Clysis comes from the same Greek word that “a flood” – hypodermoclysis refers to flooding the subcutaneous space with fluid, so that it can be absorbed systemically.
Well, it turns out, what is old is new again.
In 1913, Dr Day first described this technique for a child with severe diarrhea who could not tolerate fluids by mouth. Hypodermoclysis then began to gain popularity with a peak of use in the 1940s, until an innovative breakthrough in 1950. Dr David Massa, a resident anesthesiologist at the Mayo clinic, invented the first catheter-over-needle apparatus.
With increasing safety and ready access of IV catheters, IV quickly overshadowed SC.
The subcutaneous route of hydration has also been used effectively in geriatric and palliative care for decades, and it is only now beginning to gain popularity again in its original population: children.
In a nutshell, you place a butterfly needle or angiocatheter in the subcutaneous space and you run fluids into it. The tissues quickly absorb the fluids, making them available systemically. That’s it. Everything else is just finesse.
The ideal candidate for hypodermoclysis is the stable patient, with mild to moderate dehydration who fails a trial of fluids by mouth, or who needs a bridge to gaining IV access later, after a slow subcutaneous fluid bolus is given.
Place a topical anesthetic cream, such as EMLA, cover with occlusive dressing (IV dressing), wait 15-20 min
"Pinch an inch" of skin anywhere, but the most practical site in young children is between the scapulae
Insert a 25-gauge butterfly needle or 24-gauge angiocatheter (preferred by the author), secure
Inject 150 U hyaluronidase SC, if available
Infuse 20 mL/kg isotonic solution over one hour, repeat as needed or use "bolus" as bridge to IV access
You can set the line to gravity, and if it is dripping in, you may leave it be. If you see a very slow drip by gravity, or worse, nothing is dripping, you can set the line on a pump, to deliver up to 20 mL/kg over an hour. Infusion at this rate optimizes the balance we want in minimal discomfort while maximizing the flow rate.
This is not a “bolus” in the true sense – but then, when you compare it to the alternative – like IV therapy – and we see a time and cost savings. Dr Mace and colleagues in the American Journal of Emergency Medicine report substantially decreased cost and ED length of stay when comparing the material and human resources needed to place an IV in a squirmy young child, compared with a simple subcutaneous stick.
There will be swelling – that is the goal. It is really painless, and your patient may lie down on his back with the pump going – it is actually pretty comfortable for most children and adults to do.
Here’s a tip – since there will be swelling, we want to be careful about how we secure the line, so how you tape it down to the skin is important – we want to avoid a pulling sensation, which can be the beginning of the end of the tolerance for the procedure. Cover that with an occlusive dressing, as you would an IV site. The footprint of the occlusive dressing is relatively small, so it will travel up on top of the subcutaneous mound you’re creating. As the line exits the occlusive patch, place a thin layer of gauze between the skin and the IV tubing, so that the tubing doesn’t press into the skin. Then—as far away from the puncture site as possible—tape it down securely. The idea is not to tape on the growing mound itself, because the mound may pull at the anchored skin and set a nuclear chain reaction of annoyance and restlessness – and potentially a failed procedure.
The swelling will look indurated, a pinkish red. It’s not an allergic reaction: even with the old preparations of hyaluronidase, allergic reactions were rare, and now they are very rare with the recombinant preparation. It is supposed to swell and look ugly. The subcutaneous tissues will swell to a point where you have a steady state fluid administration rate, and as soon as you stop the infusion, the remaining fluid will start to subside as it is absorbed.
Kuensting et al. in the Journal of Emergency Nursing in 2013 compared subcutaneous fluid infusion with intravenous fluid infusion in children with difficult IV access. They found the mean time from order entry to subcutaneous fluid infusion to be 20 min, compared to the failed IV access group with an average infusion start time of 1.5 hours. The latter group eventually received subcutaneous fluids. The investigators also found a shorter ED length of stay in the subcutaneous group.
In the same study, a subgroup received subcutaneous fluids initially, and later an IV. They found a trend in ease of IV access after subcutaneous fluid therapy. In other words, if your little patient with difficult IV access is hemodynamically stable and amenable to a bolus over an hour, you may choose to start with hypodermoclysis and reevaluate.
Much has been studied and written about the predictors of difficult IV access in children. The most often cited are: age < 3 years, weight less than 5 kg, prematurity, obesity, and darker skin tones, where the contrast of vein to skin may not be so apparent.
The three main predictors of the score validated by Riker et al. in Annals of Emergency Medicine include the most practical and universal of features: vein palpability, vein visibility, and patient age.
If you’re anticipating difficult IV access in the child who can stand to wait an hour for a slow bolus, you may start with the subcutaneous route to get those veins plumper and more visible, to improve your chances of IV access in the very near future.
Certain medications have been used safely via subcutaneous infusion; always check dose, rate, and compatibility.
You don’t need to use larger needles or angiocathters for older children, adolescents or adults. A 25-gauge butterfly or 24-gauge angiocatheter works well from an infant to an elder. In one study of adults, a half a liter of saline was infused by gravity via a 24-gauge catheter. With IVs, the shorter and larger the bore, the faster the infusion.
In subcutaneous infusion, it is not the size of the catheter, but the osmotic gradient that determines the rate of absorption.
It’s actually increasingly readily found – and available in generic form. If you have it, please use it – it will make a believer out of you and others.
Hypodermoclysis will work without hyaluronidase – the process of subcutaneous rehydration just takes a lot longer to work. In a double-blind cross-over trial Thomas et al. in 2007 compared subcutaneous administration of lactated ringer’s solution by gravity with and without hyalurondase. The hyaluronidase group received their fluids 5 times faster. The average rate of the hyaluronidase group was 382 mL/h versus the fluid only group, who did not receive hyalurinodase; they were substantially slower, at 82 mL/h. It’s worth using if you have it, but still potentially useful if you don’t.
√ EMLA or any topical anesthetic used for intact skin, placed as soon as the decision is made
√ A 25-gauge butterfly needle or 24-gauge angiocatheter
√ IV tubing, gauze to pad, tape to anchor
√ 150 U hyaluronidase, the same dose, regardless of age or size
√ Isotonic fluids – you can start with 20 ml/kg
√ And finally a well informed team made up by the patient, the parents, and your staff, so that everyone knows what to expect for a successful subcutaneous fluid administration.
Allen CH, Etzwiler LS, Miller MK, Maher G, Mace S, Hostetler MA, Smith SR, Reinhardt N, Hahn B, Harb G; INcreased Flow Utilizing Subcutaneously-Enabled Pediatric Rehydration Study Collaborative Research Group. Recombinant human hyaluronidase-enabled subcutaneous pediatric rehydration. Pediatrics. 2009 Nov;124(5):e858-67.
Cabañero-Martínez MJ, Velasco-Álvarez ML, Ramos-Pichardo JD, Ruiz Miralles ML, Priego Valladares M4, Cabrero-García J. Perceptions of health professionals on subcutaneous hydration in palliative care: A qualitative study. Palliat Med. 2016 Jun;30(6):549-57.
Mace SE, Harb G, Friend K, Turpin R, Armstrong EP, Lebel F. Cost-effectiveness of recombinant human hyaluronidase-facilitated subcutaneous versus intravenous rehydration in children with mild to moderate dehydration. Am J Emerg Med. 2013 Jun;31(6):928-34.
Riker MW, Kennedy C, Winfrey BS, Yen K, Dowd MD. Validation and refinement of the difficult intravenous access score: a clinical prediction rule for identifying children with difficult intravenous access. Acad Emerg Med. 2011 Nov;18(11):1129-34.
Thomas JR, Yocum RC, Haller MF, von Gunten CF. Assessing the role of human recombinant hyaluronidase in gravity-driven subcutaneous hydration: the INFUSE-LR study. J Palliat Med. 2007 Dec;10(6):1312-20.
Zaloga GP, Pontes-Arruda A, Dardaine-Giraud V, Constans T; Clinimix Subcutaneous Study Group. Safety and Efficacy of Subcutaneous Parenteral Nutrition in Older Patients: A Prospective Randomized Multicenter Clinical Trial. J Parenter Enteral Nutr. 2016 Feb 17. pii: 0148607116629790. [Epub ahead of print]
This post and podcast are dedicated to Christina L. Shenvi, MD, PhD, for her dedication to excellence in patient care and enthusiasm in #FOAMed, Emergency Medicine, and Geriatric Emergency Medicine. There are many shared lessons learned in the care of children, elders, and families. Thank you.
Catch Dr Shenvi on the innovative GEMcast.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
S – Septic Arthritis
The most urgent part of our differential diagnosis. The hip is the most common joint affected, followed by the knee. Lab work can be helpful, as well as US of the hip to look for an effusion, but sometimes, regardless of the results, the joint just has to be tapped to know for sure.
T – Toddler’s fracture
This is usually a torque injury when the wobbling toddler pivots quickly or trips and falls. Toddler’s fractures happen in children 1 to 3 years of age, and occur in the distal 1/3 of the tibia. Sometimes a cast is needed, but currently there is a new trend in foregoing casting in mild cases.
