the ECG tracing. Calcium Chloride (20 mg/kg) was slowly administered in order to stabilize cardiac cell membranes. The baby was then transferred to the pre-warmed transport isolette and skin temperature monitoring was initiated.
A couple of issues concerning to the referring staff that were not immediately addressed was:
- the baby’s tachypnea. The transport team recognized this as a compensatory mechanism for hypoperfusion and profound acidosis. Aggressively managing this could have made the disparity in acid-base balance worse. While tachypneic, the baby was exchanging gasses appropriately.
- The “milky white” stool in the baby’s diaper. This is typically a warning sign that the newborn is not properly digesting food. A white color can indicate a lack of bile from the liver to digest food. This was more than likely due to the acute liver dysfunction that the baby was experiencing and should be self-resolving was normal liver function / perfusion is re-established. While an abnormal finding, not a priority management goal for transport.
Take Home Points
- Especially in the newborn population, it is important to understand the cause of acidosis.
- Prioritize. Think about how your priority intervention will affect other issues (these issues do not exist in “silos”).
- Do not underestimate the simplicity of intravascular volume restoration, glucose and temperature regulation. These interventions alone can be life saving to the newborn.
- A critically ill patient does NOT automatically = aggressive airway management. Think about WHY a tachypneic newborn is tachypneic. However, since newborns have little reserve so be prepared for a rapid deterioration.
References
Ahmad, M. S., Wahid, A., Ahmad, M., Mahboob, N., & Mehmood, R. (2016). Prevalence of electrolyte disorders among cases of diarrhea with severe dehydration and correlation of electrolyte levels with age of the patients. Journal of the College of Physicians and Surgeons–Pakistan: JCPSP, 26(5), 394-398.
Caramelli, F., Cecini, M. T., Fae, M., Iannella, E., & Mondardini, M. C. (2019). Anesthesiological Considerations: Stabilization of the Neonate, Fluid Administration, Electrolyte Balance, Vascular Access, ECMO, Bronchoscopy, and Pain in Neonates. In Neonatal Surgery (pp. 7-24). Springer, Cham.
Collins, A., & Sahni, R. (2017, October). Uses and misuses of sodium bicarbonate in the neonatal intensive care unit. In Seminars in Fetal and Neonatal Medicine (Vol. 22, No. 5, pp. 336-341). WB Saunders.