Welcome to the Multiprofessional Critical Care Review Course, Pediatric. Welcome to the SCCM MCCR Pediatric Review Course. This lecture is Fluids, Electrolytes, and Acid-Based Disorders. My name is Nick Ettinger, and I'm a Pediatric Intensivist at Texas Children's Hospital and Baylor College of Medicine in Houston, Texas. So the objectives for this talk are to understand the etiologies, the clinical manifestations, and treatment plans for various electrolyte abnormalities, and to understand the etiologies, clinical manifestations, and treatment plans for acid-based abnormalities. Just as a reminder, and background knowledge, remember that our body composition is two-thirds intracellular with respect to fluids, and one-third extracellular. And then of that extracellular component, three-fourths of the fluids are located in the interstitial space, and one-quarter of our fluids, of the extracellular fluids, are located in the intravascular or plasma space. A typical adult male is thought to be about 60% water, a typical adult female about 50% water, a child is thought to be 60% water, and an infant more like 70% water. So a typical textbook 70-kilo male adult would be about 42 liters of water. And I've also included typical blood volume estimates for adults and kids as well. This slide shows a table with the composition of some typical body fluids, and also some common IV fluids that are used in the ICU. As shown here, the typical plasma sample has a high sodium, a high chloride, and a low potassium, whereas intracellular fluid is the exact opposite, low sodium, low chloride, and high potassium, as well as high phosphate. Diarrhea, diarrheal fluids, can often represent a significant loss of electrolytes and buffer or bicarbonate, and as well as gastric aspirates can also result in loss of potassium, along with other electrolytes. Over here you can see the composition of typical IV fluids that are used in the ICU, in particular D5-normal saline, D5-LR, and plasmolyte. And the main thing to notice here is that the chloride composition of both lactated ringers and plasmolyte is significantly less than normal saline. Both LR and plasmolyte have some buffer, and as a result, their pHs are quite a bit more positive than normal saline pHs. So total daily fluid requirements for a hospitalized child are the sum of several different components, and the significance of each of these components depends on what's going on with the child and their clinical condition. And here we're talking about maintenance fluids, we're talking about replacement of intravascular fluid deficits, we're talking about replacement of ongoing losses, and all of that together is the total daily fluid requirements. So maintenance fluids are the fluids required to maintain normal hydration, or uvulemia, in the absence of other deficits or losses. Maintenance fluids are replacing fluids that are lost from two different sources. Sensible losses, that are daily things like sweat and moisture in breathing that are quite hard to measure, and sensible losses, which are things like water that we lose in the urine and stool that we can measure. Typically, we use the Holliday-Seger method to calculate maintenance fluids for a typical child, assuming their renal function is normal. And the estimate here uses the 4-2-1 rule, where you have four cc's per kilo for the first 10 kilos, two cc's per kilo for the second 10 kilos, and then one cc's per kilo for every kilo above 20 kilos. You can also use body surface area calculations with somewhere between 1,500 to 1,600 milliliters per meter squared per day, and then insensibles are typically calculated at 400 milliliters per meter squared per day. So deficits can be from various sources or causes. They can be gastrointestinal losses, such as vomiting, diarrhea, or NG suction. They can be blood loss, as from trauma or if you have bleeding disorders. They can be from excessive heat losses, sweating, or fever, or heat stroke. They can be from excessive respiratory losses, from tachypnea. They can be from intravascular leak in the situation of distributive shock, like in sepsis or anaphylaxis, or when you have cytokine release syndrome, or when your albumin levels are extremely low. So the type of fluid to replace deficits, which is really what kind of fluids do I need to resuscitate, have to be tailored to the individual patient and the circumstance. So for instance, a child who's injured in a car crash with significant loss of blood needs transfusion of whole blood or PRBCs. A child who presents with lots of days of vomiting needs IV fluid replacement with isotonic fluids to restore the