O – Osteomyelitis
Bacteremia – from any source – can seed into any bone. It’s not very common, but it happens: approximately 2% of children who present to an ED with limp will have osteomyelitis. Plain films, ESR, and CRP are a fair screen to start. For more than the casual concern, MRI is the best modality to evaluate, followed by radionuclide scintigraphy. Although not the first choice modality, CT can show periosteal changes, such as inflammatory new bone formation or periosteal purulence.
P – Perthes disease
This is the famous Legg-Calvé-Perthes idiopathic avascular necrosis of the hip, usually affecting children from 3 to 12 years. They present with a slow onset pain and with an antalgic gait. Patients will have trouble with internal rotation and abduction of the hip. Radiographs may be initially normal. MRI can show the culprit: decreased perfusion to the femoral head and subsequent necrosis.
L – Limb-Length Discrepancy
Parents may notice that he seems “wobblier” than he should be. It may be that we are just now appreciating a congenital anomaly. Get out the paper tape, and measure from the anterior superior iliac spine to the medial malleolus and compare both sides. Children with limb-length discrepancy only need a non-urgent referral to pediatric orthopedics to look for congenital dysplasia of the hip, or other growth abnormalities. Some are treated with orthotics. Surgical options vary. Epiphysiodesis destroys the growth plate on the unaffected side, which evens out the growth. Other options are limb-lengthening or limb-shortening procedures.
I – Inflammatory
Transient Synovitis. This is what we want them to have right? The typical age is between 3 and 6 years, sometimes just after a URI. To be comfortable with this diagnosis, we should have considered all of the dangerous diagnoses, the child should be well, afebrile, in minimal discomfort, and he should respond almost completely to an NSAID. He’s the one running up and down the department after treatment – or just from sheer boredom after observation.
M – Malignancy
Primary bone tumors such as Ewing’s sarcoma or osteogenic sarcoma typically affect older children. Limping, however, may be a presenting symptom of leukemia. If you have any suspicion of the general wellness of the child, get a screening CBC, and perhaps a peripheral blood smear. Whatever you do, make sure you get close follow up for these kids that are on your malignancy radar -- the blast crisis may not have occurred yet – but it can happen hours to days later.
Plain films are insensitive for leukemic involvement of bone but they may show diffuse osteopenia, or metaphyseal bands – symmetrical high-uptake markings around the joint. They look like stacks of paper within normal bone – you can see them also in anemia, lead poisoning, and other causes. Also look for periosteal new bone formation, sclerosis, or lysis.
P – Pyomyositis
This usually presents with vague irritability, pain, and fever, and sometimes with a subacute minor trauma. These children don’t look to well.
Also think about just run-of-the-mill myositis, usually from a viral cause, such as influenza. Typically the calves are affected and are always tender. Hydration and supportive therapy are indicated for viral causes.
For bacterial focal pyomyositis, give empiric antibiotics, admit them for major inpatient workup, and think about early surgical consultation if you think you need sepsis source control.
I – Iliopsoas Abscess
Children most often will develop a primary abscess from bacteremia from an unresolved infection. Adults more commonly form secondary abscesses from Crohn’s disease, post-op complications, a vertebral infection, or even a bad chronic urinary tract infection. Lest you think this is a dramatic presentation, think again: iliopsoas abscesses present also with vague symptoms of back, flank, abdominal, or hip pain, sometimes with fever. The median time from symptoms to diagnosis in children is a whopping 20+ days, according to one study. If iliopsoas abscess is starting to get your attention, get the CT or MRI.
N – Neurologic
Not to scare you, but children do have strokes; unlike adults, half are hemorrhagic, half are thromboembolic. Typically they’ll have some underlying pathology that will alert you, such as a cardiac lesion, sickle cell disease, or some infectious or metabolic history. The good news is that it won’t just be a limp – you’ll have some other neuro sign or symptom to go after.
Guillain Barré is another thing to consider – early lower extremity weakness may present as a limp or refusal to walk. Maybe it’s not the hip that should be tapped, but the spinal canal.
Think also about muscular dystrophy or peripheral neuropathy and its possible underlying etiology.
G – Gastrointestinal and Genitourinary
What else could be going on? Appendicitis may be faking you out here. Perhaps there is a hernia, or testicular or ovarian torsion, all of which can present as lateralizing pain and not wanting to walk. Think outside the box.
The gait cycle has three phases: contact, stance, and propulsion. Contact is the time from heel strike to just when the foot is flat. Stance is from the foot being flat to lifting the heel from the ground. The stance phase is when you bear most of your weight. The propulsion phase is when your weight transfers to your toes, and you push off.
Antalgic Gait -- "hobbling" gait; normal contact phase, but stance phase is abbreviated; propulsion is normal. The patient is trying to limit the time spent bearing weight on that side.
Trendelenburg Gait -- the affected side's hip abductor muscles are too weak or painful to stabilize the pelvis; the unaffected side dips to the floor. May be superior gluteal neuropathy, or a biomechanical problem, such as avascular necrosis, congenital dysplasia of the hip, or slipped capital femoral epiphysis.
Circumduction Gait -- the patient swings his foot laterally (due to a foot or ankle pathology), or to avoid tripping in limb-length discepancy.
Stiff-leggged Gait -- the patient walks with knees locked, in an attempt to avoid using the gastrocnemius muscles; concerning for myositis.
Equinus Gait -- toe-walking, as seen in myositis, also to avoid exacerbating pain from the calves.
Look for symmetry of internal rotation, or lateralizing pain or "guarding" with range of motion.
Keep the pelvis flush to the bed, and simultaneously rotate the lower extremity laterally, which will cause internal rotation of the hip.
Avascular necrosis will not allow full internal rotation, since the joint space is narrowed with this maneuver, causing impingement of the sensitive necrotic head of the femur.
Note any pain, asymmetry, and angle of internal rotation achieved.
In their original paper in 1999, Dr Kocher et al. performed a retrospective analysis of children who were being evaluated for a septic joint versus transient synovitis over a 15 year period, in a major referral center. They came up with four independent predictors of a septic joint, and calculated the probability of septic arthritis based on the number of features present. In 2004 the same group validated their prediction tool, with a slightly decreased sensitivity and specificity in the validation population.
In short, the Kocher criteria are not perfect, but it’s the best evidence we have at the moment.
The four predictors are:
Inability to walk
Fever of 38.5 C of greater
ESR > 40 mm/h
WBC > 12,000
Bonus mnemonic: Walk FEW: Inability to Walk | Fever | ESR | WBC
The probability of septic arthritis increases with increasing predictor. In this prediction model, each predictor has the same weight.
Probability of Septic Arthritis (Kocher et al. 1999)
0 Predictor – <0.2 %
1 Predictor – 3%
2 Predictors – 40%
3 Predictors – 93.1%
4 Predictors – 99.6%
Now, remember, this is to be used in children in whom you already have some suspicion of a septic joint. So, 0 predictors, generally you’re alright. 1 predictor, you may start to worry. Once you have 2 predictors, your chances jump for 3% to 40%. You really have to go looking.
The Kocher caveat is that there is no single test or single decision rule that will stop you from investigating if you are concerned enough. Don’t have too much faith in this imperfect decision tool – we use it because we need somewhere to start. Treat and push for the aspiration of the hip if you are left in doubt. Septic arthritis can be devastating if not identified early.
Kocher MS et al. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999 Dec;81(12):1662-70.
Kocher MS et al. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004 Aug;86-A(8):1629-35.
This post and podcast are dedicated to the estimable yet graciously humble Andrew Tagg BSC(Hons), MBBS, MRCSEd, ACEM for his dedication to #FOAMed, Emergency Medicine, Pediatric Emergency Medicine, and all things caffeinated. Thank you for your dedication, generosity, and your example.
World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.
Simply put, shock is the inadequate delivery of oxygen to your tissues. That’s it. Our main focus is on improving our patient’s perfusion.
Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen.
At the bedside, we can measure some of these things, directly or indirectly. But did you notice that blood pressure is not part of the equation? The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal.
The equation here is a formality:
DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2 x 0.003)
Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.
All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion. The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI.
Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis. Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry.
A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion. A warm and dry presentation is typically early in the course, and presents with tachycardia only.
If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress. Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure.
“Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker.
A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow. Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status.
The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up. You will see cool, mottled extremities.
Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion.
Pericardial Effusion? Get ready to aspirate.
Ventricle Size? Collapsed, Dilated,
Careful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion
Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute. Usual adult starting range will end up being 1 to 10 mcg/min.
Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload
Just say no to dopamine: increased mortality when compared to epinephrine
Mostly one of two entities: pulmonary embolism or cardiac tamponade.
Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors.
Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.
Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic. It’s seen easily enough on point of care ultrasound. If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating.
Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial. PE with symptoms: heparin.
Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.
The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle. May be due to obvious GI losses or simply poor intake.
Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter.
Tip: in infants, use pre-filled sterile flushes to push fluids quickly. In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient.
Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output.
The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes. Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components.
Children with sepsis come in two varieties: warm shock and cold shock.
Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine.
Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate. Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine.
Early antibiotics are crucial, and culture everything that seems appropriate.
Sometimes things are not so cut-and-dried. We'll use a practical approach to diagnose and intervene simultaneously.
Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance.
How FAST you FILL the PUMP and SQUEEZE
First, we look at heart rate -- how FAST?
Look at the heart rate – is it sinus? Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output? If so, use 1 J/kg to synchronize cardiovert. Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output -- which is in liters/min – is decreased. Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing.
If the heart rate is what is causing the shock, address that first.
Next, we look at volume status.
How FAST you FILL the PUMP and SQUEEZE
Look to FILL the tank if necessary. Does the patient appear volume depleted? Try a standard bolus – if this improves his status, you are on the right track.
Now, we look at contractility.
How FAST you FILL the PUMP and SQUEEZE
Is there a problem with the PUMP? That is, with contractility? Is this in an infarction, an infection, a poisoning? Look for signs of cardiac congestion on physical exam. Put the probe on the patient’s chest, and look for effusion. Look to see if there is mild, moderate, or severe decrease in cardiac contractility. If this is cardiogenic shock – a problem with the pump itself -- begin pressors.
And finally, we look to the peripheral vascular resistance.
How FAST you FILL the PUMP and SQUEEZE
Is there a problem with systemic vascular resistance – the SQUEEZE?
Look for signs of changes in temperature – is the patient flushed? Is this an infectious etiology? Are there neurogenic or anaphylactic concerns? After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation? If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis. Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock. Perhaps this is warm shock, both are supported with norepinephrine. All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.
The four take-home points in the approach to shock in children
Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830.
Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450.
Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302.
This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed. You make a difference. Thank you.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Altered mental status in children can be subtle. Look for age-specific behaviors that range from irritability to anger to sleepiness to decreased interaction.
In the altered child, anchoring bias is your biggest enemy. Keep your mind open to the possibilities, and be ready to change it, when new information becomes available.
For altered adults, use AEIOU TIPS (Alcohol-Epilepsy-Insulin-Overdose-Uremia-Trauma-Infection-Psychosis-Stroke).
Try this for altered children: remember that they need their VITAMINS!
V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)
I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)
T – Toxins (e.g. environmental, medications, contaminated breast milk)
A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)
M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)
I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)
N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)
S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)
16-month-old who chewed on his grandmother's clonidine patch
Clonidine is an alpha-2 agonist with many therapeutic indications including hypertension, alcohol withdrawal, smoking cessation, perimenopausal symptoms. In children specifically, clonidine is prescribed for attention deficit hyperactivity disorder, spasticity due to cerebral palsy and other neurologic disorders, and Tourette’s syndrome.
The classic clonidine toxidrome is altered mental status, miosis, hypotension, bradycardia, and bradypnea. Clonidine is on the infamous list of “one pill can kill”.
Treatment is primarily supportive, with careful serial examinations of the airway, and strict hemodynamic monitoring.
Naloxone can partially counteract the endogenous opioids that are released with clonidine's pharmacodynamics.
Start with the usual naloxone dose of 0.01 mg/kg, up to the typical adult starting dose is 0.4 mg.
In clonidine overdose, however, you may need to increase the naloxone dose (incomplete and variable activity) up to 0.1 mg/kg. Titrate to hemodynamic stability and spontaneous respirations, not full reversal of all CNS effects.
A 7-year-old with fever, vomiting, body aches, sick contacts. Altered on exam.
Should you get a CT before LP?
If you were going to perform CT regardless, then do it.
Adult guidelines: age over 60, immunocompromised state, history of central nervous system disease, seizure within one week before presentation, abnormal level of consciousness, an inability to answer two consecutive questions correctly or to follow two consecutive commands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language.
Children: if altered, and your differential diagnosis is broad (especially if you may suspect tumor, bleed, obvious abscess).
Influenza is often overlooked as a potential cause of altered mental status. Many authors report a broad array of neurological manifestations associated with influenza, such as altered mental status, seizures, cranial nerve abnormalities, hallucinations, abnormal behavior, and persistent irritability. All of this is due to a hypercytokinemic state, not a primary CNS infection.
14-year-old brought in for "not listening" and "acting crazy"; non-complaint on medications for systemic lupus erythematosus (SLE).
SLE is rare in children under 5. When school-age children present with SLE, they typically have more systemic signs and symptoms. Teenagers present like adults. All young people have a larger disease burden with lupus, since they have many more years to develop complications.
Lupus cerebritis: high-dose corticosteroids, and possibly IV immunoglobulin. Many will need therapeutic plasma exchange (TPE), a type of plasmapheresis.
Schwartz J et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue. Journal of Clinical Apheresis. 2013; 28:145–284.
This post and podcast are dedicated to Teresa Chan, HBSc, BEd, MD, MS, FRCPC for her boundless passion for and support of #FOAMed, for her innovation in education, and for her dedication to making you and me better clinicians and educators. Thank you, T-Chan.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Read on to go from bread-and-butter pediatric blood work to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids?
Someone with a cough and fever may simply have a viral illness, or he may have pneumonia. Our obligation is to evaluate for the pneumonia. It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia.
Depending on the disease and the particular patient, we have a threshold for testing, and the threshold for treating. Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play.
Easy to do right? They are but a click away…
Often a good history and physical exam will help you to calibrate your investigational thresholds. This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care. If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills.
First, a brief word about basic labs.
If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children.
Potassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium.
BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease)
Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!)
Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also fond in liver, placenta, kidneys)
Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood
ESR and CRP: low in healthy children, as chronic inflamation from comorbidities is not present; both increase steadily with age
Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity
Reliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography)
Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies). Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease.
In adults, we typically think of a BNP < 100 pg/mL as not consistent with symptoms caused by volume overload.
Luckily, we have data in children with congenital heart disease as well. Although each company's assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values.
One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation.
Use of BNP in children has been studied in both clinic and ED settings. Cohen et al. in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls.
Later, Maher et al. used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history.
The bottom line is:
To cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children.
The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots.
This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications. An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population.
There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors.
If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer.
If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test.
This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe.
A sick child with sepsis syndrome?
The short answer – yes.
In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients.
And it’s all about perfusion and providing oxygen to the tissues. Lactate and other laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment. There are two main reasons for an elevated lactate: the stress state and the shock state.
The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it.
We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment.
We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level.
Have you every been in this situation:
There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES
L – liver – any liver disease affects how lactate is metabolized by the Cori cycle
A – albuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp
C – “can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration
T – toxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious
A – alcohol, not an infrequent offender
T – thiamine deficiency – think of this in your cachectic or malnourished patients
E – epinephrine – a by-product of the cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip.
S – seizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive.
Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations.
Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495.
Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical Chemistry. 2009; (55) 12:2098–2112.
Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045.
Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56.
Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289.
Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463.
Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360.
Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611.
Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350.
Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168.
Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878.
Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488.
Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6.
Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899.
Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899.
Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31.
Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384.
Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16.
Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8.
Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140.
Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83.
Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280.
Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719.
Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387.
This post and podcast are dedicated to Daniel Cabrera, MD for his vision and his leadership in thinking 'outside the box'.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
On arrival, he was in compensated shock, with tachycardia.
He decompensates and needs blood.
40 mL/kg of blood products given at any time within the first 24 hours.
6-8 units of packed red blood cells (PRBCs)
The typical initial transfusion of PRBCs in children is 10 mL/kg.
Massive transfusion in children is defined as 40 mL/kg of any blood product.
Once you start to give a child with major trauma the second 10 mL/kg dose of PRBCs – start thinking about other blood components, and ask yourself whether you should initiate your massive transfusion protocol.
The goal is to have the products ready to use in the case of the dynamic trauma patient.
Direct measures the four components of clot formation. When there is endolethial damage and bleeding, the sequence that your body takes to address it is as follows:
Red wine glass: a normal tracing with a normal reaction time and a normal amplitude. That patient just needs support and monitoring.
Champagne glass: a coagulopathic TEG tracing – thinned out, with less amplitude. This patient needs specific blood products.
Puffer fish or blob: a hyperfibrinolytic tracing. That patient will needs clot-stablizer.
TEG – like the FAST – can be repeated as the clinical picture changes.
Lethal triad of hypothermia, acidosis, and coagulopathy.
Keep the patient perfused and warm.
Each unit of PRBCs contains 3 g citrate, which binds ionized calcium, causing hypotension. In massive transfusion, give 20 mg/kg of calcium chloride, up to 2 g, over 15 minutes. Calcium chloride is preferred, as it is ionically readily available – just use a larger-bore IV and watch for infiltration. Calcium gluconate could be used, but it requires metabolism into a bioavailable source of calcium.
Prothrombin complex concentrate (PCC) is derived from pooled human plasma and contains 25-30 times the concentration of clotting factors as FFP. Four-factor PCCs contain factors II, VII, IX and X, while 3-factor PCCs contain little or no factor VII.
The typical dose of PCC is 20-50 units/kg
In the severely hemorrhaging patient – you don’t have time to wait for the other blood products to thaw – PCC is a powder that is reconstituted instantly at the bedside.
Tranexamic acid (TXA), is an anti-fibrinolytic agent that functions by stopping the activation of plasminogen to plasmin, and the degradation of fibrin. The Clinical Randomisation of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) investigators revealed a significant decrease in death secondary to bleeding when TXA was administered early following trauma.
