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Pediatric Emergencies 

Pediatric Emergencies
Chapter:
Pediatric Emergencies
Author(s):

Anna Clebone

and Bradley Besson

DOI:
10.1093/med/9780199377275.003.0009
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date: 24 October 2020

Critical event checklists, developed by the Society of Pediatric Anesthesia, Quality and Safety Committee, can be found at:

and as an iPhone app:

Anaphylaxis

Definition

A rapid, possibly life-threatening allergic reaction caused by the sudden release of inflammatory mediators after exposure to an allergen, most commonly neuromuscular blockers, antibiotics, or latex.

Presentation

In an anesthetized patient:

  • Erythematous rash (may be absent in quickly progressive anaphylaxis) Wheezing, difficult ventilation, and hypoxia caused by bronchospasm

  • Face, lip, tongue, and laryngeal edema. Stridor may be present in a patient who is not intubated.

  • Hypotension (may be the only sign of anaphylaxis in the anesthetized patient)

  • Tachycardia or bradycardia (the latter occurs in 10% of patients, often associated with severe hypovolemia)

  • Cardiac arrest

Additional signs and symptoms in an awake patient:

  • Shortness of breath, tachypnea, use of accessory respiratory muscles

  • Itching

  • Nausea, vomiting, and abdominal pain

  • Dizziness or altered mental status

  • Hoarseness or stridor caused by laryngeal edema

Pathophysiology

Anaphylaxis is an immediate, life-threatening hypersensitivity reaction to a specific antigen, affecting multiple organ systems, and caused by IgE activation of mast cells and basophils and release of inflammatory mediators. Increased vascular permeability can cause a 35% decrease in circulating blood volume in 10 minutes, causing hypovolemia and shock. Arterial vasodilation produces decreased systemic vascular resistance and tissue hypoperfusion.

Immediate Management

  • Identify and discontinue antigens (e.g., antibiotic, colloid, drug infusion). Remove latex surgical equipment or urinary catheter. Wash area if latex or chlorhexidine allergy is suspected.

  • Administer supplemental oxygen or increase FiO2 to 100%.

  • Intubate the trachea if airway obstruction is imminent or if the patient is hypoxemic. Progressive laryngeal edema may make late endotracheal intubation or cricothyroidotomy impossible.

  • Epinephrine, 0.1–3 MICROgrams/kg intravenously (IV) (a fraction of the cardiac arrest dose!) depending on the severity of reaction, repeated if needed. Titrate carefully to avoid adverse hemodynamic consequences.

  • Establish large-bore IV access.

  • Begin aggressive resuscitation with IV fluids to support intravascular volume (10–20 mL/kg, repeat until blood pressure stabilizes).

  • Decrease or discontinue anesthetic agents as necessary to maintain blood pressure.

  • Treat bronchospasm with aerosolized albuterol. If intubated: Administer 4–10 puffs from a metered dose inhaler through an endotracheal tube If unintubated: Administer 0.15 mg/kg (minimum of 2.5 mg, max 10 mg) of 0.083% albuterol diluted in 3 cc normal saline through a nebulizer.

  • Potent volatile anesthetic agents (if tolerated hemodynamically) and IV ketamine may reduce bronchospasm.

  • Rarely, catecholamine resistant anaphylactic shock can occur, necessitating treatment with vasopressin, or, infrequently, methylene blue.

Differential Diagnosis

  • Rash: Mild or localized allergic reaction

  • Bronchospasm: Bronchial hyper-reactivity from recent upper respiratory infection, acute asthma exacerbation, aspiration (of a foreign body or gastric contents)

  • Hypotension: Blood transfusion reaction, red man syndrome from rapid administration of vancomycin, mastocytosis (In the latter, patients often have had previous hemodynamic events, will have negative skin tests, and tryptase is increased at baseline.)

Diagnostic Studies

  • Anaphylaxis is diagnosed based on clinical manifestations; at least two organ systems must be involved to make the diagnosis.

  • Analysis of a blood sample for histamine (send quickly; half-life is 15–20 minutes) and mast cell tryptase (half-life is 2 hours) may confirm the diagnosis.

Subsequent Management

  • After a severe reaction, begin a continuous infusion of epinephrine 0.01–0.2 MICROgrams/kg/min.

  • Administer diphenhydramine (H2 blocker) IV 1 mg/kg, maximum 50 mg and famotidine 0.25 mg/kg IV OR ranitidine (H1 blocker) 1 mg/kg IV.

  • Administer dexamethasone 0.2–1 mg/kg IV, or methylprednisolone 2 mg/kg IV, maximum 100 mg to decrease inflammation (effect occurs in 4–6 hours).

  • If a severe reaction occurs, discuss canceling or limiting the surgical procedure.

  • Refer to an allergist for skin testing in 4–6 weeks.

Risk Factors

Latex allergy is more common in children with spina bifida or other genitourinary abnormalities due to multiple exposures during surgery and catheterization.

Prevention

Obtain a detailed history of previous allergic reactions, atopy, and asthma. Question patients specifically about latex allergy, including allergy to foods with cross-reactivity (e.g., banana, kiwi, papaya, avocado) and avoid latex in those patients.

