Sick Kid Part 3

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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.
The A, B, Cs-Airway
Let’s start at the beginning. Obviously our first priority is the A, B, Cs, right. Of course. If the kid starts to lose consciousness, we may want to consider intubation. I say consider as I admit our pediatric intubation skills are most usually attributed to practicing on a manikin once or twice a year. It depends on good clinical thinking in what is really best for the patient, considering how long it is from the appropriate hospital. We can find patients in DKA who are severe enough to be unconscious. Some parents just are not bright enough to ensure their kids get their needed insulin. If the trip to the appropriate facility is far, intubation may be warranted, but if it is close, monitoring the airway and BVM may be all that is needed, as well as an NG tube if that is within your scope.

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.

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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.

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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.

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Cerebral Edema

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.

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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.

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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.

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Insulin Drip in the ED

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.

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Treating Acidosis

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.

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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:


Brandis, K., “8.2.5 Management of DKA, Acid-Base Physiology”,, 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:

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”,, 2006

Kane E., “Diabetic Ketoacidosis and Cerebral Edema”,, 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

DIABETIC KETOACIDOSIS”, University of Minnesota Department of Pediatrics Division of Endocrinology, 2003


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


ADAM said...

You're making me proud Shaggy. Great series.

Shaggy said...

I am just trying to meet your standards, and it is real difficult to do.

Ambulance Driver said...

Nice series, Shaggy. I picked up a few things!

Shaggy said...

I need to pick up a few things around my house too. Oh, you meant something else.
Accolades from you two means a lot.
I probably should have discussed treating Hyperkalemia with calcium if peaked T waves were noted, as a PICU fellow (a real fellow-the doctor kind)mentioned to me. However hypekalemia in cardiac care could be mentioned in another post by someone else. Another PICU fellow I know told me what I saw in the literature in that fluids will help flush out the K and when insulin is started, the K will go back in the cells. However, he admitted hyperkalemia should be treated if it affects conduction. Not many of us carry calcium gluconate and certainly not Kayexylate.
I think my main take home message for all EMS providers is don't assume it is just a kid with a "stomach virus".
I appologize for not discussing adult DKA, but I thought there was less to discuss and most of us are familiar with it other than precipitating factors.

Ambulance Driver said...

Another PICU fellow I know told me what I saw in the literature in that fluids will help flush out the K and when insulin is started, the K will go back in the cells."

That's pretty much the approach to hyperkalemia in DKA around here, although they will, as you pointed out, treat more aggressively if it affects cardiac conduction.