intravascular volume. A child who presents with a history of severe diarrhea will need IV replacement with isotonic fluids to restore intravascular volume, but then also may require some extra bicarbonate to replace the loss from the stool. Children who present with hypernatremia and dehydration will need careful, slow rehydration with relatively hypotonic fluid on top of their maintenance fluids to correct the fluid deficit and hypernatremia. What about replacement of ongoing losses? Similarly, ongoing losses should be replaced with fluids that are similar to the type of fluid that's lost. Generally speaking, begin with isotonic fluids and then add other electrolytes and or blood as needed. So for example, diarrhea where you have copious amounts of stool, you're losing a lot of water, you're losing a lot of electrolytes. In particular, you're often losing a lot of bicarbonate, so you may have to add bicarbonate to those replacement fluids. For hemorrhage or for trauma, you're losing blood, so you need to replace with blood and other blood products. And then in a post-surgical child, maybe a child who's got a nasogastric tube set to suction who has an ileus or a bowel obstruction, they may lose a lot of free water and electrolytes, and so you have to monitor for those losses carefully. How do we think about disorders of sodium? So as I mentioned, sodium is the main extracellular positive ion, and sodium is the primary driver of the calculation for serum osmolality, which is shown here. Serum osmolality is two times the serum sodium plus the serum glucose level divided by 18 plus the BUN divided by 2.8. And in a typical normal healthy person with normal numbers, that comes out to be about 290. So where is sodium sensed? It's sensed in two places, in the thalamus due to osmoreceptors that sense fluctuations in plasma and CSF osmolality. If there's elevated osmolality, that stimulates the pituitary to release arginine vasopressin, which then circulates through the body and then arginine vasopressin triggers the kidney to reabsorb water from the ultrafiltrate. And so therefore, if you have damage to the pituitary, damage to the hypothalamus, this can impair normal thirst mechanisms and or abilities to secrete arginine vasopressin. In the kidney, sodium is sensed via tubuloglomerular feedback via the juxtaglomerular apparatus that is in the distal collecting tubule, and the JGA senses sodium in the capillary blood flowing through the glomerulus and adjusts sodium reabsorption accordingly. First, let's talk about hypernatremia, which is defined as sodium levels greater than 145 milliequivalents per liter. Hypernatremia can be thought of as, relatively speaking, a greater loss of free water compared to sodium or an excess of sodium intake. So what are some of the causes of hypernatremia? Hypernatremia can be caused by decreased fluid intake. For instance, if there's circumstances with impaired thirst mechanisms from a neurologic injury or there's insufficient free water intake, just you don't drink enough. You can have impaired arginine vasopressin or ADH signaling from a lack of production from a central diabetes insipidus from a tumor or trauma or surgery, or if you have nephrogenic diabetes insipidus, either from genetic causes or from drug-induced nephrogenic DI. You can have loss, relatively speaking, loss of hypotonic fluid from things like DKA, lots of GI losses from diuretics, from the polyureic phase after someone experiences acute tubular necrosis, and also sometimes from burn injuries. Or you can have, relatively speaking, an excess of hypertonic sodium gain. This could be from excess sodium and chloride ingestion, from too much hypertonic saline, or from too much normal saline or sodium bicarbonate resuscitation. What's the treatment? First, you have to identify what is the likely cause from a combination of looking at the patient history, what's the physical exam, and what are the patient labs. Importantly, assessing is the intravascular volume adequate right at the beginning, and if not, first using isotonic fluids to restore that intravascular volume. Then once at least the intravascular volume is stable, the goal is slow correction of the hypernatremia by calculating the free water deficit, which is the percent total body water times the weight times the current sodium divided by the goal sodium minus one. And then correcting that deficit slowly over the course of 24 to 48 hours by giving hypertonic fluids on top of the normal maintenance IV fluids. And the goal for correction is less than 0.5 milliosmoles per kilo per hour, which works out to be something like 6 milliosmoles