Pediatric Airway, Respiratory Distress & Failure, & Hypoperfusion Emergencies

The Pediatric Airway, Respiratory Distress and Failure, & Hypoperfusion Emergencies STEVE MARCHBANK, MD www.pedsteve.com [email_address]

Etiology of Pediatric Cardiopulmonary Arrest Respiratory: 80% Cardiac: 10% Shock: 10%

Pediatric Non-Hospital Arrest Bronchiolitis & Pneumonia SIDS Severe Asthma Croup/Epiglottitis Submersion Poisoning Choking Trauma Dehydration/Shock

SIDS We STILL don’t know what causes it…… Can be difficult to distinguish from smothering “ Back to Sleep” Firm sleeping surface (no excessive blankets, pillows, soft stuffed animals, co-bedding) NO SMOKING Premies, underlying health problems, may run in families Does circulating air help???

Upper Airway Obstruction, Etiology Infectious disease accounts for 90%, with viral croup accounting for 80% Epiglottitis: 5% of severe cases 5% foreign bodies, external trauma to neck/throat, congenital anomaly

Croup Also called laryngotracheobronchitis Almost exclusively viral (parainfluenza, RSV, rhinoviruses, measles) – transmitted via respiratory droplets Begins with prodrome of mild UIR with nasal congestion, sore throat and cough Mean age is 18 months, seasonal ↑ in autumn and early winter As the infection spreads distally, the edema also spreads Characterized by hoarse voice, and brassy, seal-like cough Stridor usually develops/worsens at night May have ↑ in temperature; drooling is uncommon. May see mild expiratory wheezing

Croup, cont “ Steeple Sign” – narrowing of tracheal air column due to edema May have marked improvement with humidified air

Peds vs. Adult Airways In children, the tongue is larger, easily displaced, and the most common cause of airway obstruction in an obtunded child The narrowest point of the pediatric airway is the Cricoid ring . This means obstruction below the epiglottis is more likely than in adults

Anatomy Narrowest Point = Cricoid Cartilage Adult Child

Supraglottic vs. Subglottic Above the epiglottis, as in epiglottitis, you have inspiratory stridor, a prolonged inspiratory phase, and muffled cry or voice. Subglottic obstructions cause expiratory stridor with a normal voice, and brassy (louder) cough and cry

Upper Airway Obstruction May see the “sniffing position”, and may have drooling Expiration is usually less labored, and remember, it is normally ‘passive’ (you don’t have to ‘force’ the air out when we are breathing normally)

Warning Signs Marked retractions Absent breath sounds ↑ Tachypnea Decreasing respiratory effort/rate Head-bobbing w/ each breath Cyanosis is a LATE sign in upper airway obstruction A non-crying child may be in big trouble

Epiglottitis Usually children 3-7 years of age Haemophilus influenzae (Hib) is most common etiology Swollen epiglottis (the ‘thumb sign’ on radiograph) Usually sudden onset and progresses rapidly Muffled voice or cry (in croup it is more hoarse) Sore throat, fever, hoarseness initially Drooling from difficulty swallowing saliva (from glottic edema) May see ‘sniffing position’ Try to calm child (and not agitate) – administer high flow humidified O2 If obstruction-> Bag/mask ventilation (OR is often needed to intubate)

Croup vs. Epiglottitis Croup MUCH more common Voice = hoarse Cough = barking Fever = yes or no Saliva = minimal Neck swelling = little Begins = slowly Season = autumn/early winter Time = evening/night Epiglottitis Much less common Voice = muffled Cough = none or minimal Fever = yes, often high Saliva = TONS Neck swelling = lots Begins = rapidly Season = year-round Time = 24 hours (though may be worse at night)

Swelling/Edema in Infants Even ONE mm of airway swelling in infants can cause big problems, whereas a healthy child can tolerate much better. Also…. Healthy children will maintain their tidal volume almost completely until the point of exhaustion, at which point they progress rapidly (hypoxia, hypercapnia, acidosis)