Prophylactic medications to prevent anaphylaxis are not recommended because they may mask a true reaction and delay immediate diagnosis and treatment.

Special Considerations

  • Epinephrine is a drug with a narrow therapeutic index, and the dose to treat anaphalaxis is smaller than for cardiac arrest. Epinephrine overdose may cause severe hypertension, potentially causing cerebral or myocardial injury, pulmonary edema, and ventricular dysrhythmias.

    • Avoid atropine administration for bradycardia, especially if the patient is hypovolemic. Treat bradycardia in the setting of anaphylaxis with fluid resuscitation followed by epinephrine. Bradycardia may be protective, allowing the ventricles to fill in the setting of massive hypovolemia.

    • Between 5% and 20% of patients will have a recurrence of anaphylaxis 8–12 hours after initial presentation.

    • Respiratory abnormalities are the most common symptom of anaphylaxis in children (as opposed to adults, in whom cardiovascular instability is more common).

    • Breath sounds may be absent in a patient with severe bronchospasm because of decreased air exchange.

    • A rapid onset of anaphylaxis is associated with a more severe or possibly fatal reaction.

Further Reading

Dewachter P, Mouton-Faivre C, Emala C. Anaphylaxis and anesthesia: controversies and new insights. Anesthesiology. 2009; 111(5): 1141–1150.Find this resource:

Kounis N, Soufras G, Hahalis G. Anaphylactic shock: kounis hypersensitivity-associated syndrome seems to be the primary cause. North Am J Med Sci. 2013; 5(11): 631–636.Find this resource:

Asthma and Bronchospasm (Lower Airway Obstruction)

Definition

Increased resistance of the airways caused by hyperreactivity, inflammation, edema, and mucous plugging.

Presentation

In an anesthetized patient:

  • Wheezing

  • Diminished or absent breath sounds (indicates severe bronchospasm and minimal airflow)

  • Increased peak airway pressure

  • Hypoxemia

Additional signs and symptoms in an awake patient:

  • Dyspnea, increased work of breathing, use of accessory muscles, retractions, nasal flaring, “tripod” position

  • Tachypnea with a prolonged expiratory phase

  • Diaphoresis

  • Cough with sputum production

  • Chest pain or tightness and anxiety

  • Late bronchospasm: Obtundation, respiratory failure, and cardiac arrest

Pathophysiology

Airway obstruction leads prolonged expiratory time (increased I:E ratio) in the spontaneously breathing patient. If the I:E ratio is not manually increased in the mechanically ventilated patient, air will become trapped in the alveoli, causing hyperinflation.

Immediate Management

  • Increase FiO2 to 100%.

  • Increase the inspired concentration of potent volatile anesthetic and/or administer propofol to increase the depth of anesthesia. (Note: Desflurane is a bronchial irritant. Switch to sevoflurane if possible.)

  • Check the position of the endotracheal tube; consider the possibility of mainstem intubation, kinking, or circuit disconnection.

  • Suction the endotracheal tube.

  • Administer albuterol (β‎2-agonist). If intubated: 4–10 puffs from a metered dose inhaler through the endotracheal tube. If unintubated, 0.15 mg/kg (minimum of 2.5 mg, max 10 mg) of 0.083% albuterol diluted in 3 cc normal saline through a nebulizer.

  • Administer corticosteroids (dexamethasone 0.1–1 mg/kg IV; reduces inflammatory sequelae; effects in 4–6 hours).

If the preceding are ineffective, attempt the following:

  • Administer ketamine 1–2 mg/kg IV (bronchodilator) with atropine or glycopyrrolate (0.02 mg IV increments titrated to heart rate) to decrease secretions. CAUTION if unintubated. Ketamine will cause sedation.

  • Administer epinephrine 1 MICROgram/kg IV.

  • Consider extracorporeal membrane oxygenation (ECMO) in a patient with unremitting, life-threatening bronchospasm. Note: Alert cardiac surgical and perfusion teams early if the need for ECMO is anticipated. Caution: ECMO is resource intensive and carries many risks and therefore should be used as a last resort.

Differential Diagnosis

  • Atelectasis

  • Anaphylaxis (is accompanied by rash and hypotension)

  • Pulmonary edema caused by fluid overload (especially in an infant)

  • Foreign body aspiration (e.g., a tooth that is dislodged during laryngoscopy and intubation)

  • Pulmonary aspiration of gastric contents

  • Tracheomalacia or bronchomalacia, especially in a former premature infant

Diagnostic Studies

  • Chest radiograph may show hyperinflation of the lungs caused by air trapping

  • Arterial blood gas in decompensating patients. Multiply FiO2 by 5 to estimate expected “normal” PaO2.

  • A spontaneously breathing patient who is hyperventilating will first develop a respiratory alkalosis. Later on, increasing or “normal” PaCO2 may indicate imminent respiratory failure.

Subsequent Management

  • Administer oral steroids for several days to a week after surgery in moderate to severe cases.

  • If respiratory status does not normalize, delay extubation and/or admit the patient to the pediatric intensive care unit (PICU).

