Photo Courtesy measurelife.com
Finally, here is Part 3 of Sick Kid, following up on Part 1 and Part 2. Here we will discuss the treatment of this pediatric patient in DKA, in the field and what will be started in the ED. You may be thinking, this should be easy; the kid is acidotic, so give Sodium Bicarbonate (NaHCO3); he is vomiting, give Zofran; he is dehydrated, so give lots of fluids; and he is hyperglycemic-he needs insulin and the local ED has that. The hospital can also treat the hypekalemia you may see on the monitor as well. Right? Not quite. All are correct, but most can be wrong too. The body is very complex and reacts in diverse ways. This is the reason for the reliance on evidence based medicine as opposed to that which is based upon expert opinion we traditionally have been used to in EMS. The treatment plan is obviously based upon the clinical presentation of the child. Is the child protecting his airway? Is the child hypoxic? Is the child in hypovolemic shock? Is the child currently vomiting? These are some questions that will guide our decisions.

Breathing-Oxygen
The kid will need some oxygen. How much? Enough to keep O2 saturations as close to 100% as possible. Since the SaO2 is in the high 90s and the patient is hyperventilating in this particular case, we can be sure that the patient is capable of exhaling CO2 and large concentrations of O2 are not necessary unless we see other signs of hypoxia. In this case, a nasal cannula should be enough. Some expert literature advocates using O2 via mask, implying high concentrations. There really is not much evidence to show high concentrations of O2 are needed here and some evidence may even question if it is safe. I would also give a cannula since the patient is vomiting for obvious reasons. If the child is showing signs of hypovolemic shock, perhaps increasing the FiO2 via mask would be warranted even if the patient is not showing signs of hypoxia, but increasing fluids is the key, which leads us to circulation.

Circulation-IV Access
Now for circulation; This is where things really get tricky. We know the patient is acidotic, hyperglycemic and dehydrated, and possibly hyperkalemic. We have to take care in how we address these issues. But one thing is for sure, the child needs an IV, preferably two of them. Why two IVs? This is a seriously sick kid as anyone in DKA would be. We always get two IVs for traumas and arrests, but we rarely do it for other seriously ill patients. We should be getting two IVs in AMIs, acute Strokes or any other seriously ill patient. Well, for one reason, this kid will probably be receiving many medications later, including insulin, and later potassium and if acidotic enough, possibly HCO3, often simultaneously, so two lines will be necessary. Another important reason is to have a good line to draw serial labs while the other line can be used for fluids and medication infusions. My suggestion is in this kid is to first get the best IV you can to start fluids, even if it is a small bore IV. You can then have time to look for better access afterward, but this is just my opinion, so feel free to debate it. Don’t forget about considering an IO if you feel the kid is sick enough. This kid is sick enough to warrant it, especially in hypovolemic shock.Though I am one to often preach a 20g IV is usually the biggest you need to get on most of your patients, obtain an IV large enough to draw labs, if you can.

Blood Draw and Fluids
Though I am one to often preach a 20g IV is usually the biggest you need to get on most of your patients, obtain an IV large enough to draw labs, if you can. If you routinely draw labs for your hospitals, then draw the “rainbow”. The most important will be the chemistries (various-light green to tan). Important labs from this will be electrolytes such as Na+, K+, HCO3 and Phosphate (P-) which tend to be depleted. I did not mention P- in part 2 but a deficit shifts the oxyhemaglobin curve to the left reducing O2 delivery. Other labs from this tube will the anion gap and BUN, (as I mentioned in part 2), serum osmolality and obviously serum ketones (β-hydroxybutyrate) and glucose.

photo courtesy of yzmedical.en.alibaba.com

A CBC (purple top) is always ordered as well as this checks H/H and platelets but most importantly WBCs. Why does the ED MD care about WBCs? Viral infections, and bacterial infections, especially in kids less than 3 years old are the precipitating factors of DKA. Infections are physiological stressors that can result in sympathetic nervous system response; releasing hormones like epinephrine and cortisol counteract the effects of insulin. An important goal for an ED MD would be to not only identify the infection or any other trigger and treat it. Other useful tubes may be a clear redtop in which to draw a venous blood gas, but this is often drawn in the ED. We draw the rainbow because the ED attending will often order off the wall labs and it is often hard to predict with what the attending will order. If the hospital does not accept your labs, then don’t waste time drawing them, obviously. And don’t feel bad if you don’t have time to draw them because if you have a good line to draw from, the ED will only take less than a minute or two to draw them. That is why it is nice to bring your DKA patient in with two lines, one big enough for labs.
Blood tube order:

So, as soon as we have vascular access, we need to run some fluids. Despite a hyperosmolar state of the blood, we want to run our isotonic fluids like normal saline or ringers lactate. This will keep fluid in the vascular spaces longer, but will decrease counterregulatory hormones and lower the blood glucose level. How much do we run? Well, that depends. Is our patient in hypovolemic shock? We all should know the signs and symptoms so I won’t go over them. If so we need to correct this first by restoring extracellular fluid by running the routine 20cc/kg bolus as we learned in PALS, with one caveat. It should not be run wide but should be run over 30 minutes to an hour. Many other sources recommend over 1-2 hours. How fast should depend on how hypotensive they are. Either way, the fluids should NOT be run wide open, as we would in an adult, where would dump 1-3 liters in an hour. Ideally it should be run by a pump, programming in the volume to be infused and the time being set for 30 minutes to an hour. How many ambulances carry pumps? Too bad. If not, you have to consider the tubing drip factor and count the drips. Some experts recommend the use of microdrips for more careful control.

If the patient is not hypotensive, we still know the child is dehydrated, so we will give 10-20cc/kg over 1-2 hours, initially. The ultimate goal in IV therapy is correcting fluid deficits, which in children is usually 60-100 ml/kg of body weight, or 7-10% of body weight. The deficit can be figured out by multiplying the percentage, say 0.10 (10%) by the body weight in kg. This fluid deficit is replenished over 24-48 hours, depending on the guidelines of the facility. Some may want 36 hours. Of course, if you gave a fluid bolus to correct hypotension, it would be deducted from the calculated total fluid replacement. This is why it is important to tell the receiving facility how much fluid you administered.

Photo courtesy of www.indiamart.com

Once the first bolus has been administered, the guidelines recommend switching 0.9% NSS to 0.45 NSS (“half-normal”), though most ambulances don’t have this fluid. Unless you are doing an interfacility transfer of this kid, you won’t have to worry about that anyway. However, there is a good chance you may be the transferring service. If that is the case, this child should be on a maintenance fluid. These will be set by the referring facility and since you will not usually be expected to initiate them. Just be sure the ordered rate is in fact the rate that is running on the pump or drip set. If there is a question of the rate set by the referring hospital, consult your medical command or Children’s Hospital consult MD. Remember, many referring facilities are not confident or competent to treat seriously ill pediatric patients appropriately.This is one reason STAT Medivac and other HEMS/MICU services consult a Children's Hospital MD on interfacility transfers involving pediatric medical patients.

Photo courtesy of www.choa.org

So why the difference in fluid therapy between pediatrics and adults? The higher basal metabolic rate and large surface area relative to total body mass in kids requires greater precision in delivering fluids and electrolyte. We are also a little worried about Cerebral edema. There is some evidence that aggressive fluid therapy increases the risks or aggravates existing cerebral edema, (though recent evidence does not support this). Cerebral edema leads to increased intracranial pressure and then to herniation. Some sources state cerebral edema is normally present to some degree in all DKA patients due to idiogenic osmoles in the CNS that causes the accumulation of fluid. The exact cause is not really known and it is almost exclusively a pediatric problem, rarely seen in adults. Though severe cerebral edema is uncommon in pediatric DKA patients, with only 1-3%, it is the main cause of death in kids with DKA with a mortality rate of about 21% and a morbidity rate of 27% of kids having permanent neurological deficits.