Bronchiolitis Infection in bronchioles, characterized by very thick mucous, usually clear/white/yellowish (later) Caused by: RSV (especially during peak winter months), Influenza, rhinovirus, parainfluenza virus, adenovirus Worse in smaller infants, ex-premies, BPD (bronchopulmonary dysplasia), asthmatics, CF

What is asthma? Chronic airway inflammation Reversible airway constriction/airflow limitation Airway hyperresponsiveness Recurring symptoms over time, usually from a variety of triggers

OK… but what IS asthma? The first thing to remember (in pediatric or adult asthma) is that asthma can wear many ‘hats’ and remember that…. Not everything that ‘wheezes’ is asthma, and not every asthmatic is ‘wheezing’

Asthma Pathophysiology: 2 basic components Bronchoconstriction: Multiple biochemical pathways; bronchospasm means the air doesn’t flow as easily, which can give cough, wheeze, SOB, sleep disturbance, etc. Airway hyperresponsiveness to a variety of triggers & reversible airway obstruction/constriction Inflammation: Multiple contributing mechanisms and pathways; inflammation leads to tendency for bronchospasm & excessive mucous production

Inflammation and Mucous Membranes: The forgotten story What happens when a mucous membrane becomes inflamed? You get……… MUCOUS! This goes for asthma, infection, and any irritation of the airway

So… what MIGHT be asthma? Recurrent cough (dry or loose) Wheezing Shortness of breath, chest tightness Exercise intolerance Sleep disturbance; cough at night Colds ‘go to the chest’, and/or always last >10 days ‘ recurrent croup’ constant throat-clearing

Diagnosis of Asthma History- pattern and recurrence of symptoms Physical examination Family History Measurement/estimation of lung function (as age appropriate) Evaluation of allergies/allergic status Exclude alternative diagnoses

The “Three R’s” of asthma diagnosis Recurrence : symptoms recur over time Reactivity : the symptoms brought on by a trigger Responsive : symptoms ↓ in response to bronchodilators and/or anti-inflammatory agents (i.e. ICS)

What may only LOOK like pediatric asthma? (differential diagnoses) Allergic rhinitis/sinusitis Large airway obstruction: tracheal FB, vocal cord dysfunction, vascular rings, laryngotracheomalacia, laryngeal webs, extrinsic (lymphadenopathy/tumor) Small airway obstruction: viral bronchiolitis, obliterative bronchiolitis, CF, BPD (bronchopulmonary dysplasia), heart disease Vocal cord dysfunction Other: recurrent cough (non-asthmatic), chronic aspiration and/or severe GERD

Asthma Triggers Upper respiratory infection Allergens: animal dander, dust mites, pollen, molds Exercise Smoke : cigarette, other Temperature/humidity changes Emotional stress: anxiety, fatigue, laughter, crying Other: drugs, chemicals

How common is asthma? If neither parent has asthma, the incidence of asthma in the average child is 7-10% ~20% if one parent has asthma ~60% if both parents have asthma Significant number of infants/toddlers hospitalized for RSV bronchiolitis go on to have asthma (somewhere between 30-50%)

II. Asthma Classification The most recent NAEPP (National Asthma Education & Prevention Program) Expert Panel Report 3 (2004) classifies asthma into the following: Mild intermittent Mild persistent Moderate Persistent Severe Persistent Can be found online at: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm

The Big Picture for Primary Care….. Is Asthma Intermittent or Persistent? The take-home message of the most recent Expert Panel Report, and for the typical primary care provider is this: Once you have established the diagnosis of asthma, you should then CLASSIFY it based on the frequency of recurrence (most importantly) and severity of symptoms, as being either intermittent or persistent

Intermittent vs. Persistent Intermittent Asthma symptoms  2 times/week nighttime symptoms  2 nights/month FEV1/PEF  80% predicted PEF variability < 20% Persistent Asthma symptoms > 2 times/week nighttime symptoms > 2 nights/month FEV1/PEF variable (dependent on sub-type, mild/mod/severe) PEF variability > 20%

Why does the classification matter? The classification - intermittent or persistent - leads us to the proper management and treatment of asthma The basics: intermittent asthma = bronchodilators as needed persistent asthma = daily anti-inflammatory + bronchodilators as needed