Based on the adult literature, one guideline is to give 15 mg/kg loading dose of TXA with a max 1 g over 10 minutes followed by 2 mg/kg/h for at least 8 h or until bleeding stops.
Our goal here is damage control. Apply pressure whenever possible. Otherwise, resuscitate, identify the bleeding source, and slow or stop the bleeding with blood products or surgery.
In adults, we speak of “permissive hypotension” (also called “balanced resuscitation” or “damage control resuscitation”). The idea is that if we bring the adult patient’s blood pressure up to normal, we may be promoting clot rupture. To avoid this, we target a MAP of 65 and look for clinical signs of sufficient perfusion. Adults tolerate hypotension relatively well, and is sufficient until we send them to the OR or interventional radiology suite.
In children, this is simply not the case. Hypotension in children is a sign of pre-arrest. Remember, they compensate with an increased systemic vascular resistance and tachycardia to maintain blood pressure.
We should not allow children to become hypotensive – severe tachycardia alone should prompt us to resuscitate.
In other words, permissive hypotension is not permissible for children.
Fox et al in Academic Emergency Medicine found a sensitivity of 52%; with a 95% confidence interval [CI] = 31% to 73%.
Often children even with high-grade splenic and liver lacerations can be managed non-operatively. If they are supported adequately, they are observed in the ICU and can avoid surgery in many cases. Unfortunately, a negative FAST cannot help with detecting or grading the laceration for non-operative management. In other words, feel free to use ultrasound – especially for things that we in the ED will react to and intervene on – but CT may help to manage the traumatized child non-operatively.
CT Head and Neck, non-contrast: in concerning mechanisms of injury, patients that are difficult to assess (especially those under 3 months), those with a GCS of 13 or lower.
CT Chest, IV contrast: for suspicion of vascular injury that needs exploration, especially in penetrating trauma. Otherwise, chest xray will tell you everything you need to know in children – especially in blunt trauma. Hemo or pneumothoraces are readily picked up by US or CXR. Rib fractures on CXR predict pulmonary contusions. If you are concerned about great vessel injury, then CT Chest may be helpful; otherwise consider omitting it.
CT Abdomen and Pelvis, IV contrast: helpful in grading splenic and liver lacerations with goal to manage non-operatively. Abdominal tenderness to palpation, significant bruising, or a seat belt sign are concerning and would generally warrant a CT. Also, consider in liver function test abnormalities, or hematuria.
Extremity injuries: in general can be evaluated with physical exam and plain films. However, some injuries in high-risk anatomically complex areas such as the hand and wrist, tibial plateau, and midfoot may be missed by plain films, and CT may be helpful here.
Fox JC, Boysen M, Gharahbaghian L, Cusick S, Ahmed SS, Anderson CL, Lekawa M, Langdorf MI. Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma. Acad Emerg Med. 2011 May;18(5):477-82.
Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.
Nosanov L, Inaba K, Okoye O, Resnick S, Upperman J, Shulman I, Rhee P, Demetriades D. The impact of blood product ratios in massively transfused pediatric trauma patients. Am J Surg. 2013 Nov;206(5):655-60.
Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.
This post and podcast are dedicated to Larry Mellick, MS, MD, FAAP, FACEP. Thank you for your dedication to medical education, and sharing your warm bedside manner, extensive knowledge and talents, and your patient interactions with the world.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
When you think of trauma in children, think of Charlie Brown. Large head, no neck, his chest and abdomen form an underdeveloped, amorphous shape.
Alternatively, think of children as apples – they are rounder than they are tall, with a large increased surface area. Apples don’t have a hard shell or thick rind to protect them. If you drop them, you may not see any evidence of damage to the outside, but there can be considerable bruising just under the surface.
A 5-year-old boy who was playing with his older brother in front of their home when the ball rolled into the street. He ran after it, and was struck by a sedan going approximately 30 mph.
This is the so-called Wadell’s triad that occurs in a collision of auto versus pedestrian or auto versus bicycle. The initial impact is the greatest, and will vary depending on the child’s height and what part of his body reaches up to the bumper of the car. Depending on the height of the child and the height of the car, the initial impact will cause a femur fracture, a pelvic fracture, or direct abdominal trauma. The second impact happens as the child is flung onto the grill or the hood of the car, causing usually thoracic trauma. The third impact can be the coup de grace – to add insult to major injury, the child is then propelled forward, worsening the two previous impacts’ injuries and adding a third – severe blunt head trauma.
If your patient has any subtle change in mental status, intubate early. In pediatric trauma, we need to be proactive. Hypoxia is our enemy.
Thankfully cervical spine injuries in children are uncommon, and when they do occur, they typically occur at the child’s fulcrum, which is at C2. Compare this with an adult’s injury pattern with our fulcrum at C7. Be careful and minimize manipulation of the cervical spine, but do what you must to visualize the chords and place the tube. Keep the neck midline, and realize that the child’s usual decrease respiratory reserve is even more affected by trauma. Preoxygenate and pass that tube quickly.
Chest tube sizing in pediatrics is straightforward if we remember that the traditional chest tube size is 4 x the ETT size.
Try using a pigtail catheter.
It’s roughly where you would put on a generous dose of deodorant. Insertion here minimizes the risk of damage to nerves, vessels and organs.
In a 40-year review of ED thoracotomy, Moore et al. analyzed 1,691 patients who received ED thoracotomy. Overall all-cause adult survival was 6.1%. In children ? 15 years of age, overall all-cause survival was considerably less, at 3.4%.
In a large case series and review of the literature for pediatric ED thoracotomy, Allen et al. found a survival rate in penetrating trauma of 10.2%, with a much lower survival rate in blunt pediatric arrest, at 1.6%. Adolescents had more penetrating injuries, and younger children had more blunt trauma.
To synthesize, the rarity of ED thoracotomy in children is due to the fact that:
If you have access to resuscitative endovascular balloon occlusion of the aorta or REBOA, this may be an option to temporize the child to get him to the relative control of the operating room. REBOA involves accessing the common femoral artery, passing a vascular sheath, floating a balloon catheter to the appropriate section of the aorta, and inflating the balloon to occlude blood flow.
Brenner et al. described a case series of 6 patients from two Level I trauma centers. They used REBOA for refractory hemorrhagic shock due to either blunt or penetrating injury. After balloon occlusion, blood pressure improved sufficiently to take the patient either to interventional radiology or to the OR. Four patients lived, two died. The AORTA trial is underway to investigate its use in trauma.
Allen CJ, Valle EJ, Thorson CM, Hogan AR, Perez EA, Namias N, Zakrison TL, Neville HL, Sola JE. Pediatric emergency department thoracotomy: a large case series and systematic review. J Pediatr Surg. 2015 Jan;50(1):177-81.
American College of Surgeons Committee on Trauma; American College of Emergency Physicians Pediatric Emergency Medicine Committee; National Association of Ems Physicians; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Fallat ME. Withholding or termination of resuscitation in pediatric out-of-hospital traumatic cardiopulmonary arrest. Pediatrics. 2014 Apr;133(4):e1104-16.
Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.
Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.
Pediatric Trauma on WikEM
This post and podcast are dedicated to Dr Al Sacchetti, MD, FACEP. Thank you for promoting the emergency care of children and for spreading the message that you don’t need subspecialty training to take good care of acutely ill and injured children.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
In children with malrotation, 50% present within the first month of life, with the majority occurring in the first week after birth. 90% of children with malrotation with volvulus will present by one year of age. This is a pre-verbal child’s disease – which makes it even more of a challenge to recognize quickly.
The sequence of events usually is fussiness, irritability, and forceful vomiting. The vomit quickly turns bilious.
Green vomit is a surgical emergency.
Babies may also present unwell, with bloating and abdominal tenderness to palpation. Be aware that later stages of malrotation may present as shock – they present in hypovolemic shock due to third-spacing from necrotic bowel and/or septic shock from translocation or perforation. In the undifferentiated sick neonate, always consider a surgical emergency such as malrotation with volvulus.
In the stable patient, get an upper GI contrast study.
Rapid-fire word association for other vomiting emergencies in a neonate:
All that vomits is not necessarily from the gut.
Abusive head injury is the most common cause of death from child abuse. Infants especially present with non-specific complaints like fussiness or vomiting. Up to 30% of infants with abusive head injury may be misdiagnosed on initial presentation.
Louwers et al. in Child Abuse and Neglect developed and validated a six-question screening tool for use the in ED. The power of this tool was that it was validated for any chief complaint – it is not an injury evaluation checklist – it is a screen for potential abuse in the undifferentiated child:
On multivariable analysis, if at least one of the questions was positive, there was an OR of 189 for abuse (CI 97 – 300). In other words, if any of those six questions are problematic, get your child protective team involved.
Other important diagnoses in the infant: intussusception and pyloric stenosis (rapid review in audio).
The important diagnosis not to miss in the vomiting toddler or early school age child is the initial presentation of diabetic ketoacidosis. Children under 5 (especially those under 2) and those from lower socioeconomic groups have a higher risk of DKA as their initial presentation of diabetes.