courtesy of emedicine.medscape.com

Children’s brains have higher oxygen requirements than adults and the hypophosphatemia I mentioned above only decreases O2 delivery and hypoxia leads to cerebral edema. We also see studies that show the lower the pH, as well as low Na+ (during rehydration) and even arterial PCO2 levels, the greater prevalence of cerebral edema as well as increased BUN, indicating dehydration, being a significant risk factor. Cerebral and other autoregulatory systems do not develop well until later childhood and with these other risk factors, can predispose a child to cerebral edema. There is conflicting evidence regarding whether increasing fluid administration is a significant risk factor. It appears the fluid rates are not a primary contributor. However, since there was evidence showing some correlation between large fluid rates and cerebral edema, we still remain careful with the fluids.
What if you are transferring this child from a local facility to a children’s hospital and he shows clinical signs of cerebral edema. What are the clinical signs?
• Sudden or persistent drop in heart rate
• Altered mental status, increased drowsiness, irritability and restlessness
• Severe headache
• Emesis
• Seizures
If you see these signs, stop the infusion and raise the head of your patient 30 degrees and be sure to notify the receiving facility. Some sources recommend hyperventilating to reverse it. Most sources however, as we know, recommend against it, especially since that decreases cerebral perfusion. Manitol is the drug of choice, or other hypertonic colloid, but most services don’t carry it.

Courtesy of rn.modernmedicine.com

By the way, though rare, children with DKA have been known to develop thrombotic strokes, so this is another reason we also keep an eye on the patient's neuro status.
Have we forgotten about the nausea and vomiting? No? Good. This kid needs that addressed, too. Ondansetron (Zofran) is ideal, dosed at 0.1 mg/kg IM/IV, but in some regions, like here in Pa., you need medical command authorization. There is no consistency in prehospital anti-emetics, so use whatever you have as long as you understand the pediatric dosage. I know there are more side effects with Phenergan (promethazine), especially in pediatrics.

Potassium started in the ED
If you are doing an interfacility transfer of this kiddo, don’t be surprised if he is not receiving KCl added to the fluids. Why would that be if he was hyperkalemic? Well the potassium leaves the cells and enters the bloodstream, causing the hyperkalemia, but the fluids tend to wash it out. The cells are already lacking potassium and there won’t be any in the blood stream to draw from when the potassium is excreted in the urine. Therefore, after the first hour or two of fluids, the goal is to administer potassium via the fluids. With this see-saw balance of potassium, it is important to monitor this kid during transport to detect any arrhythmias.

Photo courtesy http://www.usza.us/

So, our patient is hyperglycemic. Isn’t large amounts of insulin the key? No. The fluids do a good job of diluting the blood and helping to excrete the glucose. The child does need insulin to normalize the blood glucose and suppress lipolysis and ketogenesis, but low dose IV insulin is the key. It is to be started after the first fluid bolus-after the first hour or two. However, most EMS services do not give insulin. Why am I bringing it up then? You may be transferring a pediatric patient on insulin as part of a MICU team. Remember that referring facilities often don’t know the current pediatric DKA treatment guidelines and may give too much. Either way, when you do a transfer of a DKA patient, you need to check the glucose. When the glucose level gets down to 300 mg/dl, IV D5 1/2 or D5 NSS should be started. If you are transporting the patient and the patient is on D5NSS, and you are wondering why, it is because between the insulin and fluids, the sugar levels drop fast. The 5% dextrose will help prevent hypoglycemia but the insulin will still continue to run to continue treating the DKA.

Photo courtesy of http://www.cvs.com/

Now the kid is acidotic, so we should treat that with bicarb, right? No. At least not in the field. The ideal treatment is fluid replacement, especially in the field. The fluids will decrease the serum ketones, which in turn will decrease the acidosis. The ED may start bicarb if the pH is low enough and critical, but since EMS currently is not doing field ABGs and generally don’t have patients too long, there is no need for field administration of bicarb. Studies show no significant in improvement in patients in DKA and in fact, bicarb administration may in fact exacerbate cerebral edema, according to some studies.