The Basics of Asthma Maintenance and Control 1. Persistent asthma = Daily , preventative anti-inflammatory asthma medication 2. The Gold-Standard for anti-inflammatory asthma medication is: inhaled corticosteroid

Treatment of Asthma in the Acute Care or ER Setting History h/o chronic respiratory diseases (BPD-Bronchopulmonary Dysplasia, RSV) h/o Atopy, allergies FHx asthma Presence of pets or smokers in the home Known triggers Home Medications

Risk Factors for severe or persistent status asthmaticus h/o ↑ use of home bronchodilators without success h/o previous ICU admissions h/o previous intubation Asthma exacerbation despite recent or current corticosteroid use Frequent ED visits and/or hospitalization h/o syncope or seizures during exacerbation O 2 saturation below 92% despite supplemental O 2 If patient has severe exacerbation without wheezing (the silent chest) – may imply such severe airway obstruction or fatigue such that they are unable to move enough air to wheeze

Physical Exam Always go back to the basics….. A irway B reathing C irculation

“ A” Airway Evaluation Foreign bodies and secretions: FB, especially in toddlers; thick secretions in RSV infection, CF (Cystic Fibrosis), other infections; Airway edema may cause wheezing/compromise in CHF (which is not that common in children) Don’t forget about a possible FB in the L or R mainstem bronchus (or trachea), which can mimic asthma and other respiratory conditions Mouth: make sure no obstruction, if patient obtunded or unconscious, jaw thrust/neck tilt Nose: clearing of secretions, being aware of any anatomical abnormalities that may interfere with breathing and/or interventions. Also remember that neonates are ‘obligate nose breathers’, so they will preferentially breathe through their noses, not mouths. Neck/Throat: positioning, is air being exchanged adequately; extrinsic compression from vascular rings, lymphadenopathy, tumors

Airway Maneuvers Head Tilt-Chin Lift Jaw Thrust

“ B” Breathing Evaluation Adequacy of air movement Respiratory Rate Equality of Chest Movement Auscultation of Patient (can be difficult with loud upper respiratory noises – sometimes using the bell of the stethoscope can help unmask the air movement you’re wanting to hear) Use your EYES, not just your ears (respiratory effort, retractions/accessory muscles, sitting up and forward, nasal flaring) Pulse Oximetry, End-Tidal CO 2, Peak Flow Measurement

“ C” Circulation Perfusion Capillary Refill: remember that peripheral perfusion may be significantly affected by volume depletion/dehyrdration, so core cap refill may be more accurate and diagnostic Also….. Neonates especially have preference for core circulation, so acrocyanosis even in a normal, healthy infant may cloud the picture Color Heart Rate Blood Pressure

Cardiac Pulsus paradoxus: ↓ in SBP during inspiration, due to ↓ in cardiac stroke volume with inspiration due to greatly ↑ LV afterload generated by the dramatic ↑ in negative intrapleural and transmural pressure in a patient struggling to breathe against significant airway obstruction. Pulsus paradoxus of > 20 mm Hg correlates well with the presence of severe airways obstruction

What is next? Be aggressive about your initial treatment of the very ill asthmatic, aka status asthmaticus: the first few minutes can make all the difference in ‘breaking’ the patient out of their crisis, in order to get to the stabilization/maintenance mode of treatment Don’t be too afraid to give β 2 agonists (Albuterol, Xopenex), and lots of them, especially early in the game.

Mainstays of Treatment Again, remember the 2 mechanisms of asthma: Bronchoconstriction and Inflammation Therefore, our therapeutic agents are going to target both of these components

Oxygen What is V/Q Mismatch? In the normal lung, the areas being ventilated are also being perfused, so that Oxygenated hemaglobin can be delivered to the rest of the body With V/Q mismatching, there are areas of shunting and ‘dead space’, such that areas receiving ventilation are getting little to no perfusion, or areas that are being perfused well are getting no ventilation.

Oxyhemaglobin Dissocation Because of the flat upper portion of the Oxyhemoglobin dissociation curve, blood leaving the relatively healthy alveoli will have an oxygen saturation of about 97%. Blood leaving alveoli that do not have optimum V/Q ratios will have a much lower oxygen saturations. The admixture of all the blood leaving the alveoli results in low oxygen saturations and hypoxemia.