per kilo for every 12 hours of correction. What about hyponatremia, which is defined as a sodium less than 135? Causes of hyponatremia, it's key to first assess what is the total overall body fluid status. Is the patient hypervolemic, are they uvolemic, are they hypovolemic? And that sometimes can be a clue to diagnosis. If the patient is hypovolemic, this can result from extrarenal or non-kidney fluid losses like GI losses or third spacing. It can result from renal losses through the action of diuretics or adrenal insufficiency or renal tubular acidosis. It could be from cerebral salt wasting in the context of a tumor or trauma or subarachnoid hemorrhage or meningitis. If the patient is uvolemic, then the hyponatremia could result from a relatively excess amount of hypotonic fluid intake, as is the case with hypotonic IV fluids, potentially with incorrect baby formula, with incorrectly made TPN, or from SIADH, which can result from various causes such as meningitis, pneumonia, or head trauma syndrome of inappropriate ADH. If the patient is hypervolemic, this can result from congestive heart failure and fluid retention. It could result from hepatorenal syndrome, or it could result from acute or acute on chronic acute kidney injury. There's also the condition of pseudohyponatremia, which is artificially low serum sodium measurements due to very high hyperlipidemia or hyperproteinemia or excess amounts of osmotically active substances like glucose in the context of hyperglycemia and DKA. So what's the workup for hyponatremia? First assess total body fluid status. Is the patient hypervolemic, uvolemic, hypovolemic? Assess their history and labs. Was this an acute change? Was this slower or a chronic change? In particular, look at serum chemistry, serum osmolality, urine sodiums, and urine osmolality. A little more details on the workup will be on the next slide. Then in terms of treatment, if the cause is deemed to be syndrome of inappropriate ADH secretion, SIADH, the answer is restrict fluid intake. In particular, if the cause is deemed to be inadequate sodium intake, looking at total daily needs and examining what the intake is from. If sodium levels are extremely low, in particular if serum sodium levels are less than 120, the goal would be to urgently correct those levels to at least above 120, especially if the patient is seizing, to prevent spontaneous seizures. This can be estimated by 0.6, the volume of distribution, times the weight, times what your goal sodium minus what your actual measured sodium is. For example, if the serum sodium is 116 and the goal is 130, you're not necessarily trying to get to normal, you're just trying to get out of the danger range and you have a 15-kilo child. This would be 0.6 times 15 times the difference of 116 from 130, which would equal 126 milliequivalents, which as 3% sodium is about 0.5 milliequivalents per mL, that would end up being approximately 250 mLs of 3% sodium that you could give semi-urgently to the patient to prevent seizures. This slide presents an overall workup for hyponatremia. Again, the first step is assessing total body fluid status, are they hypovolemic, are they uvolemic, are they hypovolemic, and assessing their history and labs. Is it acute change? Is it a slower or chronic change? And looking at serum chemistry, serum osmolality, urine sodium, and urine osmolality to figure out the specific cause. What about disorders of sodium in terms of tips for the boards? So the boards like questions about sodium disorders. In particular, if there's a question about SIADH, this is typically considered to be a uvolemic condition on the boards where you have relatively too much water, or you have inappropriate urinary water retention leading to intercellular volume overload, but not significant intervascular volume overload. What are some tip-offs that this is SIADH? You'll have a hypoosmolar serum and an inappropriately concentrated urine. Why inappropriate? If your serum osmolality is low, the kidneys should be trying to lose water to raise that serum osmolality, not concentrate the urine. You might see hyponatremia with a low to no urine output, and for the boards, the treatment for SIADH is always going to be fluid restriction rather than sodium administration to correct the hyponatremia. By contrast, cerebral salt wasting is usually a hypovolemic condition where you have too little sodium. The tip-offs here will be some sort of history, like a car accident with head trauma, non-accidental trauma, a patient who's had CNS surgery of some kind, like a tumor removal or a CNS bleed, something like that. In terms of lab values, you'll