Photo courtesy http://www.dixieems.com/

Now where does this child get transported to? The local hospital? Sure, if the local hospital is appropriate or the appropriate hospital is over an hour away. Well, what is the appropriate hospital? For one, a hospital that has pediatric endocrinology with written guidelines for pediatric DKA, and one with a laboratory for frequent and timely evaluation of lab results. And that is just for the more stable kids. Those with severe symptoms (kussmaul respirations, acetone breath, large ketones on urine dip stick), like this particular case I gave, would need to go to a Pediatric Intensive Care Unit (PICU). If you are not sure of the severity, and this is very difficult just on clinical presentation alone, err on the side of assuming this kid will need a PICU admission. Therefore, transport the child to a Children’s hospital or one that has a PICU. EMS providers seem to have a problem with transporting patients to the appropriate facilities and often don’t know the capabilities of the hospitals in their region. I suggest that should be one of the first things learned or taught during field training.

Children's Hospital of Pittsburgh, before it opened this year.

Here is a sample DKA ALS protocol.
So, to summarize, this kid will need O2 to keep sats as close to 100% as possible, Two IVs with labs drawn and IV NSS started to run at 20cc/kg run over an hour or two, unless the kid is in shock. In that case, run the fluids twice as fast perfusion is improved. Treat nausea and vomiting with an anti-emetic, and just as important: transport to the appropriate facility; one that has a PICU. Here is that boring but informative doctor again to summarize medical treatment for DKA:

References:

Brandis, K., “8.2.5 Management of DKA, Acid-Base Physiology”, http://www.anaesthesiaMCQ.com, November 2008

Chansky Michael E, Lubkin Cary L, "Chapter 211. Diabetic Ketoacidosis" (Chapter). Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 6e: http://www.accessmedicine.com/content.aspx?aID=606036.

Chiasson J, Aris-Jilwan N, Bèlanger R, Bertrand S, Beauregard H, Ekoè, J, Fournier, H, Havrankova, “Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state”, CMAJ. 2003 April 1; 168(7): 859–866.

Children with Diabetes Website, “Treatment of DKA”, 6 August 2006

Crandall, J., “Diabetic Ketoacidosis (DKA)”, The Merk Manual, May 2007

Finberg, Laurence, Appropriate Therapy Can Prevent Cerebral Swelling in Diabetic Ketoacidosis, The Journal of Clinical Endocrinology and Metabolism. - San Francisco : [s.n.], 2000 . - No. 2 508-509 : Vol. Vol. 85.

Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N; “Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics., Predicting cerebral edema during diabetic ketoacidosis”. N Engl J Med. 2001 Jan 25;344(4):264-9.

Green SM; Rothrock SG; Ho JD; Gallant RD; Borger R; Thomas TL; Zimmerman GJ, “Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis”. Annals of Emergency Medicine. 1998; 31(1):41-8

Ho Josephine , Pacaud Danièle, Hill Michael D., Ross Catherine, Hamiwka Lorie, and Mah Jean K. “Diabetic ketoacidosis and pediatric stroke” CMAJ. 2005 February 1; 172(3): 327–328.

Hopley L, Schalkwyk, J., “Diabetic ketoacidosis: pathophysiology”, jo2@anaesthestist.com, 2006

Kane E., “Diabetic Ketoacidosis and Cerebral Edema”, pedsccm.org, November 6, 1996

Kitabchi A, Wall B., “Management of Diabetic Ketoacidosis, American Family Physician”, August 1999

Kravitz J, “Diabetic Ketoacidosis: Still Serious After All These Years”, Emergency Medicine 39(11):10, 2007

McNally, P, “Aggressive Fluid Resuscitation in Initial Treatment of Children Presenting in DKA May Cause Herniation”, Michigan Department of Pediatrics Evidence-Based Pediatrics Web Site

Moran, Tony, “GUIDELINES FOR THE TREATMENT OF PEDIATRIC
DIABETIC KETOACIDOSIS”, University of Minnesota Department of Pediatrics Division of Endocrinology, 2003

Morris, A, Olshan, J., “CRITICAL CARE GUIDELINE FOR THE MANAGEMENT OF DIABETIC KETOACIDOSIS (DKA) IN THE PEDIATRIC PATIENT” at the Barbara Bush Children’s Hospital, March 2005

Munk, M, “Pediatric DKA: The presentation, assessment & prehospital management of diabetic ketoacidosis in children”, JEMS June 2006 Vol. 31 Issue 6 2006 Jun 1

Pischke M., “Diabetic Ketoacidosis”, Physician Assistant, Volume 25, Number 11, 2001