Risk Factors

  • Pre-existing upper respiratory infection (URI) or reactive airway disease/asthma increase the risk of bronchospasm. The airway will be hyper-reactive for 6 weeks after a URI.

  • Bronchospasm can be caused by endotracheal intubation or other airway instrumentation.

  • Atopy, including pre-existing asthma, environmental allergies, and eczema.

Prevention

  • Postpone elective surgery if a patient is wheezing preoperatively. For emergency surgery, administer inhaled albuterol in the preoperative area and advise the parents that extra oxygen, a prolonged postoperative stay, or prolonged intubation and PICU admission may be required.

  • Continue home medications, including inhaled corticosteroids (fluticasone) and leukotriene inhibitors (monteleukast), in patients with known reactive airway disease or asthma. If a patient is at high risk for intraoperative bronchospasm, several days of oral steroids (e.g., prednisone 1 mg/kg/day) should be administered before surgery.

Special Considerations

  • Airway instrumentation and endotracheal intubation can precipitate bronchospasm by irritating the airways. It may be possible to avoid bronchospasm by using mask ventilation or a laryngeal mask airway for the duration of the anesthetic. If the trachea will be intubated, removing the tube during stage 3 of anesthesia (i.e., a “deep” extubation) may decrease bronchospasm, but may increase the risk of laryngospasm during emergence.

Further Reading

Nievas IF, Anand KJ. Severe acute asthma exacerbation in children: a stepwise approach for escalating therapy in a pediatric intensive care unit. J Pediatr Pharmacol Ther. 2013; 18(2): 88–104.Find this resource:

Regli AL, von Ungern-Sternberg BS. Anesthesia and ventilation strategies in children with asthma: part II—intraoperative management. Curr Opin Anaesthesiol. 2014 Mar 29.Find this resource:

von Ungern-Sternberg BS1, Boda K, Chambers NA, Rebmann C, Johnson C, Sly PD, Habre W. Risk assessment for respiratory complications in paediatric anaesthesia: a prospective cohort study. Lancet. 2010; 376(9743): 773–783.Find this resource:

Burns

Definition

Thermal injury that compromises the skin, airway, and other organs, predisposing to infection and impairing the body’s ability to regulate temperature and maintain fluid and electrolyte balance. Extensive local tissue damage can lead to hypermetabolism and multiorgan failure. First-degree burns involve only the epidermis, second-degree burns cross into the dermis, third-degree burns involve the subcutaneous tissue, and fourth-degree burns involve the bone or muscle.

Presentation

  • First degree: painful, red skin. Second degree, Superficial: erythema, pain, blisters. Second degree, Deep: white, leathery skin, less pain (indicates nerve damage). Third degree: white, leathery, painless. Fourth degree: may be fatal. Bone and muscle are involved. Tissue injury may be worse than surface appearance in electrical or chemical burns.

If severe, systemic manifestations:

  • Airway: Progressive edema and airway obstruction over the first 24 hours are caused by smoke inhalation injury and resultant inflammation. This is indicated by burnt nose hairs, facial burns, ashes around the mouth or soot in the sputum.

  • Pulmonary: Dyspnea, bronchospasm, stridor, hypoxemia. Toxin damage to the tracheobronchial tree is symptomatic 12–36 hours post injury. Carbon monoxide (CO) poisoning may be present despite normal SaO2. Hydrogen cyanide (HCN) poisoning can cause severe metabolic acidosis. Pulmonary injury, CO toxicity, or HCN poisoning can occur without external injuries.

  • Cardiac: Decreased cardiac output, hemoconcentration, and edema caused by fluid shifts into the burned tissue. Myocardial depression. Hypoperfusion and hypotension leading to metabolic acidosis and end-organ damage.

  • Neurologic: Hypoxic encephalopathy (hallucinations, seizures, coma). Chemical inhalation or CO poisoning can cause altered mental status.

  • Renal: Injury caused by hypoperfusion, myoglobinuria, or hemoglobinuria.

Pathophysiology

  • The airway can be injured by thermal injury from steam, smoke particles, chemicals, and gases that are toxic. Necrotic respiratory epithelium will begin shedding approximately 3 days after injury and may cause airway obstruction.

  • Hypothermia is caused by fluid evaporation from injured tissue. Hypothermia may develop quickly in children because the body surface area is high relative to height. Hypermetabolism occurs in proportion to the severity of injury, and involves the hypothalamic mediated release of glucagon, cortisol, and catecholamines. Catecholamine and vasoactive mediator release cause a capillary leak around the burned tissue during the first day after injury.

Differential Diagnosis

  • Acute respiratory distress syndrome (may indicate progression of inhalation injury).

  • Stevens-Johnson syndrome: A severe, red, blistering rash and epidermal necrosis that occurs as an immune-mediated reaction to systemic infection or certain medications.

Immediate Management

Treat Life-Threatening Systemic Conditions

  • Intubate the patient immediately with a microcuffed endotracheal tube if the patient has signs of an inhalation injury (see Special Considerations) or facial burns. Advanced airway equipment (fiberopic, glidescope) must be available. Caution: Succinylcholine may be used only within 24 hours of the burn. Mask ventilation may be difficult if the face is burned.