have hyponatremia with an inappropriately high urine sodium. Why inappropriately high? If you're hypovolemic and hyponatremic, your kidneys should be trying to retain sodium. The question will often have excessive urine output. And in reality, it's true that nobody quite understands the true pathophysiology of cerebral salt wasting, but it is a condition that we do see in the ICU, and hence it's on the boards. And the answer in terms of treatment for cerebral salt wasting is hypertonic fluid administration, and often you need a 3% continuous infusion either in place of or on top of regular maintenance IV fluids. Next we'll talk about disorders of potassium and start with hyperkalemia. So remember that potassium is the primary intracellular positive ion. Sodium is the primary extracellular positive ion. Potassium is key for both muscle and nerve excitation, and the normal serum range is 3.5 to 5. So in terms of a workup, it's important to look at the history, to look at what meds the patient is on or has been receiving, and what is the renal function of the patient. And in general, hyperkalemia is unusual if the kidneys are functioning properly. They have a very good ability to compensate. Typical causes of hyperkalemia can be, relatively speaking, an excess potassium load. This could be from too much IV replacement or too much entero replacement. It could be from administration of older PRBCs with lots of excess potassium in the fluid. It could be from muscle or tissue crush or necrosis and from tumor lysis syndrome from an oncology patient. It could be from decreased renal excretion. This is very common with AKI or adrenal insufficiency. It could be drug-induced, things like too much spironolactone, ACE inhibitors, beta blockers, or the classic boards question will be hyperkalemia from digoxin excess. Or it could be from a shift from intracellular stores to extracellular levels. This is common in situations like DKA or acidosis or severe excess catabolism. What's the danger of hyperkalemia? Obviously, it can cause ventricular tachyarrhythmias, which can lead to cardiac arrest. And this is a very characteristic progression on EKGs. In terms of treatment, the priority is stabilize the myocardium before you try and treat the levels by giving IV calcium. That's step number one. And this is typically calcium chloride or calcium gluconate. Then once you stabilize the myocardium, the goal is to reduce extracellular concentrations of potassium by giving an insulin-dextrose combination, or giving albuterol, or administering sodium bicarbonate fluids, or giving diuretics like Lasix. You can also give a normal saline bolus to expand the extracellular volume and dilute the potassium a little bit. And if the GI tract is functioning, you can give potassium binders like K-exolate to help reduce extracellular concentrations of potassium. So again, there is a characteristic progression of the EKG findings when you have hyperkalemia. In the beginning with mild increases in potassium, you start to see peaked T waves. Then as you progress from mild to moderate, you see P wave widening, then P wave flattening, prolongation of the PR interval, and also continued peaked T waves. And then if levels become severe, you start to develop Bradyarrhythmias with QRS complex widening, eventual AV block that then evolves to a sinusoidal shape EKG and eventually PEA. And here are some pictures with the precordial leads showing peaked T waves in hyperkalemia with small flattened P waves. What about hypokalemia? Hypokalemia is relatively common in the hospital, but often is pretty mild with minimal clinical effects. The causes of hypokalemia, generally speaking, are due to inadequate intake of some kind, whether you're NPO with IV fluids that don't have any potassium in them, or similarly you're on TPN that doesn't have adequate amounts of potassium in them. It could be from GI losses, particularly with diarrhea or NG tube suctioning or lots of vomiting. In the case of NG suction, you are primarily losing gastric chloride, but this can create a relative alkalosis, which then leads to increased sodium bicarbonate that's being delivered to the distal renal tubule. And then that leads to increased potassium secretion in the urine. Lastly, you can have hypokalemia from increased renal excretion or from increased renal wasting from diuretics, or as is common in the osmotic diuresis from DKA. So often the history itself is pretty illustrative of what the cause of the hypokalemia is. If the etiology is unclear, you can calculate something called the trans-tubular potassium gradient, which is a ratio of the potassium