Wolfsdorf J, Glaser N, Sperling M., “Diabetic Ketoacidosis in Infants, Children, and Adolescents: A consensus statement from the American Diabetes Association, Diabetes Care” May 2006 vol. 29 no. 5 1150-1159

History of Present Illness
As we approach the patient, we illicit more information from the mother in order to think of the differentials besides or in addition to gastroenteritis. Asking about PO and output would reveal valuable information such as the three "P"s: Polydipsia, Polyphagia, and Polyuria. As we know, these are classic signs of a hyperglycemic patient with Type 1 DM. Asking abouf family history would also have revealed that there was a family history of diabetes. Another clue. Walking in we see a thin kid. This is also a clue. Why? Well, if he is a Type 1 diabetic, he lacks insulin which has many functions including the following which are pertinent:

• Controlling cellular uptake of glucose


• Increasing glycogen synthesis from increased serum glucose


• Increased fatty acid synthesis and conversion to triglycerides to be stored as fuel through esterification


• Decreased proteolysis
  
  
• Decreased lipolysis
  
  
• Decreased gluconeogenesis


• Increased Potassium (K+) uptake in cells

So what does this mean? It means that lack of insulin leads to the opposite of those functions listed above. There is a decreased uptake of glucose needed for cellular respiration (including the Kreb's Cycle) to provide the energy the body needs to function.

Okay, so we know that without insulin, the cells are starving in a land of plenty. They cannot gain access to the glucose. Since the cells are starving, and insulin is lacking, we see a breakdown of glycogen in liver and muscle tissue to create more glucose for the cells, but yet, the cells cannot take it in. This leads to a continuing cycle of accumulting glucose. So we do a bedside glucometer reading and find it is "CRITICAL HIGH". A patient in DKA will have a blood glucose > 250 mg/dl, or for those up North or across the pond, >13.8 mmol/l.

Courtesy of http://realitycheck.org/

Courtesy of www.inkeehong.com

Ketogenesis
Normally with high serum levels of glucose, acetyl-CoA metabolizes the glucose to make FFAs to then be stored as fat in adipose tissue. But, as we discussed the cells are starving so there is a breakdown of adipose tissue into FFAs to be used as energy by muscle and cells and also to be transferred to the liver bound to albumin to be broken down into acetate, to be broken down further into the ketnone body, acetoacetate. The brain can use ketone bodies as fuel when glucose levels are low. There, and other places low in adipose tissue the ketoacids are oxydized back into acetyl-CoA to be used in cellular respiration. I know this is getting deep, but...well try to hang in there. Acetyl-CoA needs the organic chemical oxaloacetate to push it through the Kreb's Cyle. But oxaloacetate is used up during gluconeogenesis, so there is not enough to process the acetyl-CoA, which means the excess goes back to ketone body formation. Here is the reaction:
Acetyl CoA < > Acetoacetic Acid (acetoacetate) < > Beta-hydroxhybutyric Acid
This leads to ketosis, the build-up of excess ketones. Not usually a bad thing as it is can be common in fasting or ketogenic diet, but this time it is a bad thing.

Along with glucose, the kidneys try to excrete the excess ketones and on a urine dipstick, ketones >3+ indicate ketoacidosis. Urine dipstick? They are commonly done in the ED. Since the patient has polyurea, collecting a urine sample is quick and it only takes a minute to dip the urine stick and read it. I foresee, if our roles in EMS increase, we may have the option of using these in 10 years. Far fetched I am sure, but if we take advantage of the patient's need to urinate, we can learn many things from the dipstick such as not only determining DKA by identifying large quantaties of ketones and glucose in the urine, but recognizing kidney stones and UTIs as well.

Courtesy of www.medicalgeek.com

Acetone
I mentioned a smell when we walk in the room similar to that of nail polish. This is acetone. While acetone smell is a highly reliable sign of ketosis, not everyone has the gene to smell it on someone's breath. It is estimated that only about 30-50% of people have the gene to smell it, but if it is smelled, it is a significant sign. What causes that "fruity odor"?