  • Administer 100% oxygen. If possible, humidify inspired gases to minimize irritation.

  • Establish large-bore IV access. Begin aggressive fluid resuscitation according to the Parkland formula. Titrate urine output to 0.5–1 mL/kg/h.

  • If necessary, support hemodynamics with inotropic agents (can have depressed cardiac function).

  • Prevent hypothermia by increasing the room temperature. Cover the patient with a warming blanket. Warm all fluids.

  • If HCN poisoning is suspected, immediately administer hydroxocobalamin IV 70 mg/kg (max 5 g).

  • Remove all affected clothing and begin a primary trauma survey (see Major Trauma, page [link]).

  • Apply cold, running water (12–18° C) to the burned tissue for at least 20 minutes for analgesia and to reduce burn depth Caution: Avoid hypothermia. This should be done as soon as possible, but may be beneficial for up to 3 hours after injury.

  • Cover the burn with clear plastic wrap or sterile plastic bags to reduce fluid and heat loss.

  • Administer analgesia as tolerated. Intranasal fentanyl can be given if intravenous (IV) access is not yet established, but monitor carefully for apnea.

Diagnostic Studies

  • Treatment decisions are partially based on the percentage of total body surface area (TBSA) injured (blistering or worse). Children have relatively smaller limbs and bigger heads than teenagers or adults, which alters this calculation (see Figure 9.1, Rule of 9s).

  • Complete blood count, electrolytes creatine kinase, urine myoglobin (rhabdomyolysis), co-oximetry (CO poisoning).

  • Serial arterial blood gas measurements guide ventilation and oxygenation (PaCO2, PaO2) and treatment of metabolic acidosis.

  • Chest radiograph demonstrates lung opacities in severe inhalation injury. (Lungs will appear normal in less severe inhalation injury.)

Figure 9.1 Rule of Nines: Body Surface Area in Adults versus Children

Figure 9.1 Rule of Nines: Body Surface Area in Adults versus Children

Subsequent Management

Fluid Resuscitation

  • Estimate crystalloid fluid requirements with the Parkland formula: 4 mL/kg × percent burn × wt (kg) = first 24-hour additional requirements (beyond maintenance), with half given in the first 8 hours. Can be up to one-third higher if a concomitant inhalation injury exists. Titrate IV fluids to vital signs, urine output (0.5–1 mL/kg/h), pulse oximeter and arterial line respiratory variations, central venous pressure.

  • Add glucose to IV fluids if needed, especially in younger patients.

  • If necessary, administer colloids (albumin 5%) to keep serum albumin >2.0 g/dL.

  • Add potassium to IV fluids as necessary to compensate for loss in the urine or from burned tissues.

  • Administer blood products as indicated for anemia or coagulopathy.

  • Consider inserting a central venous catheter in patients with burns of >30% of the body’s surface area.

Breathing

  • Check endotracheal tube cuff pressures frequently. Maximum airway edema typically occurs 24 hours after injury, and then decreases. It may be necessary to secure the endotracheal tube with cloth ties because tape will not stick to injured tissue.

  • Circumferential, deep burns to the abdomen and chest may impair ventilation by limiting chest wall excursion, and may require urgent surgical escharotomy.

Toxicity

  • In patients with severe HCN toxicity, consider administering sodium thiosulfate 1.65 cc/kg IV to a maximum of 12.5 g, in addition to hydroxocobalamin (may be synergistic)

Neurologic

  • Multimodal pain management: Consider fentanyl and hydromorphone (less histamine release than morphine), ketamine, midazolam, and dexmedetomidine. Patients may need continuous narcotics and sedation. Tolerance develops quickly; doses will need to be increased over time.

Risk Factors

  • Half of pediatric burns occur in children <5 years old.

  • Twenty percent of pediatric burns are due to child abuse. Glove and stocking burns, especially without splash marks and if full thickness, or on the soles of both feet or on the backside should raise the suspicion of abuse.

Special Considerations

  • Patients are at increased risk of aspiration due to delayed gastric emptying or recent oral intake. They are also at risk for difficult ventilation and intubation due to inflammation and swelling. An inhalation induction, maintaining spontaneous ventilation until the airway is secured, may be safer if the airway is compromised. Note: Equipment necessary to establish a surgical airway should be immediately available. Under-resuscitation or delayed fluid resuscitation will lead to tissue hypoperfusion, acidosis, and increased mortality. Over-resuscitation with intravenous fluids can lead to increased tissue swelling, compartment syndrome, and even pulmonary edema.

  • Intravenous access may be difficult. It may be necessary to insert a catheter through burned tissue to avoid delays in resuscitation. Consider an intraosseus catheter or venous cutdown if adequate access cannot be obtained.

  • Inhalation injury can occur even in the absence of skin burns and should be suspected if soot is present in or around the airway. Emergency airway equipment should be immediately available, and the team should be ready to manage a possible difficult airway. Secure the airway immediately if respiratory distress, severe burns to the face or neck, or swelling or blistering inside the mouth are present. If ulcerating burns are present in the airway, an early tracheostomy is indicated to avoid further airway trauma. Even if immediate intubation is not indicated, maintain a high level of suspicion for airway injury. If steam inhalation is suspected, perform a fiberoptic bronchosopy to assess the degree of thermal injury of the tracheobronchial tree. Caution: Laryngoscopy or bronchoscopy can precipitate laryngospasm, bleeding, or swelling and subsequent airway obstruction. Younger children will not tolerate these procedures and may require general anesthesia.

