Photo courtesy of Las Vegas Review-Journal

Recently I was the assisting Paramedic for a neighboring service on a cardiac arrest call. Immediately after determining the patient was in a possible witnessed cardiac arrest, CPR was started and the monitored showed asystole. Within a couple of minutes, before IV access was obtained or intubation attempted the medic started shouting, “let’s load and go!” I looked at my partner dumbfounded, and asked the medic if he was sure he did not want to try for ROSC and consider TOR later. It was his call and he said his service transports all arrests. Of course I had to approach their supervisors, and they denied that claim. Recently, at a PALS class, all the medics in their class stated they transport all arrests except the obvious DOAs. Again, I was dumbfounded, so I thought I would discuss this issue here.

Photo Courtesy of www.life-save.org

In fact, now it is no longer acceptable to transport cardiac arrest patients to the hospital (Grudzen, 2006). It is considered unethical for many reasons (AHA, 2000): It ties up a needed bed in an overcrowded ED; it ties up needed members in the ED who must continue the resuscitation; it incurs unnecessary hospital charges; it increases time that EMS crews are not available for another call; it gives the family a false sense of hope and causes them much inconvenience in coming to a crowded ER out of touch with their loved one. It can also be dangerous for the family driving to the hospital in a stressed state of mind (Dick, 2007), and most importantly, dangerous to the public and EMS crew travelling to a hospital lights and sirens with attendants providing resuscitation efforts in the back, unrestrained.

Courtesy of gayaruangkepelbagaim.wordpress.com

Photo courtesy of Michael Ging at photo.net

According to a survey done by Smith (2005), about half of EMS providers felt that their role should include notifying the family of the death, but “three-quarters reported they had not been trained adequately to make a death notification.” She and Feldman (2004) evaluated the change in behavior of EMS providers following death education training were more confident and planned to change their behavior at the scene of death. There are many training programs offered to EMS. However, there is no standardized or required grief support training for EMS, and it is severely deficient in initial EMS training. Cudos should go out to the AHA for including death notification in their 2000 Guidelines PALS video. Since most ALS providers need PALS training, their only grief support training was provided in this video. Still, death notification and grief support training is not consistent and lacking.

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.

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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.

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

Allow me to introduce myself. My name is Chris Kaiser, or Ckemtp, and I write the EMS blog http://www.lifeunderthelights.com/ - I am a Nationally Registered Paramedic holding licensure in Illinois, Iowa, and also in Wisconsin. A few months ago I was asked to become a contributor to write for this blog and I jumped at the chance to intermingle my stuff with the venerable names here. Unfortunately, it has taken me a while to get something up here with the work needed to move from my old site to the new site. Today I'm fixing that and I would like to repost this article here with a few updates. I hope you find it educational.

Visitors to my blog probably know that at my ambulance service we tend to bring back a lot of codes. I talk about it a lot. Back in 2004 our medical director, Dr. Michael Kellum, got us involved in a “Demonstration Project” to bring Continuous Compression CPR or Cardiocerebral resuscitation to a rural area. Since that time, the results have been more than dramatic. Depending on what statistics you look at, we may be “Saving” almost 50% of witnessed arrests found to be in ventricular fibrillation.

It’s all explained at http://www.callandpump.org/, but if you want to go right to the whitepaper that explains what we do, why we do it, and how it’s done then you want to go here: http://callandpump.org/assets/Proposal_Current.pdf – This link is explains the demonstration project initiated by Dr. Kellum et al. in the two county area that I work in. This paper was published in 2004 at the beginning of the project.

This is a link to the results published in the Annals of Emergenc Medicine in 2008 – http://www.ncbi.nlm.nih.gov/pubmed/18374452?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

You may be interested in this part:

“RESULTS: In the 3 years preceding the change in protocol, there were 92 witnessed arrests with an initially shockable rhythm. Eighteen patients survived (20%) and 14 (15%) were neurologically intact. During the 3 years after implementation of the new protocol, there were 89 such patients. Forty-two (47%) survived and 35 (39%) were neurologically intact. CONCLUSION: In adult patients with a witnessed cardiac arrest and an initially shockable rhythm, implementation of an out-of-hospital treatment protocol based on the principles of cardiocerebral resuscitation was associated with a dramatic improvement in neurologically intact survival.”

The management of the newborn with Hypoplastic Left Heart Syndrome can be divided into the initial stabilization period and the operative / post-operative period.

Even while diagnostic tests may be going on, the rapid stabilization of infants with Hypoplastic Left Heart Syndrome must begin as soon as the diagnosis is suspected.

Catheters are placed, usually in the umbilical blood vessels, which allow medications to be given and blood to be obtained for testing. An infusion of prostaglandin, a medication that prevents the patent ductus arteriosus from closing, is begun, thus maintaining the pathway for blood to reach the body from the right ventricle.

Even though the infant may have low oxygen saturations, supplemental oxygen is avoided since it tends to promote more blood flow to the lungs which may steal blood flow from the body and place excessive demands on the already stressed single right ventricle.

Manipulations of medications and respiratory treatments (including possible mechanical ventilation) are performed to optimally balance the flow of blood to the body and the flow of blood to the lungs.

Close monitoring is essential to detect any organ dysfunction and maintain cardiopulmonary stability because infants with this anomaly may be very unpredictable and undergo quite sudden changes.

There are essentially three treatment options that have been proposed for children with Hypoplastic Left Heart Syndrome.

In the past, due to poor outcomes with available treatments at that time, no treatment was often recommended. Today it is rare that a family may choose not to treat a child with Hypoplastic Left Heart Syndrome, though in cases when the infant is unable to be satisfactorily stabilized no treatment may be advised.

Cardiac transplantation in the newborn period is performed as primary treatment for Hypoplastic Left Heart Syndrome at some centers in this country. While transplantation has the advantage of replacing the very abnormal heart of a child with Hypoplastic Left Heart Syndrome with one of normal structure, this treatment is limited by the scarcity of newborn organs available for transplantation and the life-long need for anti-rejection therapy. Additionally, although outcomes for transplantation continue to improve, and the incidence of rejection is lowest in patients transplanted as newborns, the average life span of the transplanted heart is limited (currently less than 15 years).

The most commonly pursued treatment for Hypoplastic Left Heart Syndrome is "staged reconstruction" in which a series of operations, usually three, are performed to reconfigure the child's cardiovascular system to be as efficient as possible despite the lack of an adequate left ventricle. These surgeries do not correct the lesion, and are instead considered "palliative".

The first operation in the staged approach is known as the Norwood operation and is typically performed in the first week of life. With the Norwood operation, the right ventricle become the systemic or main ventricle pumping to the body. A "new" or "neo" aorta is made from part of the pulmonary artery and the original, tiny aorta, which is reconstructed / enlarged to provide blood flow to the body. Finally, to provide blood flow to the lungs, a small tube graft is placed either from an artery to the lung vessels (called a modified Blalock-Taussig shunt) or from the right ventricle to the lung vessels (called a Sano modification). Because of the extensive reconstruction of the aorta that must be done, this operation is one of the most challenging heart surgeries in pediatrics.

The subsequent operations in the staged reconstruction plan are the bi-directional Glenn procedure, typically done at 3 to 6 months of age, and the Fontan operation, typically done in children older than 2 or 3 years. These operations are described in more detail in the Heart Encyclopedia chapter on "Single Ventricle Cardiac Anomalies."