Courtesy of http://www.invelos.com

So as I mentioned above, when the acetoacetate that cannot be metabolized back into Acetyl-CoA or used as fuel are then broken down further into Beta-hydroxybutyrate, a ketoacid like ketoacetate, and acetone as a byproduct. Acetone, as a byproduct cannot be synthesized back to acetyl-CoA. No problem. It is easily excreted in the urine. Acetone also has a high vapor pressure meaning it is easily evaporated through exahalation. Alsa, the infamous "fruity" or acetone odor. This odor is very specific to identifying ketosis. If you are like me in that you cannot smell it, don't feel to depressed. Though I have seen and heard varying numbers, the consensus seems to be more than half the population does not have the gene to smell it. But if you do, and you smell it, then consider it a very important indication of ketoacidosis.

Acidosis
If you are weak on acid base basics, here is a basic overview:

Courtesy of http://www.mountnittany.org/

Our patient is very weak in bed. Why is he weak? A couple of reasons. He is dehydrated and lacking energy since the the cells are having a tough time getting at the glucose they need. There may be a build-up of lactate which fatigues muscle cells. But not only that, Acetoacetate and betahydroxybuterate are ketoacids. They are very acidic and with enough ketoacid accumulation, the pH drops to dangerously low levels, leading to the state of Ketoacidosis. Acidic states hinder enzymatic reactions, and this includes skeletal muscle contractions. The acidotic state leads to the GI symptoms such as the abdominal discomfort, nausea and vomiting, though the exact etiology of these are unknown. Part of the diagnostic criteria for DKA is an arterial pH<7.30.>

Now the body will try to buffer this acidotic state, and one way is Kussmaul breathing. Actually, a peson will develop tachypnea or hyperventilation first,and then the Kussmaul breathing at later stages. Hyperventilation and Kussmaul breathing are not necessarily the same. Kussmaul breathing is more like deep, fast and labored breathing and is a later sign and can lead to respiratory fatigue. Still, you will see hyperventilation of some sort, like we saw in our sick kid. Why? To blow off CO2 of course. Most of us know that but for those providers who are not sure of the relevance of "blowing off CO2", let me explain briefly. An acidic environment in the blood means more excess H+ ions. To counter this acidosis, the H+ ions need rid of. The body has many buffering systems to keep the pH between 7.35-7.45, but we will focus on the following equation:

We see when H+ ions accumulate after being donated by the ketone bodies, to become hydronium H3O, they are buffered by HCO3 (bicarbonate, a.k.a bicarb), which binds to the H+ to become H2CO3 (carbonic acid) and H2O, then to be broken down to CO2 and H2O, both of which are exhaled. The increases in H+ ions stimulate central chemoreceptors (tha aortic bodies in the aortic arch and carotid bodies in the carotitids) which in turn stimulate the respiratory centers in the medulla and pons in the brain stem to increase rate and depth of respirations. So the more the body hyperventilates to compensate, the more O2 is inhaled to eventually bind with H+ to make H3O and the more H2O and CO2 is exhaled, trying to raise the pH or keep it level. Remember, a low pH state is actually acidotic. So thus, the reason for the hyperventilation and Kussmal breathing. Usually we start to see the Kussmal breathing when the patient is starting to fatigue from the hyperventilation.

Courtesy of www.Jumpstarttriage.com

What is interesting is the HCO3 is used up in the buffer system- one for each H+ buffered so serum labs and ABGs will show a decrease in HCO3 as well as a normal or decrease in the CO2. This is due to the compensatory mechanism via buffers and hyperventilation. But you knew that. A bicarbonate level of 18 mEq per L or less is part of the diagnostic criteria of DKA, but again, we in the field usually don't have access to serum labs. Another one of the blood tests done in the ER will be an Anion Gap, wich in DKA, will be >12. It is used to help diagnose metabolic acidosis.

Now if you put the kid on the monitor, you may see peaked "T" waves. Why? Insulin pushes K+ back into cells, but there is no insulin, remember. Not only that, but the acidosis pulls the K+ out of the cells. This leads to hyperkalemia, which gives us the peaked "T" waves on the EKG. But remember, the, body's cells don't have the needed K+ as it is in the vacular space. Making matters worse, along with the glucose and ketones, the patient will excrete the K+ and the Na+, leading to hypokalemia and hyponatremia later, especially after fluids are started. But we will discuss that later.