  • Consider carbon monoxide or hydrogen cyanide poisoning in patients with smoke inhalation (may occur in up to 35% of patients). SaO2 will not be decreased in CO poisoning because a standard pulse oximeter cannot differentiate between oxyhemoglobin and carboxyhemoglobin. Carbon monoxide poisoning should be suspected if there was a prolonged exposure to smoke or the patient has mental status changes, chest pain (from hypoxia), headache, or nausea. Send blood for co-oximetery on blood gas or use a noninvasive pulse co-oximeter to diagnose CO inhalation. A child with chronic exposure to tobacco smoke will have an already elevated CO level of approximately 1.5%. Consider hyperbaric oxygen if the CO level is >25%, there are mental status changes, signs of end-organ injury, or myocardial ischemia, or if pH is <7.1. HCN is present in smoke when materials containing both carbon and nitrogen are burned. HCN poisoning presents with stomach pain, mental status changes, and an initially elevated respiratory rate, heart rate, and blood pressure followed by cardiopulmonary collapse, rhabdomyolysis, and multi-system organ failure. Laboratory studies will reveal an anion gap metabolic acidosis, elevated lactate (often >10 mmol/L), a decreased venous to arterial PO2 gradient, and a blood cyanide level. Amyl nitrite and sodium nitrite can cause methemoglobinemia and should not be used if concomitant CO poisoning is suspected. Patients may also require intubation and mechanical ventilation and hemodynamic support with vasopressors. Caution: Co-oximetry may be inaccurate after the patient has received hydoxycobalamin.

Further Reading

Caruso T, et al. Airway management of recovered pediatric patients with severe head and neck burns: a review. Paediatr Anaesth. 2012; 22(5): 462–468.Find this resource:

Kim L, Martin C, Holland A. Medical management of paediatric burn injuries: best practice. J Paediatr Child Health. 2012; 48: 290–295.Find this resource:

Shank E, Sheridan R, Cote C, Jeevendra M J. Burn injuries. In: Cote CJ, Lerman J, Todres ID, eds. A practice of anesthesia for infants and children. 4th ed. Philadelphia: Saunders Elsevier; 2009:715–733.Find this resource:

Epiglottitis (Supraglottitis): Nonperioperative Onset of Stridor

Definition

Epiglottitis is a relatively rare, but immediately life-threatening cause of stridor that can lead to rapidly progressive airway obstruction (Table 9.1).

Table 9.1 Nonperioperative Onset of Stridor in Children

Croup (laryngotracheobronchitis)

Epiglottitis

Inhaled Foreign Body

Incidence

Common (>80% of stridor)

Rare

Varies

Fever

High

High

None

Acuity

Often benign

Can be life-threatening

Can be life-threatening

Onset

After 12–24 hours of rhinitis and “cold” symptoms

Sudden without prodrome

Sudden

Cough

Common (due to involvement of the trachea and bronchi) and high-pitched (due to turbulent air flow through the narrowed subglottis)

Rare

Common

Drooling

Absent

Typical

No

Dysphonia

Hoarse

Muffled

Dysphagia

Sometimes

Severe

Dyspnea

Present

Present

Present

Stridor

  • Loud inspiratory stridor (due to inflammation and edema at the extrathoracic narrowed cricoid ring)

  • Fast respirations (due to the involvement of the trachea and bronchi)

Soft inspiratory stridor (epiglottis is extrathoracic, but airflow is decreased due to inflammation)

Expiratory (or biphasic) stridor if foreign body is in the bronchus, due to intrathoracic obstruction

Age

<3

2–8

Varies

Radiography (only in a stable patient)

Tracheal narrowing “steeple sign”

Epiglottis swollen “thumbprint sign”

If object is radio-opaque, often seen in bronchi or trachea

Intervention

  • Humidified oxygen

  • Racemic epinephrine

  • Intravenous steroids

To operating room, intubate, ICU, antibiotics

To operating room, inhalation induction, remove with rigid bronchoscopy by ENT

Presentation

Airway

  • Classic appearance of “4Ds”: drooling, dyspnea, dysphonia (muffled voice), and dysphagia. The patient may complain of a severe sore throat, and will have inspiratory stridor.

Breathing

  • Normal respiratory rate

Systemic

  • High fever often >39° C, toxic appearance

  • Patient may be found sitting up and leaning forward with the chin protruding in a sniffing position.

Pathophysiology

Epiglottitis is an inflammatory edema of the supraglottic structures, including the arytenoids, aryepiglottic folds, uvula, and epiglottis, commonly caused by Haemophilus influenzae type B. Other bacteria (e.g., Group A β‎-hemolytic streptococcus, staphylococcus aureus), viruses (e.g., herpes simplex, varicella-zoster), and mechanical trauma or thermal injury can also cause epiglottitis.