This is true for any child that isn’t quite acting right – check a finger stick blood sugar as a screen.
If you have access to checking a serum beta-hydroxybutryrate – the unsung ketone – it can help in diagnosis in unclear cases.
Cerebral Edema Criteria:
Cerebral Edema Action Items:
As you can see, vomiting in the young child can be really anything! Keep your differential broad, and think by age and by system.
The general approach to the child with chiefly vomiting starts with the decision: sick or not sick. If ill appearing, establish rapid IV access, or if needed IO. Rapid blood sugar and if available a point of care pH and electrolytes. Be the detective in your history and doggedly go after any red flags as you go methodically by organ system.
In other words, use your best judgement, have the dangerous differentials in the back of your mind, and pull the trigger when red flags mount up. Otherwise, a good history and a good exam will get you where you need to be.
Applegate KE, Anderson JM, Klatte EC. Intestinal malrotation in children: a problem-solving approach to the upper gastrointestinal series. Radiographics. 2006; 26(5):1485-500.
Glaser NS, Wootton-Gorges SL, Buonocore MH et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. 2006 Apr;7(2):75-80.
Louwers ECFM, Korfage IJ, Affourtit MJ et al. Accuracy of a screening instrument to identify potential child abuse in emergency departments. Child Abuse & Neglect. 2014; (38): 1275–1281.
Lee HC, Pickard SS, Sridhar S et al. Intestinal Malrotation and Catastrophic Volvulus in Infancy. J Emerg Med. 2012; 43(1): e49–e51.
Marcin JP, Glaser N, Barnett P et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr. 2002; 141(6):793-7.
Parashette KR, Croffie J. Intestinal Malrotation in Children: A Problem-solving Approach to the Upper Gastrointestinal. Pediatrics in Review. 2013; (34)7: 307-321.
Wolfsdorf JI, Allgrove J, Craig ME et al. ISPAD Clinical Practice Consensus Guidelines 2014. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2014 Sep;15 Suppl 20:154-79.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Household electricity uses alternating current, or AC. Voltages across the world range anywhere from 100 to 240 V. Here in North America, most outlets and appliances use 120 volts, which is the measure of electrical tension, or the potential difference in electrical charge.
Cut-off between low voltage and high voltage is 1000 V.
Industrial energy may be AC or direct current, DC. DC current propels the victim -- think of this as a blast injury. The same voltage in AC is three times as damaging as that voltage at DC, because AC causes muscle tetany, and prolonged contact time.
Did the current pass through the thorax? -- Think dysrhythmias. Through the head or neck? -- Think damage to the CNS and risk for later central respiratory arrest; acoustic nerve damage; cataract formation. Did the current pass along an extremity? -- Think compartment syndrome and rhabdomyolysis.
The electrical charge meets resistance and converts to thermal energy, which causes tissue necrosis, increasing with the contact time. Was your patient extricated? Was there tetany? Was he found in a pool of water or liquid? Longer contact time correlates with extensive injuries that may only be apparent hours later.
Think of electrical injury as a trauma – major trauma rarely occurs in isolation. Was the patient flung after contact? Did he have a syncopal episode? -- Think precipitated dysrhythmia and fall. Was there any chest pain? -- Consider stress-induced ischemia.
An electrical burn to the angle of the mouth cauterizes superficial bleeding vessels, and hours later the wound becomes covered with a white layer of fibrin, surrounded by erythema. Edema and thrombosis will continue, and at 24 hours there is typically a significant margin of tissue necrosis. Most patients do well, and the burn heals by secondary intention. The eschar will slough off in 1 to 2 weeks. The labial artery is just deep to the burn, and as the eschar sloughs off, it can be exposed. It’s a high-flow artery to the face, and if disrupted, the child may have significant bleeding and possibly hemorrhagic shock.
These children need close wound care follow-up, and potentially outpatient coordination with Head and Neck Surgery and/or Plastic Surgery consultants.
Precautionary advice: take the moment to talk to parents about the risk, and show them how to apply pressure to the wound, pinching the inner and outer cheek together with the thumb and index finger until the child arrives to the hospital.
A a “kissing burn” occurs when the electrical charge creates an arc and jumps to a more proximal portion of the extremity.
The kissing burn typically occurs at flexor creases such as the wrist or the antecubital fossa. There is often extensive underlying tissue damage even under the skin where it doesn’t appear to be involved. Compartment syndrome and subsequent rhabdomyolysis and renal failure are the highest-risk complications.
Nitrogen capsules propel two barbs into the dermis, which deliver short bursts of energy; most patients have no harm from the electricity delivered.
How to remove a dart: The darts are typically 9 mm long, but the small barb is typically not buried very deep in the skin. Hold the skin taught, use a hemostat to grasp the end as close to the skin as possible, align the dart perpendicularly to the skin, and pull quickly and firmly.
If the patient can’t tolerate this or the barb appears particularly embedded, inject with local lidocaine and make a small superficial incision with an 11-blade scalpel just large enough to allow passage. Ultrasound can be used to troubleshoot when needed.
Taser dispo: People who have been tased do remarkably well and complications are rare. In a review of tasers used by law enforcement, Vilke et al. found that there was no need for routine laboratory testing or observation, as there was ‘no evidence of dangerous laboratory abnormalities, physiologic changes, or immediate or delayed cardiac ischemia or dysrhythmias after exposure to electrical discharges of up to 15 s.” Subsequent studies with minors less than 16 years of age found similar results.
Special note on the patient with agitated delirium or stimulant intoxication: treat these patients carefully, as the organic problem that got them tased in the first place still needs to be addressed, and substances such as PCP, cocaine, and methamphetamines are all cardiac irritants and may predispose them to dysrythmias.
Patients who are struck by direct current like lightening should be treated aggressively, because the reason for their cardiac arrest is often reversible if treated quickly. Either the current sent the victim into a dysrhythmia, or it caused a temporary paralysis of the thoracic muscles, resulting in a primary respiratory arrest.
For victims of a lightning strike, classically we use reverse triage – normally, those in full arrest are triaged as black, deceases. In high-voltage and lightening injuries, we tend to those in full arrest first, because you might quickly reverse them, and can move on to the next patient triaged red, or immediate.
High-voltage injuries are a multi-trauma – other sequelae include pulmonary edema, paralysis, ileus, and cataracts, in addition to the more immediate cardiac, musculoskeletal, neurologic, and renal considerations.
Regardless of the exposure, obtain an ECG and look for bundle branch block, heart block, and dysrhythmias, since those will change disposition. In those who are injured, consider a basic metabolic panel, looking for potassium, calcium, and creatinine. A creatine phosphokinase or total CK will screen for rhabdomyolysis. Troponin is not predictive of the extent of direct myocardial damage, but get it if you think there might be a stress-induced, or type II MI. Radiography as needed depending on the presenting associated trauma.
1. Injury from electrical burns can be subtle. Think of patients as having occult multi-trauma. Be thorough in history and examination. Plan to re-examine either during observation in the ED, or in close outpatient follow-up.
2. Discharge patients with low-voltage injury, no symptoms, and a normal ECG. Counsel outpatients and provide close follow-up as appropriate.
3. Admit patients with low-voltage injury with signs or symptoms such as loss of consciousness, ECG changes, or evidence of end-organ damage on laboratory screening. Admit all patients with high-voltage injury, even if asymptomatic and a normal laboratory screen.
4. Transfer patients with high-voltage injury or significant burns to a regional burn center or trauma center.
Celik A, Ergün O, Ozok G. Pediatric electrical injuries: a review of 38 consecutive patients. J Pediatr Surg. 2004;39(8):1233-1237.
Ericsson KA. Deliberate Practice and Acquisition of Expert Performance: A General Overview. Acad Emerg Med. 2008; 15:988-994.
Fish RM. Electric injury, part I: treatment priorities, subtle diagnostic factors, and burns. J Emerg Med. 1999;17(6):977-983. doi:10.1016/S0736-4679(99)00127-4.
Fish RM. Electric injury, part II: Specific injuries. J Emerg Med. 2000;18(1):27-34. doi:10.1016/S0736-4679(99)00158-4.
Fish RM. Electric injury, part III: cardiac monitoring indications, the pregnant patient, and lightning. J Emerg Med. 2000;18(2):181-187. doi:10.1016/S0736-4679(99)00190-0.
Horeczko T. “Electrical Injuries: Shocking or Subtle?” In Avoiding Common Errors in the Emergency Department, 2nd Edition. Mattu M, Swadron SP (eds). Lippincott, Williams & Wilkins. Phiadelphia. 2016. (In Press).
Rai J, Jeschke MG, Barrow RE, Herndon DN. Electrical Injuries: A 30-Year Review. J Trauma Acute Care Surg. 1999;46(5):933-936.
Vilke GM, Bozeman WP, Chan TC. Emergency department evaluation after conducted energy weapon use: review of the literature for the clinician. J Emerg Med. 2011; 40(5):598-604.
This post and podcast are dedicated to Joelle Donofrio, MD, FAAP for her tireless care of children, in the ED and in the field. A special thank you and dedication to Cliff Reid, BM, FRCP(Glasg), FRCSEd(A&E), FRCEM, FACEM, FFICM, FCCP, EDIC, DCH, DipIMC, RCSEd, DipRTM, RCSEd, CCPU, CFEU for his transformative intelligence and educational verve.
Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother. On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions. Her heart rate is 160, RR 50, oxygen saturation is 88% on RA. She has fine tissue-paper like rales throughout her lung fields. Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse.
She is in respiratory failure from bronchiolitis and likely viral sepsis. She needs her airway taken over.
Is this child stable enough for intubation?
We have a few minutes to optimize, to resuscitate before we intubate.
Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS. Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child.
Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV.
The consensus recommendation for the induction agent of choice for sepsis in children is ketamine.
Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock. It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines.
The succinylcholine versus rocuronium debate…
Succinylcholine and its PROS
Succinylcholine and its CONs
Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug. The side effects are rare, but they can be deadly. So, what’s the alternative?
Rocuronium and its PROs
Rocuronium and its CONs
Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him.
He is brought in by paramedics, who are now bagging him.
Are your surgeons in an uproar about a long-acting agent and the pupillary response? Relax, it’s a myth.
Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response. Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response.
In a critically ill child or adult, perfusion suffers and it affects how we administer medications. The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives.
We need to adjust our dosing for a critically ill patient:
Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing.
The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology.
The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump. The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome.
Typical “normal” saturations are 75 and 85% on RA. Ask the parents or caregiver.
Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others.
A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism.
Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive.
Children after palliative surgery for cyanotic heart disease are volume-dependent. Even if there is a component of cardiogenic shock, they need volume to drive their circuit. Give a test dose of 10 mL/kg NS.
A blue baby – with a R –> L shunt – needs some pinking up with ketamine
A pink baby – with a L –> R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate.
Myocarditis or other acquired causes of cardiogenic shock – etomidate.
Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today.
On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic.
Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol.
Rocuronium (in general), as there are concerns of a neurologic comorbidity.
What size catheter doe I use? If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5.
Remember this: 2, 3, 4 – Tube, Tape, Tap
Medicine is evolving. As technology advances, we need to meet the challenge of taking care of our patients who have come to rely on this technology for their basic needs. Before we go further, remember to assess the parent and the child as a unit. The caregiver who is usually the parent, is a rich source of knowledge about the child’s particular condition and past experience. Take them seriously, and be on the lookout for caregiver burnout.
4-month-old baby boy born full term with Pierre Robin Sequence, febrile, not eating anything, now with breathing difficulty.
Place on trach collar oxygen, suction those secretions; flush with small amounts of saline, and repeat.
Any child symptomatic with a trach? Remember to monitor for hypoxia and bradycardia.
Tracheostomy indications: obstruction, primary respiratory compromise, or a neurologic disorder. The obstruction may be a tumor, post-infectious, or addressing a congenital anomaly. Children may have bronchopulmonary dysplasia, a restrictive lung disease such as scoliosis. A wide array of neurologic problems can result in a child’s having a trach, such as cerebral palsy, TBI, or spinal muscular atrophy.
Early complications of trachs especially in the first few months – include bleeding, pneumomediastinum, accidental decanulation, wound breakdown, and subcutaneous emphysema. The most common later complications include infection and granuloma formation. Tracheo-esophageal fistulas and trachea-innominate fistulas are thankfully very rare.
11-year-old girl with a history of prematurity, intraventricular hemorrhage, and subsequent flaccid paralysis with neurogenic bladder. She is brought in by her mother because of constipation and “not acting her usual self”. She is afebrile, abdomen is soft, full of stool.
The most common shunt is the ventriculoperitoneal shunt, originating in a lateral ventricle and tracking subcutaneously down the neck and chest until the distal end enters and coils in the peritoneal space. Less common types include ventriculoatrial, ventriculopleural, ventriculocisternal, ventriculo-vesicular (to gall bladder) and the lumbo-peritoneal, usually reserved for spina bifida.
The common denominator: hydrocephalus. The most common causes are tumor, congenital anomalies, hemorrhage, or post-infectious obstructions.
The two most common complications of VP shunts are malfunction (due to obstruction, fracture, or kinking) or infection. The slit-ventricle syndrome results from overdrainage, causing headaches and ataxia and the slit-ventricle syndrome. An abdominal pseudocyst forms when cells floating in the peritoneal cavity aggregate on the distal tip of the VP shunt, forming a biofilm that fills with CSF. VP shunts, like any foreign body, can migrate and erode through intestines and skin.
Classically in severe hydrocephalus an infant or toddler will have sun-setting eyes – the irises look like a setting sun against the prominent bulbar conjunctiva. However, the presentation is usually much more subtle; if the child just feels off or if the parent tells you he is not acting right, this is a shunt malfunction until proven otherwise.
Garton et al. in the Journal of Neurosurgery followed 344 children with shunts, and found that in the first six months after a shunt is placed, the presence of nausea or vomiting carried a positive LR pf 10.4 for shunt malfunction. Irritability conveyed a positive LR of 9.8 for shunt malfunction. Decreased LOC was 100% predictive.
Most shunt infections occur within a few weeks after placement. 90% of infections occur within the first 9 months. Fever is only 60% sensitive, but CRP is 95% specific.
If the child has severe mental status changes, hypertension, and/or bradycardia, tap the shunt emergently.
Head of the bed is 30 degrees; sterile fashion: don a cap, mask, faceshield, and sterile gloves, chlorhexidine or betadine to clean. Use a 23 or 25 g butterfly attached to a manometer, and advance slowly. Pressures above 25 mmH20 are reliably indicative of a distal shunt obstruction. If there is no return of CSF, or there is poor flow, there probably is a proximal obstruction. Make note of the pressure you get, allow the pressure to equilibrate, remove the needle, and dress it sterilely. Be ready to take over the airway if needed, and use standard ICP lowering temporizing tactics until a neurosurgeon is found.
A 3-year-old boy with ALL undergoing consolidation chemotherapy has had vomiting with abdominal pain since yesterday; he is febrile, tachycardic, and pale; there is mild tenderness to palpation in the right lower quadrant, and his capillary refill is 3 seconds. He is in compensated shock.
The Huber needle is not a resuscitative line. Obtain proper access to give fluids -- do not rely on the port-a-cath.
Vascular devices are notoriously troublesome. In the European Respiratory Journal, Munck et al. reviewed cases of patients who needed to have their vascular devices out. 43% of them got them out for was for occlusion, 21% infection; other reasons included displacement, rupture, and skin necrosis. Only 2.5% of them were removed for clinical improvement.
When a child or an adult is at risk for a massive air embolism, we should do three things: clamp the device proximal to the fracture or defect, hyperoxygenate, and perform Durant’s maneuver, or left lateral decubitus in Trendelenberg. This forces a presumed air embolus to stay in the apex of the right ventricle until we figure out what to do. You can put the US probe on and look for a whirlwind of tiny bubbles to confirm – it is very sensitive and can detect as little as 0.05 ml/kg of air. Some references advocate for hyperbarics to allow the embolus to resolve, others comment on using a needle to aspirate air. The main thing for us is to suspect it, detect it, control it, and if the child arrests, to do vigorous CPR to mechanically disrupt the bubbles.
A 17-year-old boy with a history of botulism had a rough ICU course, home after rehabilitation, with some residual dysmotility issues, still partially g-tube dependent. No complaints in the ED, but there is irritation around the stoma, and discomfort with g-tube manipulation.
G-tubes are placed for one of three reasons: insufficient intake, increased demand, or increased loss. Insufficient intake may be due to anatomical problems, prematurity, or failure to thrive. Increased demand may be temporary, such as in burns, s/p cardiac surgery, or ay prolonged recovery. Increased losses may be from enteropathies, or short gut syndrome.
Gastrostomy or g-tubes end directly in the stomach. Whatever you can take by mouth can go into the g-tube, including medications and bolus feeds.
Jejunostomy tubes, or J-tubes are placed by IR or surgery for babies with severe reflux – this is for drip feeds, usually done at night.
Gastro-jejunostomy tubes or G-J tubes use the G port for medications, and the J port for continuous feeds.
We do not pull or replace or touch G-J or J tubes in the ED, but we can place a Foley catheter in the stoma to keep it patent if needed.
“Buried bumper syndrome” occurs when the patient has not changed his g-tube for much longer than recommended, or if there is a dramatic change in habitus. The inner balloon is pulled up and away from the stomach lumen, so that it is displaced and fixed – causing pain, inadequate feeds, obstruction, and sometimes peritonitis.
Tracheostomy: the stoma matures in one month – you can change out after that, suction, suction, suction, and you can place an ETT if the patient is critical.
Ventriculoperitoneal Shunts: 90% of infections occur within the first 9 months.
Vascular Devices: assume the line is not functional, and use another to resuscitate, especially in port-a-caths.
Gastrostomy Tubes: buried bmpers are bad business – be aware of the painful, obstructed, poorly mobile g-tube. The stoma matures in one month is open, three months of it’s a PEG. If it has fallen out, you have 1-3 hours before the stoma begins to close – temporize with a foley catheter.
When it comes to the technologically dependent child in the ED, familiarity breeds…confidence!