Courtesy of www.learnTheHeart.com

Another EKG finding that though not common, but occasionally occurs, is a prolonged QTc. You should know about prolonged QT from Adam in Long QT Part 1 Part 2, Part 3. This is a reason these kids need cardiac monitoring.Just remember that hyperkalemia is in no way diagnostic criteria but something you may see before rehydration and insulin therapy. Afterward you may see hypokalemia (hopefully not), such as when you may be tasked with doing an interfacility transfer of this kid.

Courtesy http://www.medinfo.ufl.edu/

Again, this is not something to expect to see and not used for diagnostic criteria but just another reason to monitor your pediatric DKA patient.

So, to rehash, I just went over some of the obvious signs we will see and why we see them. Basically what is going that is reflected in the signs and symptoms. I understand for many of you this may have been a little deep, and quite boring. However, maybe not as boring as this guy (who is thorough though).

Referrences:

Barbour, L.A., Friedman, J.E., Chapter 26, "Management of Diabetes in Pregnancy", Influence of Metabolic Changes in Pregnancy on Diabetes Management. March 6, 2003: http://www.endotext.org/diabetes/diabetes36/diabetesframe36.htm

Brandis, Kerry. "8.2.1. What is ketoacidosis?, Acid-base pHysiology", Anaesthesia Education Website<>, http://www.anaesthesiamcq.com/AcidBaseBook/ab8_2.php

Chansky Michael E, Lubkin Cary L, "Chapter 211. Diabetic Ketoacidosis" (Chapter). Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 6e:
http://www.accessmedicine.com/content.aspx?aID=606036

Crandall, Jill P. MD, "Diabetic Ketoacidosis (DKA)", The Merck Manuals Online Medical Library, May 2007, http://www.merck.com/mmpe/sec12/ch158/ch158c.html

"Diabetic Ketoacidosis Pathophysiology", slide presentation, The Diabetes Monitor: http://www.diabetesmonitor.com/dmemerh/tsld005.htm

Faulke, Dan. DKA Mechanisms Anaesthetist.com June 2008
http://www.anaesthetist.com/icu/organs/endocr/dm/Findex.htm#dka.htm

Gundstream, Stanley, E., Anatomy and Physiology: With Integrated Study Guide, 4th Ed., McGraw Hill, 2010

King, Michael W., Ph.D / IU School of Medicine / miking at iupui.edu, Gluconeogenesis, The Medical Biochemistry Page
http://themedicalbiochemistrypage.org/gluconeogenesis.html

Klabunde, Richard, E., “Chemoreceptors”, Cardiovascular Physiology Concepts, http://www.cvphysiology.com/, 04/01/07

Kuppermann, N, Park, J, Glatter, K, Marcin, J, Glaser, N. Prolonged QT Interval Corrected for Heart Rate During Diabetic Ketoacidosis in Children,
ARCH PEDIATR ADOLESC MED/VOL 162 (NO. 6), JUNE 2008
Downloaded from http://archpedi.ama-assn.org/ at University of Pittsburgh, on October 20, 2009

Musa-Veloso, K, Likhodii, S., Cunnane, S. "Breath acetone is a reliable indicator of ketosis in adults consuming ketogenic meals", American Journal of Clinical Nutrition, Vol. 76, No. 1, 65-70, July 2002: http://www.ajcn.org/cgi/content/full/76/1/65

Patlak, Joe, "ISF-Plasma Exchange/Capillary Pressures", Body Fluids lectures of Medical Physiology 301, http://physioweb.med.uvm.ed%2011/01/00

Place Frederick, Mayer Thom, "Chapter 128. Diabetic Ketoacidosis" (Chapter). Tintinalli JE, Kelen GD, Stapczynski JS, Ma OJ, Cline DM: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 6e: http://www.accessmedicine.com/content.aspx?aID=597225

Sateesh, B, "Glucose Homeostasis and Diabetes", Pharmainfo.net, Vol. 5 Issue 4, 08/09/2007: http://www.pharmainfo.net/reviews/glucose-homeostasis-and-diabetes