So, who cares about the V/Q Mismatch and Oxyhemaglobin? V/Q mismatch is responsible for most cases of respiratory failure, and is by far the most common cause of hypoxemia. So….. Some O 2 delivery in the right way is a very, very good thing.

O 2 Delivery Nasal Cannula: 1-5 L/min can deliver up to a maximum of about 40% P a O 2 Is influenced by RR, tidal volume and pathology Venturi Mask: Mixes O2 with room air, and can achieve a maximum of about 40% P a O 2 Often used when concerned about CO 2 trapping/retention

O 2 Delivery Simple Face Mask: O 2 Typically delivered at 5-10 L/minute, which can give a maximum of about 40-60% F i O 2 Influenced by RR, tidal volume, and pathology Non-rebreathing Mask: Indicated when you need a F i O 2 greater than 60% O2 flow of 8-10 L/minute, and can give an F i O 2 of about 90% Uncomfortable; may have CO 2 trapping/retention

Bag-Mask Ventilation Sellick Maneuver Pressing down on Cricoid cartilage, which compresses the esophagus against the cervical spine

Intubation Reasons to Intubate?? Failure to Oxygenate (Hypoxia/hypoxemia) Failure to remove CO2 (Hypercarbia) ↑ Work of Breathing CNS Failure; Neuromuscular Weakness Cardiovascular Failure

ET Tube Children >2 Years: ETT Size: (Age+16) / 4 ETT Depth (lip): ETT size x 3 Size of the tip of pinkie = ETT size

Laryngoscope Blades Better in infants/toddlers/younger children with a floppy epiglottis Straight Blade

Curved Blade Better in older children (teens/adults) with stiff epiglottis

Confirmation of ETT Placement in the field Auscultation Chest Rise End-Tidal CO 2 detector Water vapor in tube O 2 sats improving

Failure or Deterioration after Endotracheal Intubation pneumonic: D O P E D isplacement O bstruction P neumothorax E quipment failure

Reasons for inadequate improvement after ET Intubation Inadequate PEEP Air leak or disconnection Inadequate O2 flow Air trapping and ↓ Cardiac Output

β 2 agonists Albuterol 0.5mg in 2.5cc Saline (or 1 ampule of pre-mixed albuterol, 0.083%, the equivalent of 0.5mg) Continuous Albuterol Xopenex (l-Albuterol) Delivered in 0.25 mg, .125mg and 0.63mg Ampules 0.25mg Xopenex is equivalent to 0.5mg of Albuterol Supposed to have fewer CNS side effects due to being a non-racemic medication (i.e. the r-Albuterol has been removed)

β 2 agonists Again, be AGGRESSIVE with your usage of β 2 agonists Give first dose of either Albuterol or Xopenex, and be ready/willing to give a 2 nd , 3 rd or 4 th dose of them very quickly if inadequate clinical response to the first dose Consider giving Albuterol or Xopenex as a continuous nebulized solution to the critical patient

Other Inhaled Agents Atrovent (Ipatropium Bromide) What is Ipatropium? It’s quaternary Atropine (4 units bound together), an anti-cholinergic, and does not cross the BBB (Blood-Brain Barrier) May give in addition to β 2 agonists to enhance effect in acute setting Dosing: Adults, 1 ampule (500mcg, or 0.5mg) q1-2 ̊ - may give in addition to β 2 agonists Pediatrics: ½ ampule – 1 ampule for children down to 2 Neonates: ¼ - ½ ampule

Other inhaled agents, cont. L-epi or racemic epi may have a role in severe bronchospasm in the emergent setting, especially if IV access has not been obtained Racemic Epi: 0.5cc in 3ccNS L-epi: 1:1000 nebulized HeliOx (Helium-Oxygen mixture) usually a 70:30 helium-oxygen mixture – can be very effective in O 2 exchange, unless higher O 2 concentrations are needed to treat hypoxemia. If need more than 30% O 2 , then will not be very useful. Works because Helium-Oxygen is about 1/3 rd as dense as Nitrogen-Oxygen (Helium mw=2; Nitrogen mw=14)