Babu R, Spicer RD. Implanted vascular devices (ports) in children: compications and their prevention. Pediatr Surg Int (2002) 18: 50-53
DiBaise JK, Scolapio JS. Home Parenteral and Enteral Nutrition. Gastroenterol Clin N Am 36 (2007) 123-144l
Feinberg A et al. Gastrointestinal Care of Children and Adolescents with Developmental Disabilities. Pediatr Clin N Am 55 (2008) 1343–1358
Garton HJ. Piatt JH. Hydrocephalus. Pediatr Clin N Am 51 (2004) 305– 325
Kusminsky RE. Complications of Central Venous Catheterization. J Am Coll Surg. January 17, 2007.
Marek A. Mirski MA et al. Diagnosis and Treatment of Vascular Air Embolism. Anesthesiology 2007; 106:164–77
Marks JH. Pulmonary Care of Children and Adolescents with Developmental Disabilities. Pediatr Clin N Am 55 (2008) 1299–1314
Munck A et al. Follow-up of 452 totally implantable vascular devices in cystic fibrosis patients. Eur Respir J 2004; 23: 430–434
Shinkwin CA, Gibbin KP. Tracheostomy in children. J Royal Soc Med. Volume 89 April 1996
Simpkins C. Ventriculoperitoneal Shunt Infections in Patients with Hydrocephalus. Pediatr Nurs Nov 2005 Vol 31, No 6
Trachsel D, Hammer J. Indications for tracheostomy in children. Paediatric Resp Rev (2006) 7, 162–168
Wright SE,VanDahm K. Long-term care of the tracheostomy patient. Clin Chest Med 24 (2003) 473– 487
Intranasal medications, if understood and employed properly, are a great choice to avoid and IV or as a bridge until IV access is obtained. Learn the strengths and limits of intranasal fentanyl, midazolam, ketamine, and dexmedetomidine.
Pain Management in Children
Goal: the “ouchless ED”.
Two main barriers in pain treatment in children:
1. We consistently under-recognize children’s pain. We may not detect the typical behaviors that children exhibit when they are in pain, especially in the pre-verbal child: crankiness or fussiness; changes in appetite or sleep; decreased activity; or physiologic findings such as dull eyes, flushed skin, rapid breathing, or sweating.
2. We under-treat pain in children. This is mostly from an old culture of misunderstanding or fear of overdose.
Four Components to Successful Pain Management and Intranasal Medication Administration
Right drug, right dose, right patient, right timing
Right Drug – Not every medication is easily amenable to intranasal administration. We can use intranasal drugs for analgesia, for anxiolysis, for seizures – but not all drugs used for those purposes will perform well – or at all – via the IN route.
Right Dose – Dosing with IN meds will vary considerably from the IV route. Rule of thumb: the IN dose is 2-3 times the IV dose.
Right Patient – Is this patient and family appropriate for “just taking the edge off”? What is the level of anxiety in the room? How is the child relating to the parent, usually it’s the mother there. What else is going on in that clinical snapshot as you walk in?
Right Timing – Mostly IV and IN onset times are very similar. Notable exception: intranasal midazolam may take 10-15 minutes to take effect – something to keep in mind when you plan your procedure.
Intranasal Medications bypass first-pass metabolism, and a portion of the drug is delivered into the CSF immediately via the nose-brain pathway.
Ideal Volume for Intranasal Medication: 0.25 to 0.3 mL per naris
Absolute maximum: 1 mL per naris (but expect some run-off)
Preload the device with 0.1 mL solution for dead space
Administer intranasal medications in the sniffing position. Lie the patient flat with occiput posterior, put patient in the sniffing position, seat the mucosal atomizing device cushion in the naris, aim toward the pinna of the ear, and shoot fast – you have to push the drug as fast as you can to atomize the solution.
Safe, effective at 2 mcg/kg. Most commonly stocked concentration of fentanyl is 50 mcg/mL. A 40-kg-child will reach the maximum volume possible for administration (40 kg x 2 mcg/kg = 80 mcg; at 50 mcg/mL – that makes 1.6 mL – if we divide the dose, it’s not ideal, but is still under our maximum of under 1 mL per naris.) You graduate from intranasal fentanyl in elementary school.
Sufentanil for adults (half the volume of fentanyl) – 0.5 mcg/kg, which can be repeated as needed.
Intranasal Midazolam or versed for anxiolysis is dosed at 0.3 mg/kg (up to 0.5 mg/kg for procedural sedation)
Here, another practicality weighs in. The IV preparation for midazolam is 5 mg/5 mL – this a very dilute solution. You need to use the 5 mg/mL concentration to have any success with intransal midazolam because of the volume needed for the right effect.
A 20-kg-child will near the maximum volume for intranasal midazolam (0.3 mg/kg is 6 mg, at 5 mg/ml, 1.2 mL, or 036 mL per naris). Kindergarten graduation is when to drop the intranasal midazolam.
The IV dose for ketamine for pain control is 0.15 to 0.3 mg/kg, usually as an infusion over an hour. The intranasal dose of ketamine for pain control is 1 mg/kg.
Low-dose ketamine may be used for pain control as an adjunct and opioid-sparing agent.
Dexmedetomidine is an alpha-2 receptor agonist, a smarter clonidine. Clonidine is also an alpha-2 agonist, and it can cause a marked decrease in blood pressure with some mild sedation. Dexmedetomidine targets receptors in the CNS and spinal cord, and so it provides deep sedation, with very minimal blood pressure effects. It induces a sleep-like state. In fact, EEGs done under dex show the same pattern as seen in stage II sleep. Dex is safe, if titrated, and does not depress airway reflexes or respiration. Dose is 2.5 mcg/kg IN, and can add another 1 mcg/kg if needed. The downside is that it can last 30 minutes or more, but it may be a good choice for an abdominal ultrasound or CT head in unruly toddlers.
Before You Go: The “Semmelweiss reflex”.
Weisman SJ, Bersnstein B, Schechter NL. Consequences of Inadequate Analgesia During Painful Procedures in Children. Biol Neonate. 2000 Feb;77(2):69-82.
Anand KJ, Scalzo FM. Can adverse neonatal experiences alter brain development and subsequent behavior? Expert Opin Drug Deliv. 2008 Oct;5(10):1159-68. doi: 10.1517/17425247.5.10.1159 .
Wu H, Hu K, Jiang X. From nose to brain: understanding transport capacity and transport rate of drugs. J Opioid Manag. 2012 Jul-Aug;8(4):237-41. doi: 10.5055/jom.2012.0121.
Stephen R, Lingenfelter E, Broadwater-Hollifield C, Madsen T. Intranasal sufentanil provides adequate analgesia for emergency department patients with extremity injuries.
Do you have a plan for your little patient when he just won’t stop seizing? What do you do when your typical treatment is not enough? Get up-to-date in the understanding and management of pediatric status epilepticus.
Definition of status epilepticus:
Continuous seizure activity of 5 minutes or greater
– OR –
Recurrent activity without recovery between intervals. (This definition includes clinically apparent seizures as well as those seen only on EEG.)
During a seizure, GABA receptors in the neuron’s membrane are internalized and destroyed. Seizure activity itself starts this self-defeating process – this is the first reason we need to act as quickly as possible and take advantage of the GABA receptors that are still recruitable.
Excitatory receptors – the NMDA receptors – are acutely upregulated and mobilize to the neuron’s surface. This is the second reason to act quickly and avoid this kindling effect.
In other words – time is brain.
Or… is it something else as well?
Pediatric status epilepticus is analogous to the multi-organ dysfunction syndrome in severe sepsis. Status epilepticus affects almost every organ system.
Cardiac – dysrhythmias, high output failure, and autonomic dysregulation resulting in hypotension or hypertension.
Respiratory – apnea and hypoxia, ARDS, and potentially aspiration pneumonia.
Renal – rhabdomyolysis, myoglobinuria, and acute renal failure.
Metabolic – lactic acidosis, hypercapnia, hyperglycemia, sometimes hypoglycemia, hyperkalemia, and leukocytosis.
Autonomic – hyperpyrexia and breakdown of cerebral circulation.
DeLorenzo et al.: Mortality correlated with time seizing. Once the seizure has met the 30 min mark, Delorenzo reported a jump from 4.4% mortality to 22%! If the seizure lasts greater than 2 hours, 45%. Time spent seizing is a vicious cycle: it’s harder to break the longer it goes on, and the longer it goes on, the higher the mortality.
Think about treatment of pediatric status epilepticus in terms of time: prehospital care, status epilepticus (greater than 5 min), initial refractory status epilepticus (greater than 10 min), later refractory status (at 20 min), and coma induction (at 25 minutes).
Case 1: Hyponatremic Status Epilepticus
Give 3 mL/kg of 3% saline over 30 min.
Stop the infusion as soon as the seizure stops.
Case 2: INH toxicity
Empiric treatment -- you are the test. If we know the amount of ingestion in adults or children, we give a gram-for-gram replacement, up to 5 grams.
If a child under 2 years of age arrives to you in stats epilepticus, give 100 mg of IV pyridoxime for potentially undiagnosed congenital deficiency.