My goal with this 3 part post is to discuss a particular disease state focusing on the pathophysiology and the current treatment guidelines and their rationale. Let's start with the presentation:

Introduction
You are the medic working with with an EMT on a 12 hour shift in an urban low income, mixed race neighborhood. You have been running non-stop for 9 hours, doing two BLS and 5 ALS trips, and you are hungry, tired, and have 4 PCRs to type up yet (while your partner only has two). It is a typical cold winter day with snow flurries. The heater is on to not only warm you guys but as a half hearted attempt to keep your food warm that is sitting on the dash over the defroster duct. You have been nibbling at your sandwich over the past couple of hours. Just as you take a bite, you get a call for a 9 YOM "sick and vomiting". Your partner slams her hand on the steering wheel while you yell out a few expletives. "This kid better be sick!" Your partner yells out, "Who calls an ambulance for vomiting?" Why ask? We get these calls everyday, and will continue for a long time.

You pull up to an old row house in this old mill town and see a somewhat neat front porch atop a flight of stairs with bikes in the front yard. You are already thinking you aren't carrying someone down these stairs for just feeling sick. This kid is going to walk. You grab the clipboard while your partner grabs the jumpbag and you ascend the stairs to the house. The door opens and an overweight but neat appearing woman in her late 20s opens the storm door. She appears concerned and tells you it is her son who is sick. She holds the door open as you and your partner pass through. She tells you he is upstairs in bed and scurries past you to lead the way to his room. Great. More steps. This kid is definitely walking.

Chief Complaint
As you climb the stairs, you try to illicit a history of present illness. She tells you he has been sick the past few days, progressively getting worse. "So why now are you calling?" You ask. She turns around to see the expression on your face as she senses a slight sarcasm in your voice. You quickly add, "I mean, what prompted you to call now? What is worse this evening?"
"He has been throwing up all day and now and is weak, laying in bed all day," she says as she turns the corner and heads down the hall. "He won't even play his video games."

"Has he had a recent fever?", you ask. She tells you she didn't notice and does not have a functioning thermometer. "Do you think it is the flu?" she asks. You shrug your shoulders. You ask about his medical history. He has none other than a T&A (tonsillectomy/Adenoidectomy) done last year.
Your partner asks, "Did you call your PCP for guidance?" and the woman answers that she thought she should just take her child to the ER. Yeah, the ER-the abused modern day clinic. Your partner asks if she has a car to drive him to the hospital and the woman says no. Of course not. If she needed a ride to Walmart she would have no problem getting one, but to the hospital, the ambulance is always free. Or so it seems to many. You keep those thoughts to your self. You are used to this.

General Impression
As you walk in the room, you see the thin child, of normal size for his age, laying in bed. He shares the room with his younger brother and it is expectedly messy. Though it is a boy's room, you can smell someone was painting nails or something similar. He makes eye contact with you but gives a half hearted smile, showing signs he is tired of being sick. Looking at him makes you overcome with pity. You have forgotten you are a health care provider, often called to replace the MD who did house calls in the past. Despite how busy you are, it is not this kid's fault he is sick. He did not plan this. Despite whether a patient needs transport or not, you have a responsibility to alleviate pain and suffering, and this kid appears to be suffering in some way. This family called you for help and you have an obligation to help them.

Assessment
You talk to the kid and he is alert and oriented but appears slightly pale and tachypneic. Actually, he appears to be hyperventilating at 28 and regular but he denies any SOB and you have seen much worse on healthier patients. His skin is warm and dry and he tells you he is thirsty and hungry but cannot keep anything down.
In the meantime, your partner get vitals:
P=110, S/R
BP=90/58, manually
R=28, deep and regular
T=37.6
Pulsox=97% RA

Your partner asks you if you want to make this ALS or BLS and how do you want to get him to the truck. What is your answer? What is your general impression of this patient? Are the vitals within normal limits for a 9 year old. Does he need to go the hospital or should you call his pediatrician about scheduling an urgent office visit the next day? Would you refer the child to bee seen at the local urgicare center or clinic in the morning? Are there any additional isolation precautions you should consider? What other assessment information would you like (or need) to guide your treatment plan for this patient?