Other inhaled agents, cont. Inhaled Steroids – is there a role? Definitely, especially if IV access is difficult or cannot/has not been obtained Pulmicort Respules: (comes as 0.25mg, 0.5mg and 1mg) Give 1mg respules Dosing: 2, 3 or 4 respules given consecutively or continuously – may be mixed with other inhaled agents (Albuterol, Xopenex, Atrovent)

Quick side note… Croup Inhaled steroids in Croup Has a definite role, especially in the emergent setting. Would dose with 2-, 3- or 4- 1mg Pulmicort Respules consecutively or continuously – again, may combine with other inhaled agents (L-epi or racemic epi) May use as delivery vehicle for other inhaled agents, i.e. 0.5cc of racemic epi combined with a 1mg Pulmicort respule, or 0.5cc Albuterol/Xopenex with 1mg Pulmicort Respule

Fear of steroids, inhaled or otherwise I have seen much resistance (sadly) to the use of higher doses of inhaled steroids for status asthmaticus or croup, due to fear of ‘steroid side effects’, yet we readily pump 60 or 80 mg of methylpred into someone intravenously Which is more important – the acute, life or death setting, or worrying about GI side effects, secondary bacterial infection or thrush 8 hours later? Yes, there may be some sequelae from intensive steroid use, but these can be dealt with once a patient is out of crisis mode – I would much rather have to give Nystatin or Zantac to a patient who’s life has been saved, rather than having a dead patient with no thrush. Which do you think has a greater impact on the body: 4-6mg of inhaled steroid (or even more), or 80 mg of Methylpredinisone? It’s not rocket surgery. 

Intravenous Agents Steroids Decadron: Pediatrics: 0.6mg/kg up to 20mg Methylprednisilone: 2mg/kg up to 80mg Side effects: Acutely, GI upset/bleed, bacterial 2 nd infection Chronic use: Cushing’s syndrome, weight gain, edema

Intravenous Agents Terbutaline β 2 receptor agonist – may still have some tachycardia, arrhythmia, ECG changes at higher doses due to weak β 1 effect IV: Loading dose: 5-10 mcg/kg over 10 minutes; maintenance: start at 0.4-1 mcg/kg/min, may increase in increments of 0.2-0.4 mcg/kg/min to a max of 4 mcg/kg/min. Some studies have shown efficacy and success up to 20 mcg/kg/min SQ: 0.01mg/kg/dose q15-20 min prn; max dose 0.25mg MUCH better than Isoproterenol, which has been used in the past

Intravenous Agents Magnesium Sulfate Causes smooth muscle relaxation (hence, bronchodilatory effect) by competing with Ca ++ at Ca ++ -mediated smooth muscle receptor sites 25-75mg/kg infused over 20 minutes (max 2.5 g/dose) May cause significant increase in PEF, FEV1, and FVC Adverse effects: Hypotension, flushing, tingling, nausea

Intravenous Agents Ketamine Short acting pentachlorophenol (PCP) derivative that exerts bronchodilatory effects by ↑ endogenous catecholamines, which bind β -receptors and cause smooth-muscle relaxation and bronchodilation Also has sedative effect to reduce anxiety/agitation which can be present (tachypnea and ↑ work of breathing) – may prevent respiratory failure in children with status asthmaticus Dosing: IV: 0.5-2 mg/kg– produces effect within 30 seconds, lasts 10-20 minutes IM: 4-12mg/kg which gives effect within 3-4 minutes, lasting 12-30 minutes Remember, although Ketamine has some respiratory/aspirative-sparing effects, you must be wary of aspiration, loss of airway, etc. as with any sedative

Intravenous Agents Epinephrine Dosing (1:10,000): IV for adults usually ranges from 0.1 to 0.25 mg (1 to 2.5 mL of 1:10,000 solution), injected slowly. Neonates may be given a dose of 0.01 mg per kg of body weight; for the infant 0.05 mg is an adequate initial dose and this may be repeated at 20 to 30 minute intervals Dosing (1:1000) SQ: 0.01mg/kg (max 0.3mg/dose) ET : 0.05-0.1mg/kg dose, followed by NS flush