Immediate Management

  • If complete airway obstruction is imminent, call personnel skilled in advanced airway management and an otorhinolaryngologist to the bedside.

  • Administer O2 via facemask or “blow-by” as tolerated. Avoid airway examination or manipulation (may precipitate laryngospasm).

  • Transport the patient to the operating room. An anesthesiologist and otolaryngologist should remain with the patient at all times. Advanced airway management equipment, including several endotracheal tubes of expected size for age and smaller, and stylets, should be immediately available during transport.

  • If possible, allow a parent to accompany the patient to the operating room to minimize agitation and the risk of airway compromise. Allow the patient to remain in the sitting position. Avoid painful procedures (IV placement) until anesthetized in the operating room.

  • Ensure that all equipment necessary for a possible rigid bronchoscopy or surgical airway is immediately available.

  • Induce general anesthesia via inhalation with sevoflurane, even in a patient with a full stomach. Keep the child in the sitting position on the parent’s lap during induction. Maintain spontaneous ventilation with a deep plane of anesthesia (spontaneous ventilation may facilitate location of the vocal cords in a patient with an edematous airway). Caution: Do not use intravenous agents or muscle relaxants until the airway is secured.

  • Establish intravenous access after patient is adequately anesthetized.

  • Carefully perform an endotracheal intubation, lifting the tongue gently without touching or traumatizing the epiglottis.

Differential Diagnosis

  • Croup (more common, 80% of children with stridor)

  • Foreign body in the airway or esophagus (history of choking while eating; sudden, persistent cough)

  • Retropharyngeal abscess

Diagnostic Studies

  • Primarily a clinical diagnosis. DO NOT DELAY TREATMENT.

  • Lateral neck radiograph can show an enlarged epiglottis appearing as a “thumbprint,” obscuring the vallecula (Note: This is not required for diagnosis and should only be attempted in stable patients.) Ultrasonography can show an “alphabet P sign.”

  • After securing the airway, blood cultures and throat cultures can assist in identifying the causative organism and antibiotic sensitivities.

Subsequent Management

  • Intubation may be required for 24–36 hours until airway inflammation is resolved. Signs of decreased swelling include an air leak around the cuff of the endotracheal tube after deflation.

  • Humidify inspired gases.

  • Transfer to the intensive care unit.

Risk Factors

  • Winter months

  • Immunosuppression

Prevention

Universal vaccination to decrease H. flu infection.

Special Considerations

  • Late complications of epiglottitis can include subglottic granulomas or stenosis, as well as tracheomalacia.

Further Reading

Charles R, Fadden M, Brook J. Acute epiglottitis. Br Med J. 2013; 19: 347.Find this resource:

Li CJ, Aronowitz P. Sore throat, odynophagia, hoarseness, and a muffled, high-pitched voice. Cleve Clin J Med. 2013; 80(3): 144–145.Find this resource:

Tibballs J1, Watson T. Symptoms and signs differentiating croup and epiglottitis. J Paediatr Child Health. 2011; 47(3): 77–82.Find this resource:

Inhaled Foreign Body

Definition

The presence of a foreign body in the hypopharynx, larynx, trachea, or lungs, or posterior compression of the trachea caused by an object obstructing the esophagus.

Presentation

  • A witnessed choking episode may be reported.

  • Stridor, shortness of breath, coughing, wheezing

  • Late presentation could be a chronic nonasthmatic wheeze or persistent pneumonia

  • If severe obstruction of trachea or both bronchi, child may be cyanotic.

Immediate Management

Partial Airway Obstruction

  • Monitor respiratory status closely.

  • Transport the patient to the operating room. The patient should be transported by personnel skilled in airway management and emergency airway equipment must be immediately available.

  • Perform an inhalation induction of general anesthesia. Keep the patient spontaneously breathing.

  • To facilitate rigid bronchoscopy, begin a propofol infusion (200–300 MICROgrams/kg/min or as tolerated) to maintain spontaneous respirations on 100% O2 and provide a deep plane of anesthetic (so the patient does not move or cough, which could cause airway injury).

  • If the airway is injured or edematous, intubate the trachea after the foreign body has been removed.

Complete Airway Obstruction (No Air Movement)

  • If the patient is awake, perform the Heimlich maneuver.

  • Request an emergency otolaryngology consult to perform direct laryngoscopy and rigid bronchoscopy (to attempt to stent the airway open and either remove the object or push the object distally so that air movement can occur).

Differential Diagnosis

  • Acute asthma exacerbation (wheezing, respiratory distress, prolonged expiratory phase).

  • Croup (gradual onset, barking cough, hoarseness, rapid respiratory rate).

  • Foreign body in the esophagus (drooling, dysphasia, dyspnea).

  • Epiglottitis (acute onset, toxic appearance, sore throat, stridor).

  • Anaphylaxis (sudden onset, exposure to allergen, urticaria, possible hypotension).

  • Retropharyngeal abscess (airway obstruction, stridor).

Diagnostic Studies

  • Radiography may be nondiagnostic and should be attempted only in a stable patient. Eighty-nine percent of foreign bodies may not be visualized on radiography, and sequalae (e.g., hyperinflation or atelectasis) may not be seen in 17% of patients.