Case 3: Headache and Arteriovenous Malformation
Unlike in adults, stroke in children is divided evenly between hemorrhagic and ischemic etiologies.
The differential is vast: cardiac, hematologic, infectious, vascaulr, syndromic, metabolic, oncologic, traumatic, toxic.
Treatment: stabilization, embolization by interventional radiology, elective extirpation when more stable. Other options for stable patients include an endovascular flow-directed microcatheter using cyanoacrylate. Radiosurgery is an options for others.
Non-convulsive Status Epilepticus
Risk factors include age < 18, especially age < 1, no prior history of seizures, and traumatic brain injury. This would prompt you to ask for continuous EEG monitoring for non-convulsive status epilepticus, especially when there is a change in mental status for no other reason. Also, a prolonged post-ictal state or prolonged altered mental status. Other considerations are those who had a seizure and cardiac arrest - ROSC without RONF, those with traumatic brain injury, and those needing ECMO – all within the context of seizures.
The longer the seizure lasts, the harder it is to break – act quickly
Have a plan for normal escalation of care, and Search for an underlying cause
Recognize when the routine treatment is not enough.
Before You Go
“Healing is a matter of time, but it is sometimes also a matter of opportunity.”
“Extreme remedies are very appropriate for extreme diseases.”
– Hippocrates of Kos
Abend NS et al. Nonconvulsive seizures are common in critically ill children. Neurology. 2011; 76(12):1071-7
Baren J. Pediatric Seizures and Strokes: Beyond Benzos and Brain Scans. ACEP Scientific Assembly. October 8th, 2009. Boston, MA.
Brophy et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocrit Care. 2012; DOI 10.1007/s12028-012-9695-z
Capovilla G et al. Treatment of convulsive status epilepticus in childhood: Recommendations of the Italian League Against Epilepsy. Epilepsia. 2013; 54 Suppl 7:23-34
Chin RFM et al., for the NLSTEPSS Collaborative Group. Incidence, cause, and short-term outcome of convulsive status epilepticus in childhood: prospective population-based study. Lancet. 2006; 368: 222–29.
Chen JW, Chamberlain CG. Status epilepticus: pathophysiology and management in adults. Lancet Neurol. 2006; 5:246-256.
DeLorenzo RJ. Comparison of status epilepticus with prolonged seizure episodes lasting from 10 to 29 minutes. Epilepsia. 1999 Feb;40(2):164-9.
LaRoche SM, Helmers SL. The New Antiepileptic Drugs: Scientific Review. JAMA. 2004;291:605-614.
Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care. 2010; 26(5):380-1.
Ogilvy CS et al. Recommendations for the Management of Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Stroke Council. Stroke. 2001; 32: 1458-1471
Rosati A et al. Efficacy and safety of ketamine in refractory status epilepticus in children. Neurology. 2012; 79:2355-2358.
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Trommer BL, Pasternak JF. NMDA receptor antagonists inhibit kindling epileptogenesis and seizure expression in developing rats. Brain Res Dev Brain Res. 1990 May 1;53(2):248-52.
Waterhouse EJ et al. Prospective population-based study of intermittent and continuous convulsive status epilepticus in Richmond, Virginia. Epilepsia. 1999 Jun;40(6).
You have all of the skills you need to care for an acutely ill infant. Learn a few pearls to make this a smoother endeavor.
The Pediatric Assessment Triangle is a rapid, global assessment tool using only visual and auditory clues to make determinations on three key domains: appearance, work of breathing, and circulation to the skin.
The combination of abnormalities determines the category of pathophysiology: respiratory distress, respiratory failure, CNS or metabolic problem, shock, or cardiopulmonary failure.
Tone - the newborn should have a normal flexed tone; the 6 month old baby who sits up and controls her head; the toddler cruises around the room.
Interactiveness - Does the 2 month old have a social smile? Is the toddler interested in what is going on in the room?
Consolability - A child who cannot be consoled at some point by his mother is experiencing a medical emergency until proven otherwise.
Look/gaze - Does the child track or fix his gaze on you, or is there the "1000-yard stare"?
Speech/cry - A vigorously crying baby can be a good sign, when consolable - when the cry is high-pitched, blood-curling, or even a soft whimper, something is wrong.
If the child fails any of the TICLS, then his appearance is abnormal.
Work of Breathing
Children are respiratory creatures - they are hypermetabolic - we need to key in on any respiratory embarrassment.
Look for nasal flaring. Uncover the chest and abdomen and look for retractions. Listen - even without a stethoscope - for abnormal airway sounds like grunting or stridor. Grunting is the child's last-ditch effort to produce auto-PEEP. Stridor is a sign of critical upper airway narrowing.
Look for abnormal positioning, like tripodding, or head bobbing
Circulation to the skin
Infants and children are vasospastic - they can change their vascular tone quickly, depending on their volume status or environment. Without even having to touch the child, you can see signs of pallor, cyanosis, or mottling. If any of these is present, this is an abnormal circulation to the skin.
Pattern of Abnormal Arms = Category of Pathophysiology
Differential Diagnosis in a Sick Infant: "THE MISFITS"
Trauma - birth trauma, non-accidental - check for a cephalohematoma which does not cross suture lines and feels like a ballotable balloon, as well as for subgaleal hemorrhage, which is just an amorphous bogginess that represents a dangerous bleed. Do a total body check.
Heart disease or Hypovolemia - is there a history of congenital heart disease? Was there any prenatal care or ultrasound done? Does this child look volume depleted?
Endocrine Emergencies - Could this be congenital adrenal hyperplasia with low sodium, high potassium, and shock? Look for clitoromegaly in girls, or hyperpigmented scrotum in boys. Could this be congenital hypothyroidism with poor tone and poor feeding? Any history of maternal illness or medications? Congenital hyperthyroidism with high output failure?
Metabolic - What electrolyte abnormality could be causing this presentation? Perhaps diGeorge syndrome with hypocalcemia and seizures?
Inborn Errors of Metabolism - there are over 200 inborn errors of metabolism, but only four common metabolic pathways that cause a child to be critically ill. Searching for an inborn error of metabolism is like looking for A UFO - amino acids, uric acids, fatty acids, organic acids. If the child's ammonia, glucose, ketones, and lactate are all normal in the ED, then his presentation to the ED should not be explained by a decompensation of an inborn error of metabolism.
Seizures - Neonatal seizures can be notoriously subtle - look for little repetitive movements of the arms, called "boxing" or of the legs, called "bicycling"
Formula problems - Hard times sometimes prompt parents to dilute formula, causing a dangerous hyponatremia, altered mental status, and seizures. Conversely, concentrated formula can cause hypovolemia
Intestinal disasters - 10% of necrotizing enterocolitis occurs in full-term babies - look for pneumatosis intestinalis on abdominal XR; also think about aganglionic colon or Hirschprung disease; 80% of cases of volvulus occur within the 1st month of life
Toxins - was there some maternal medication or ingestion? Is there some home remedy or medication used on the baby? Check a glucose ad drug screen
Sepsis - Saved for last - You'll almost always treat the sick neonate empirically for sepsis - think of congenital and acquired etiologies.
The hyperoxia test is the single most important initial test in suspected congenital heart disease - we can test the child's circulation by his reaction to oxygen on an arterial blood gas. Place the child on a non-rebreather mask, and after several minutes, perform an ABG. (Ideally you obtain a preductal ABG in the right upper extremity, and compare that with one on the lower extremity, but this may not be practical.)
In a normal circulatory system, the pO2 should be high - in the hundreds - and certainly over 250 torr. This effectively excludes congenital heart disease as a factor. If the pO2 on supplemental oxygen is less than 100, then this is extremely predictive of hemodynamically significant congenital heart disease. Between 100 and 250, you have to make a judgement call, and I would side on worst first.
If you are giving this child 100% O2, and he doesn't improve 100% -- that is, his ABG is not at least 100 - then he has congenital heart disease until proven otherwise.
Give prostaglandin if the patient is less than 4 weeks old (typical presentation is within the first 1-2 weeks of life). Start at 0.05 mcg/kg/min. PGE keep the systemic circulation supplied with some mixed venous blood until either surgery or palliation is decided.
* When you see a sick infant, keep THE MISFITS around to keep you out of trouble.
* Before you decide on sepsis, ask yourself, could this be a cardiac problem?
* When in doubt, perform the hyperoxia test.
* All the rest, you have time to look up.
Before You Go: The Availability Heuristic
Brousseau T, Sharieff GQ. Newborn Emergencies: The First 30 Days of Life. Pediatr Clin N Am. 2006; 53:69-84.
Cloherty JP, Eichenwald EC, Stark AR: Manual of Neonatal Care, 5th edition. Philadelphia, PA, Lipincott Williams & Wilkins, 2004.
Horeczko T, Young K: Congenital Heart Disease, in Pediatric Emergency Medicine-A Comprehensive Study Guide, 4th Ed. ACEP/McGraw-Hill, 2013.
McGowan et al. Part 15: Neonatal Resuscitation: 2010 American Heart Association Guidelines. Circulation. 2010;122:S909-S919.
Okada PJ, Hicks B. Neonatal Surgical Emergencies. Clin Ped Emerg Med. 2002; 3:3-13.