Hypoperfusion Emergencies Shock in Children: Hypovolemic: Most common loss of intravascular volume, hemorrhage, electrolyte imbalance, loss of plasma (burns, nephrotic syndrome) Septic: includes multiple forms (hypovolemic, distributive, cardiogenic) Cardiogenic: CHD, cardiomyopathies, dysrhythmias Distributive: loss of vasomotor tone, 3 rd spacing, neurological, drugs

Early Treatment of Shock Does the type of shock alter your initial treatment?? Answer: Not really! There is sometimes a fear about ‘over bolusing’ a child that may be cardiogenic shock, which can cause increased afterload problems. However, if the child is in shock, they need fluids . The cardiogenic pathology can be addressed once transport to tertiary care center has been done In other words, I’d rather have an alive, fluid overloaded child in cardiogenic shock, then one who is dead from shock.

Hypovolemic Shock Hypovolemic shock results from deficiency of intravascular blood volume Top 5 leading causes for pediatric mortality in the United States (6-20 million deaths worldwide from gastroenteritis) Most commonly from gastroenteritis (vomiting/diarrhea), most of which are viral in nature (Rotavirus, norwalk agent, other) Clinical History: often have vomiting, profuse diarrhea; blunt or penetrating trauma; fever may indicate a bacterial infection that gives septic shock; immunocompromised patients at risk; history of congenital heart disease (CHD); neonates with large liver or cardiac murmur may have a congenital obstructive ductal-dependent heart lesion (patent ductus arteriosus closes within first 2 weeks of life)

Clinical Evaluation Compensated vs. Decompensated Shock Need to determine central blood pressure: 5 th centile for SBP in children: Newborn = 60 mm Hg Infant (1 mo – 1yr) = 70 mm Hg Children (>1yr) = 70 + 2 x age (in years)

Tachycardia Almost always seen in shock Very early sign in shock However… this is not always sensitive or predictive in children, because tachycardia may exist for a myriad of other reasons: fever, pain, agitation, infection Adults: 60-100 bpm 6-12 Months: 110-170 Age 8-15: 60-130 1-6 Months: 120-180 Age 2-7: 70-150 1-3 Weeks: 110-180 Age 1-2: 90 – 150 Neonate: 120-170

Findings in shock Common misconception, that shock only occurs with low BP (hypotension) - because infants/children have enormous capacity to compensate through increased vascular tone, hypotension is usually a late finding. Therefore, tachycardia (with or without tachypnea) may be the 1 st or only sign of early, compensated shock You will also see signs of decreased perfusion, although again, compensation may delay some of these findings in early, compensated shock Therefore, if you see severe hypotension in the presence of other signs of shock, you are probably in a critical stage of shock (may have other reasons besides hypovolemia also contributing, such as septic and/or cardiogenic components)

Hypovolemic Shock, Signs and symptoms Tachycardia Tachypnea Poor peripheral pulses and perfusion Cool extremities Oliguria or anuria Hypotension Mental status changes

Mild, Moderate & Severe Shock Mild Shock Mild hemorrhage, compensated shock, mild hypovolemia (<30% blood volume loss) Moderate Shock Moderate hemorrhage, Decompensated Shock, Marked Hypovolemia (30-45% blood volume loss) Severe Shock Severe hemorrhage, cardiopulmonary failure, severe hypovolemia (>45% blood volume loss) Cardiovascular Mild tachycardia Moderate tachycardia Severe tachycardia Weak peripheral pulses Thready peripheral pulses Absent peripheral pulses Strong central pulses Weak central pulses Thready central pulses Low or normal BP Hypotension Profound Hypotension Mild acidosis Moderate acidosis Severe acidosis Respiratory Mild tachypnea Moderate tachypnea Severe tachypnea Neurologic Irritable, confused Agitated, lethargic Obtunded, comatose Skin Cool extremities, mottling Cool extremities, pallor Cold extremities, cyanosis Renal Mild oliguria, ↑ spec grav Marked oliguria, ↑ BUN Anuria