Subsequent Management

  • Unless otherwise contraindicated, administer a steroid (e.g., dexamethasone 0.5–1 mg/kg) to decrease late inflammatory edema.

  • Treat bronchial hyper-reactivity and resultant wheezing (from the foreign body and from instrumentation) with inhaled albuterol (4–10 puffs from a metered dose inhaler through an endotracheal tube, or 0.15 mg/kg [minimum of 2.5 mg] of 0.083% diluted in 3 cc normal saline through a nebulizer for an unintubated patient).

  • Upper airway irritation causing stridor can be treated with nebulized racemic epinephrine 0.5 mL of 2.25% solution diluted in 2 mL normal saline (0.3 mL for infants).

Risk Factor

  • Age <4 years

Prevention

Check the mouth carefully for loose teeth prior to laryngoscopy, especially in young or developmentally delayed patients.

Special Considerations

  • Removal of the foreign body in the operating room with full anesthesia and surgical equipment including a rigid bronchoscope and tracheostomy kit is the safest option. Agitation, multiple attempts at removal, positive pressure ventilation, and endotracheal intubation may cause the object to move, rapidly converting partial airway obstruction into complete airway obstruction.

  • Spontaneous ventilation should be maintained because intravenous anesthestic agents or neuromuscular blocking agents may cause relaxation of airway muscles and lead to complete obstruction.

  • Complications that may occur during removal of the foreign body include aspiration, bronchospasm, severe edema of the larynx, laceration of the trachea or bronchi, pneumothorax, pneumomediastinum, or hypoxia.

Further Reading

Fidkowski CW, Zheng H, Firth, PG. The anesthetic considerations of tracheobronchial foreign bodies in children: a literature review of 12,979 cases. Anesth Analg. 2010; 111(4): 1016–1025.Find this resource:

Near-Drowning

Definition

Interruption of breathing due to immersion in liquid. Pulmonary, cardiac, neurologic, and global end-organ injury may occur due to hypoxia and hypothermia (see chapter 5). Presentation may be asymptomatic or catastrophic, depending upon on how quickly the patient was rescued.

Presentation

Pulmonary

  • Hypoxemia

  • Apnea when body temperature falls to <28° C.

Cardiac

  • Dysrhythmias or cardiac dysfunction (a result of hypoxemia, hypothermia, or acidosis). Osborn (J) waves on electrocardiogram may be present when core temperature is <32° C. Cardiac arrest caused by myocardial ischemia.

  • Hypovolemia due to brisk diuresis (hypothermia decreases antidiuretic hormone production early in submersion).

Neurologic

  • Altered mental status (core temperature <32° C), coma (core temperature <30° C).

Pathophysiology

Water aspiration causes loss of surfactant and atelectasis. Pulmonary edema and damage to alveoli may increase intrapulmonary shunt to 75%. Patients commonly develop acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) after a near-drowning episode. Hypoxic encephalopathy may also occur.

Differential Diagnosis

  • Spinal cord injury (e.g., after diving in shallow water)

  • Head injury after a slip and fall accident near water

  • Toxic ingestion (e.g., alcohol poisoning, especially in adolescents)

  • Seizure

Immediate Management

  • Immobilize the cervical spine if head or neck trauma is suspected.

  • Clear debris and fluid from the airway.

  • Assess airway, breathing, circulation, perform pediatric advanced life support (PALS) if indicated (see page [link]).

  • Initiate mask ventilation if the patient is apneic; begin chest compressions if pulseless.

  • Measure rectal temperature. Do not discontinue PALS until the patient is rewarmed to at least 32° C.

  • Evaluate for associated traumatic injuries.

Diagnostic Studies

  • Monitor for late end-organ consequences of hypoxia: GI bleeding, coagulopathies, myoglobinuria, hemoglobinuria, and renal failure.

  • Arterial blood gas, electrolytes, and toxicology screen (including ethanol)

  • Chest radiograph

Subsequent Management

Systemic

  • Rewarm the patient: Use forced air warming, radiant warming (warming lights), warm, humidified O2, and a fluid warmer. Caution: Monitor blood pressure carefully because vasodilation may cause hypotension. If temperature is very low (<32° C), consider warming with cardiopulmonary bypass or hemodialysis.

Cardiac

  • In patients who are in cardiac arrest: Continue advanced cardiac life support (ACLS) at least until the core temperature has reached 37° C.

Respiratory

  • Treat bronchospasm with albuterol (4–10 puffs from a metered dose inhaler through an endotracheal tube, or 0.15 mg/kg (minimum of 2.5 mg) of 0.083% diluted in 3 cc normal saline through a nebulizer in an unintubated patient. Patients with severe hypoxia may require CPAP (continuous positive airway pressure). If the patient is not intubated, consider using a BiPAP mask. Consider PEEP (positive end-expiratory pressure) in an intubated patient to decrease ventilation-perfusion mismatch.

Special Considerations

  • Acute respiratory distress syndrome and pulmonary edema can occur up to 24 hours after a near-drowning episode, even in children who first present without apparent injury. Maintain a low threshold for overnight admission.