in the urine to serum divided by the ratio of the osmolalities in your urine to sodium. So how to work this up? History often gives you a clue, meds give you a clue, is there any renal dysfunction or not? And then in terms of treatment, the goal, generally speaking, is to give enteral replacement, usually 0.5 milliequivalents per kilo every Q4 to Q6 hours. However, if there's arrhythmias or if there's any cardiac dysfunction, giving IV replacement quickly with 0.5 milliequivalents per kilo per hour. And you have to follow serial potassium levels to prevent creating supernormal levels and hyperkalemia. Next, we'll talk about calcium disorders. And to talk about calcium, it's important to talk quickly about normal calcium flux. So in the extracellular space, 40% of calcium is bound to albumin, about 10% is bound to other anions, and about 50% exists as soluble ionized calcium floating around in the extracellular fluid. The bones are the primary storage site of calcium in the body and contain something like 99% of total body stores. So it's easiest to understand disorders of calcium by talking about hypocalcemia first. The parathyroid glands detect a low serum calcium, a low ICAL, and as a result, they release parathyroid hormone. Parathyroid hormone then acts on the kidneys to increase the level of active vitamin D, active calcitriol, in the serum, which then dramatically increases the amount of calcium being absorbed from the intestinal tract, from GI sources. It also increases the amount of flux from the bone to the extracellular space and decreases urinary filtration, urinary excretion of calcium, all of which has the net effect to raise extracellular serum calcium levels. So in terms of specific disorders that cause hypocalcemia, the causes are generally either low dietary intake, low or absent vitamin D levels or some form of genetic vitamin D resistance, low or absent parathyroid hormone or defective parathyroid hormone secretion for some reason, and it's often helpful to think of stratify causes of hypocalcemia by age. So in the neonatal period, there can be transient neonatal hypocalcemia, a very common, and especially on the boards, question would be deGeorge causing hypocalcemia. You can also have pseudo-hypoparathyroidism, which is genetic resistance to parathyroid hormone action, and also hypomagnesemia from maternal causes. In older children, hypocalcemia can result from AKI. It can result from dietary deficiencies. It can result from acute pancreatitis. It can result from autoimmune problems. It can result from malignancies. It can result from Wilson's disease, as copper will impair parathyroid hormone secretion. It can result from sepsis and inflammation and SERS, where you suppress parathyroid hormone production. And it also can be iatrogenic from too much loop diuretics, too much CRT, or too much laxative administration. What are the symptoms of hypocalcemia? Initially, they're pretty nonspecific. You can have paresthesias. You can be irritable and be tired. But then as the hypocalcemia progresses and becomes more severe, you can develop tetany, which can be especially a problem thinking about the airway and maintaining a patent airway, and eventually, if things become more severe, having hemodynamic compromise with hypotension, bradycardia, and other arrhythmias. The treatment is either IV calcium chloride or IV calcium gluconate if it's urgent or emergent for treatment, especially if there's any kind of cardiac compromise, and then chronically treatment with oral calcium gluconate and vitamin D. What about hypercalcemia? Similarly, it's helpful to think about hypercalcemia in terms of stratifying by ages. In the neonatal period, there are several genetic causes of hypercalcemia, which all result in increased parathyroid hormone production, which then results in increased calcium levels. In older children, hypercalcemia can result from multiple different kinds of cancers, there can be parathyroid hormone adenomas, multiple endocrine neoplasias, Hodgkin's, Ewing's, rhabdomyolysis, acute lymphoblastic leukemia, all of which can result in increased parathyroid hormone production, which then increases bone resorption, which increases serum calcium levels. You can have hypercalcemia with thyrotoxicosis, you can have hypercalcemia with adrenal insufficiency. An important cause in the ICU can be prolonged immobilization, leading to increased bone resorption and increased calcium levels. And then also, especially in the resource-limited settings, granulomatous diseases like TB, fungal diseases, and even sarcoid can lead to ectopic vitamin D production, which then can increase