Initial Management ABC’s are always first Always give 100% supplemental O 2 , as decreased blood volume will mean inadequate core and peripheral oxygenation is likely occurring (even if O 2 sats are normal) Obtain IV access quickly, followed by fluid bolus of 20ml/kg of isotonic fluid (NS or LR) given quickly (over 5 minutes) In severe shock, if IV access is not obtained within 90 seconds, IO access should be considered If first bolus does not change clinical findings quickly, a 2 nd fluid bolus should be given (20 ml/kg) A total of 3 or 4 fluid boluses may be necessary (60-80 ml/kg) within the first 60-90 minutes in order to stabilize the patient Fluid boluses should be titrated, or gauged, by improvements in clinical findings: improved HR, level of consciousness, perfusion, BP, cap refill Once first bolus is in, consider 2 nd large-bore IV access

Isotonic Fluids Always always always give isotonic fluid boluses!! (either NS or LR) Non-isotonic fluids can and will cause fluid shifts, 3 rd spacing, electrolyte imbalance, edema, cerebral edema, and possibly death Do not bolus with Dextran/Glucose unless severe hypoglycemia exists – may add dextran to maintenance IV fluids later

Fluids, fluids, fluids As above, begin with 20ml/kg bolus, then re-evaluate Be ready to repeat the cycle quickly if no significant clinical improvement seen A child with severe hypovolemia may require more than 60 ml/kg or volume in the first hour, or even within the first 15 minutes, to save their life One study has shown that children who received an average of 65 ml/kg of volume in the first hour had a statistically significant increased chance of survival compared to those receiving less than 40ml/kg in the first hour ( Carcillo JA, Davis AL, Zarisky A; JAMA Sep 4, 1994: 266(9): 1242-5 )

Pharmacologic Therapy Inotropic agents: increase myocardial contractility and cardiac output – have variable effects on PVR (Peripheral vascular resistance) Some Inotropic agents vasoconstrict (epinephrine, norepinephrine) and others vasodilate (dobutamine, milrinone) The Catecholamines: Dopamine, Dobutamine, Epinephrine, and Norepinephrine – work through mediating α - and β -receptors Dopamine has variable effects, dependent on dosing Which agents to use depends on the etiology of shock, the clinical/fluid volume state, and the contractile state of the heart and vasomotor state in the body

Dopamine Used either alone or with other inotropic agents; is 1 st inotrope of choice in fluid-refractory septic shock Low dose (2-5 mcg/kg/min) is useful for mixed, vasodilatory effect on end-organ perfusion (renal and splanchnic vasculature) Intermediate Dose (5-10 mcg/kg/min): more of a β 1 -agonist effect, improving myocardial contractility, cardiac output, and enhancing conduction ( ↑ SA rate) High Dose (10-20 mcg/kg/min) the α 1 -agonist effect increases, and may ↑ peripheral vasoconstriction and central blood pressure

Epinephrine For fluid-refractory, dopamine resistant non-vasodilatory shock Epinephrine stimulates both α - and β -receptors, so you see ↑ myocardial contractility and ↑peripheral vasoconstriction Peripheral vasoconstriction brings blood back into the central circulation, but at the expense of peripheral end-organ perfusion. You may see Ventricular dysrhythmia, and at higher doses, ischemic extremities Typical dosing is 0.1 mcg/kg/min IV, and titrated upward to effect (and watching for adverse effects). Max dosing may approach 2-3 mcg/kg/min or even higher in severe shock

Dobutamine Almost purely inotropic agent, primarily with β 1 –agonist effects, which ↑ cardiac contractility. Also provides some weak β 2 -mediated peripheral vasodilation that may ↓ SVR and afterload, and may improve tissue perfusion Minimal α -agonist affect occurs Perfect drug for cardiogenic shock, because it enhances myocardial contractility (↑ inotropy) Much less likely to provoke Ventricular dysrhythmias than epinephrine Typical Dosing: 5 mcg/kg/min IV, may gradually ↑ up to 20 mcg/kg/min May see normotensive or hypotensive effects, so sometimes is used in conjunction with Dopamine to preserve peripheral vascular tone (for α -agonist effects)