calcium levels. And then lastly, it's important to remember there can be iatrogenic causes like inappropriate TPN, too much thiazides, lithium, and vitamin D intoxication. In terms of symptoms of hypercalcemia, it depends on how rapid the increase is. The classic symptoms for hypercalcemia are moans, stones, groans, and bones, which refers to altered mental status or seizures for the moans, kidney stones or calciuria for stones, abdominal pain and constipation with the groans, and then bone pain for bones. In terms of treatment, key is identifying what's the underlying disorder in the first place, using hydration to dilute the calcium, and then administering calcitonin to oppose any hyperparathyroidism. What about disorders of magnesium and phosphate? Hypermagnesemia is pretty rare unless there's renal dysfunction or renal failure, or there's some kind of massive soft tissue injury or necrosis. The typical symptoms are nausea and vomiting, progressing to hyporeflexia, which then progressed to neuromuscular blockade and hemodynamic depression if things are severe. Treatment includes calcium gluconate to block hypermagnesemia if restricting intake, and then diuretics. What about low magnesium? This is much more common in the hospital setting and often results from malnutrition, can result from GI losses in the setting of DKA or various different causes of increased renal excretion of magnesium. Often this is iatrogenic from multiple different kinds of drugs. Calcineurin blockers that are used in transplant patients are frequent offenders. Diuretics, amphotericin B, and then also cisplatin can lead to hypomagnesemia. The symptoms of hypomagnesemia often overlap with hypocalcemia and hypokalemia, and so it can be a little bit difficult to tease all three of those out, causing generalized weakness, neurochanges, and then EKG changes and T-wave inversions. The treatment is IV magnesium or in the chronic phase, oral supplementation, and the goal is to relieve symptoms. What about low phosphate, hyperphosphatemia? Typically this results from decreased intake or malabsorption in conditions like anorexia, bulimia, or GI dysfunction of some type, or from increased renal losses, either from diuretics or DKA, or from increased demand with inadequate supplies in the context of refeeding syndrome, a very important cause of hypophosphatemia. In terms of symptoms, phosphate is key for energy production to make ATP, and so symptoms include weakness, hypoventilation, and if things become very severe, myocardial dysfunction and seizures leading to coma. In the acute or severe context, you can give IV sodium phosphate or potassium phosphate, or for chronic problems, enteral sodium phosphate. Hyperphosphatemia is, generally speaking, the result of renal dysfunction where you have decreased phos excretion, or you have increased production from cell lysis or hemolysis and hyperproduction, things like tuberculosis, crush injuries, or rhabdomyolysis. If renal function is normal, you can give calcium chloride or calcium gluconate because often you will have low calcium levels from the precipitation with the phosphate and a fluid bolus, but you have to be careful to monitor calcium phosphate product. If that product is greater than 60 to 70, you have an increased risk of precipitation, which then can trigger acute kidney injury. If renal dysfunction is severe, you might have to give phosph binders via the GI tract or potentially even use dialysis to correct the hyperphosphatemia. Lastly, we're going to talk about acid-based disorders. So, this equilibrium, hypothetically, should go both ways, this equilibrium between bicarbonate and CO2. But in reality, because we breathe, we are an open system, we're not a closed system, the equation goes primarily to the right. Our lungs can excrete CO2 via ventilation. PCO2 levels are low, PCO2 levels are sensed centrally, and our body tries to maintain our PCO2 pretty rigorously between 35 to 45. Our lungs react very quickly and can quickly change PCO2 levels. By contrast, the kidneys are involved with actively excreting hydrogen ions and filtering bicarbonate, and the kidneys react slowly to changes in bicarbonate levels. So, in terms of an acid-base analysis, key for assessing what's happening with a blood gas is what type of gas did you get? So, is it really an arterial gas sample? That's only going to be, generally speaking, if you have an umbilical art line or a peripheral art line, and this is the most accurate type of sample. Is it a capillary gas sample? This is very commonly used in the NICU. If it's done properly, it can give you numbers that are close to an arterial sample, but if the child bleeds poorly, or it's a bad sample, or the technique is not good, then you can be prone to clotting and clumping and having very distorted values. Or is this a venous blood gas, which is more common for older patients and less acute patients? What are the standard parts of a blood gas? The first number is the pH. The second number is the PCO2, the partial pressure of carbon dioxide. The third number is the PO2, the partial pressure of oxygen. The next number is the serum bicarbonate that's calculated by the machine from pH and PCO2. And then the last number is the base excess. And this is, quote, the amount of acid or base that's required to titrate one liter of blood to a pH of 7.4 at 37 degrees at the given hemoglobin. And so it's a means, or it's a number, to help you quantify the metabolic component of an acid-base disturbance that's separate from the PCO2. So what are general steps to analysis? Number one, what kind of blood gas did you get? Is it arterial? Is it venous? Is it capillary? Number two, what is the pH? Is it a low pH, acidotic? Is it a high pH, alkalotic? Or is it normal? Next, what is the PCO2? Is the PCO2 high? Is the PCO2 high? Is the PCO2 low? Is the PCO2 normal? And a kind of corollary question, does the pH make sense given what the PCO2 is? Next, what is the bicarbonate? Is it high? Is it low? Is it normal? And again, asking the question, does the pH make sense given what the bicarbonate level is? Next, what is the base excess? And I find this generally mostly only helpful in contexts of acidosis, not so much for alkalosis. And then integrating all of those numbers with what you know about the clinical context for the patient. Is the patient sedated? Is the patient paralyzed? Are they on a ventilator? Do you know what their primary diagnosis is or not, etc. Integrating all those things together. So first of all, after you've figured out what kind of gas you have, is the patient acidotic or alkalotic? What's the pH? So acidotic is a pH less than 7.35. Alkalotic is greater than 7.45. With the caveat that for capillary gases or venous blood gases, we tolerate a wider pH range than normal. And we tolerate down to about 7.25, all the way up to 7.45 as normal. Metabolic acidosis is when you have a low pH and a low serum bicarbonate as well. pH is low, bicarb is low. This is common. And conceptually, this is when something is either making more acid, making more H plus in the blood. This could be from ischemia, could be inborn error metabolism, could be DKA, could be renal tubular acidosis type 1, whatever. Something's making more acid. Or you have a failure to get rid of the acid that you have. This could be from acute renal failure, acute kidney injury. Or you have something that's causing, relatively speaking, a loss of bicarbonate. Diarrhea with loss of bicarbonate in the stools or RTA type 2. One way to help figure out what the cause of the acidosis is, is looking at the anion gap. So here is a picture of the cations and anions in normal plasma. So the cations are sodium, potassium, and unmeasured cations. And then the anions are primarily chloride, bicarb, and then all the other unmeasured anions. And the purple bar there is the anion gap. So if you sum up sodium plus potassium minus the chloride plus the bicarb, you get somewhere between 8 to 12 milliequivalents per liter. And that's normal. If you have an acidosis with no anion gap, then you're going to have a decrease in the serum bicarbonate. It's an acidosis, but the amount of unmeasured anions has stayed the same, and your chloride has dropped as well. And your... or chloride has increased, excuse me, has increased. And so your anion gap stays the same. If you have an acidosis with an increased anion gap, this is a situation where you have a reduction in bicarbonate because it was acidosis, but you have some unmeasured increase in unmeasured anions from some cause, and that's what's causing your gap acidosis to increase. To help figure that out, we have a typical mnemonic that is used, either mud piles or muck piles, where the M stands for methanol, U stands for uremia, D or K, depending on how you do it, can be ketoacidosis or diabetes. And this is diabetes or starvation are also from ethanol. Also from ethanol. P means propylene glycol. I means INH, so too much INH can give you a metabolic acidosis with anion gap. L means lactic acidosis from ischemia, from anemia, from shock, from infection, whatever the cause, increased lactic acidosis. E is ethylene glycol, and S is salicylates. Metabolic alkalosis, you have a high pH and a high bicarb. pH greater than 7.45, bicarb