Norepinephrine Predominantly an α -agonist that gives ↑ peripheral vascular constriction, thus ↑ PVR (and ↑ blood pressure) Recommended for fluid-refractory, Dopamine-resistant vasodilatory (“warm”) shock Predominant role as pressor agent to ↑ BP in shock that persists after adequate fluid replacement Some people use Norepinephrine for the α -mediated vasoconstrictive effect, and add Dobutamine for improved myocardial contractility Dosing (like epinephrine): 0.1 mcg/kg/min IV, and titrated upward to effect

Phosphodiesterase Inhibitors (Milrninone and Inamrinone) Different mechanism than the catecholamines ( α - and β - mediated mechanism) Work by ↑ cAMP, which ↑ intracellular Ca ++ levels, which ↑ inotropy as well as ↑ing peripheral vasodilation May be useful in scenario of adequate intravascular volume, but poor cardiac contractility and peripheral perfusion Milrinone: Loading dose of 25-50 mcg/kg over 10 minutes followed by continuous infusion of 0.375 – 0.75 mcg/kg/min Adverse effects: arrhythmia, thrombocytopenia Be cautious – has long half-life, and may be appropriate to skip the loading dose and start with an infusion for a more controlled, gradual effect

Dextrose Because infants and toddlers may have limited glycogen stores that become rapidly depleted during shock, hypoglycemia may result Always be ready/able to check a sugar in shock IV Dextrose: 0.5 – 1 g/kg IV initially May then be provided as continuous infusion once patient stabilized

Calcium Ca ++ mediates contraction/excitation in cells (including cardiac and smooth muscle) Shock may cause alterations or shifts in available ionized even if total serum calcium is normal Ca ++ even if total serum calcium is normal Blood products (or anything that contains citrate) may bind available free Ca ++ , which ↓ available ionized Ca ++ Ca ++ is indicated for documented hypocalcemia, and in arrhythmias seen in hyperkalemia, hypermagnesemia, or Ca ++ blocker toxicity. May either give as Calcium Chloride or Calcium Gluconate (I prefer Calcium Chloride, as it may produce higher and more consistent levels of available ionized Ca ++ ) Dose: 10-20 mg/kg (0.1-0.2 ml/kg of CaCL 10%) IV, not to exceed 100 mg/min

Sodium Bicarbonate Controversial, because even though acidosis may be present in severe shock, treatment with Sodium Bicarb may worsen intracellular acidosis while it corrects serum acidosis This occurs because the bicarbonate ion does not readily transverse semi-permeable cell membranes. Thus, the bicarbonate combines with acid in the serum/plamsa, resulting in H 2 0 and CO 2 (Henderson-Hasselbalch equation) If the ↑ CO 2 is not removed by adequate ventilation, then the CO 2 will readily enter the cell, and drive the Henderson-Hasselbalch equation in the other direction, creating intracellular acidosis. Dosing would be 0.5-1 mEq/kg/dose IV over 1-2 minutes Studies have not really supported improved survival rates with the use of bicarb and severe shock or arrest.

Prostaglandin E 1 (PGE 1 ) Neonates who present with a ductal-dependant lesion may have obstructive cardiogenic shock because of the closing (closed) ductus arteriosus If this is suspected, then an infusion of PGE 1 may be life saving Dosing: 0.05-0.1 mcg/kg/min IV as continuous infusion Adverse effects: apnea, hypotension due to vasodilation, fever

Patent Ductus Arteriosus Ductus Arteriosus: Connects the Pulmonary Artery and Aorta in the fetus This closes normally within 12-24 hours after birth, and closes (seals) completely after 2-3 weeks of life If circulation with a congenital heart lesion depends on this staying open, then closure of the PDA is a true cardiac emergency

The End Remember… a lot of this is straightforward, repeatable, and is medical ‘common sense’, but…. Don’t be afraid to ask questions or ask for help! Steve Marchbank, MD [email_address] www.pedsteve.com

Pediatric Airway, Respiratory Distress & Failure, & Hypoperfusion Emergencies

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