greater than 26. This is often iatrogenic and is often due to loss of some kind of acid, from vomiting or too much NG suction. Cystic fibrosis can give you too much loss of acid, or you have too much diuretics and LASIX. One way to help determine if the history does not give you the clue is looking at a basic metabolic profile plus your arterial gas and looking at your urine chloride as well. If your urine chloride is low, that alkalosis is from volume loss. If your urine chloride is above 20, that might be consistent with a genetic syndrome or some tumor. What about respiratory acidosis? Here you have a low pH and high bicarbonate. This is common in the hospital, and something is making the child hold on to carbon dioxide or to hypoventilate or both. So examples could be if you have primary pulmonary disease from things like BPD or interstitial lung disease or bronchiolitis obliterans, or from non-BPD or interstitial lung disease or bronchiolitis obliterans, or from non-pulmonary causes, things like hypoventilation. The breaths are too small, or they're too infrequent, or both, or you're over sedated, or you have poor neuromuscular tone and you can't take a breath, or you have pain and you can't take a breath. Also important to note that patients with respiratory acidosis potentially could be hypoxic as well, and remember the definition of the minute ventilation is your respiratory rate times your tidal volume or respiratory rate times breath size. So something is wrong with your minute ventilation if you have a respiratory acidosis. Respiratory alkalosis is generally speaking due to hyperventilation from some cause. This could be inappropriate ventilator settings if you're breathing for the patient. This could be from tissue hypoxemia. This could be too much lung receptor stimulation. This could be inappropriate CNS stimulation from a tumor that's causing you to hyperventilate. It could be from liver failure. It could be pain, stress, anxiety, whatever the cause is you're hyperventilating. And then lastly, as we mentioned, putting it all together, what do you know about the clinical situation? In other words, how do you interpret the numbers if you have more than one abnormality? Some helpful hints are the pH generally tells you what the primary problem is. Then after looking at the PCO2 and the bicarbonate and the base excise, thinking about what meds are they on? Are they on a ventilator? Are we breathing for the patient? Are they breathing spontaneously? Are they sedated? Are they not sedated? Are they paralyzed? And also, what are their ins and outs? Are they very fluid positive? Are they very fluid negative? That can be helpful. These can all be helpful pieces of information. Here's a series of real-life examples, which you guys can work through. The A and the V mean venous and arterial. And then the answers are listed below. Here's a board-style question on some of these topics. A four-day-old infant presents to the emergency department with feeding intolerance, tonic rigidity, and possible seizures. The ED physician secures the infant's airway with a 3.5 millimeter endotracheal tube, but has difficulty viewing the larynx. She then administers 20 mLs per kilo of normal saline as an IV bolus, as well as antibiotics for potential sepsis, and transfers the infant to the PICU. On physical examination, the infant has slightly low set ears, mild hypertelarism, and a short philtrum. There is a cardiac systolic ejection murmur, and pulses are symmetric in all four extremities. Results of the initial laboratory studies are white blood cell count of 8.9 thousand, hemoglobin 12.8 grams per deciliter, platelet count of 312 thousand, sodium of 136, potassium of 4, chloride of 105, bicarbonate of 24, ionized calcium of 0.72, and a glucose of 84. Chest radiography results are normal, with good position of the endotracheal tube. So, of the following choices, the most likely cause of this infant's condition is hypoparathyroidism. The answer is number four, hypoparathyroidism. It is true that hyperphosphatemia, hypomagnesemia, and vitamin D deficiency are all possible causes that could cause some of these phenotypes, but based on the age, the physical stigmata, and the potential structural heart disease described for the infant with the systolic murmur, DeGeorge syndrome with resultant hypoparathyroidism is the most likely cause in this case. The hypoparathyroidism therefore results in hypocalcemia, which results in the seizures and tetanus.

fluids

electrolytes

acid-base disorders

pediatric patients

body fluids composition

fluid balance

electrolyte abnormalities

acid-base imbalances