  • Hypoxia for >5–10 minutes is associated with a worse outcome, as are laboratory values showing a very low pH, high lactate, and high blood sugar.

Risk Factors

  • Healthy children ages 1–4 who cannot swim and who are not closely supervised.

  • Children with a seizure disorder or developmental delay.

  • Hypothermia from swimming in cold water in a child with long QT syndrome (body temperature <35° C increases the QT interval).

Further Reading

Burford AE, Ryan LM, Stone BJ, Hirshon JM, Klein BL. Drowning and near-drowning in children and adolescents. Pediatr Emerg Care. 2005; 21(9): 610–616.Find this resource:

Hoek, TL, et. al. 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 12: Cardiac arrest in special situations. Part 12.9: Cardiac arrest in accidental hypothermia. Circulation. 2010; 122: S829–S861.Find this resource:

Topjian AA, Berg RA. Pediatric out-of-hospital cardiac arrest. Circulation. 2012; 125(19): 2374–2378.Find this resource:

Neonatal Resuscitation

Definition

Factors such as prematurity (birth at <37 weeks postconceptual age), congenital abnormalities, peripartum fetal asphaxia, or the failure to warm and dry the newborn can impair the transition from fetal to neonatal circulation and may require advanced resuscitation measures.

Presentation

  • At birth, assess for the following: Born full term? Breathing or crying? Good muscle tone? If the answer to any of these questions is “no,” proceed immediately to the Immediate Management section.

If in distress, may also see:

  • Blue, floppy, minimal movement, ineffective or absent respirations

  • Bradycardia (heart rate <100 beats per minute [bpm]). In children and neonates, hypoxia is the most common cause of bradycardia.

  • See Table 9.2 for APGAR score.

Table 9.2 Apgar Score

Clinical Feature

0

1

2

Color

Pale/blue

Acrocyanosis (Pink body, blue extremities)

Pink

Heart rate (beats/minute)

Absent

<100

>100

Response to stimulation

None

Grimace

Pulls away, crying

Muscle tone

Limp, flaccid

Some flexion of extremities

Active movement

Respiratory rate

Absent

Poor effort, slow, irregular

Good, crying

Differential Diagnosis

Rare conditions that may cause neonatal cardiovascular collapse:

  • Hypovolemia from hemorrhage before birth

  • Diaphragmatic hernia (difficult to ventilate, scaphoid abdomen, bowel sounds present on ausculation of the chest)

  • Hydrops fetalis (leading to hemolytic anemia)

  • Congenital complete heart block (suspect this when heart rate does not increase to >60 bpm)

  • Pneumothorax (may occur during resuscitation, decreased breath sounds)

  • Residual drug effects or withdrawal (i.e., opioids administered to the mother prior to delivery or maternal addiction to drugs or alcohol)

Immediate Management

First 30 seconds:

  • Warm and dry the infant.

  • Suction the airway if needed.

  • Stimulate (rub the back, tap the feet).

  • Cover a preterm baby’s torso and limbs with plastic wrap to maintain heat.

Second 30 seconds:

  • Evaluate heart rate (auscultate or feel for an umbilical pulse), respirations, and color

  • If heart rate is <100 or infant is gasping or apneic, begin positive pressure ventilation (rate of 40–60 breaths/minute) and monitor SaO2. Begin with room air and increase FiO2 as needed. Caution: Avoid high peak pressures.

  • If breathing is labored or the neonate remains cyanotic, suction the airway, monitor SaO2, and consider CPAP.

Third 30 seconds (after 30 seconds of adequate ventilation):

  • If the heart rate is <60, begin chest compressions. Place two thumbs on the lower one-third of the sternum. The depth of compressions should be one-third of the chest while maintaining a rate of 120/min. Give three chest compressions for each breath. The mnemonic for this is: “one-and-two-and-three-and-breathe-and”

Persistent heart rate <60 bpm:

  • Administer epinephrine 0.01–0.03 mg/kg IV (preferred) or 0.1 mg/kg via the endotracheal tube. Repeat every 3–5 minutes.

  • Intubate the trachea if the chest does not rise with positive pressure ventilation. A supraglottic airway (laryngeal mask airway) can be used as a rescue device.

  • Confirm endotracheal tube position above the carina by looking for bilateral chest rise. Mainstem intubation is common in newborns, and is not reliably detected by auscultation. Avoid peak airway pressures >20–25 cm H2O.

  • Consider the possibility of complications such as pneumothorax (treat with needle thoracostomy) or hypovolemia (administer fluid or blood with 10 cc/kg boluses).

  • Assess respirations, heart rate, and color every 30 seconds. Continue coordinated chest compressions and ventilations until spontaneous heart rate is >60 bpm.

  • Consider administering surfactant through the endotracheal tube (beractant 4 mL/kg intratracheal) for severe respiratory distress in preterm infants (especially if <28 weeks gestation). Divide into four aliquots and administer in different positions to ensure adequate distribution.

  • Infants with meconium in their amniotic fluid require intubation and suctioning of the endotracheal tube only if they do not successfully transition to postpartum physiology (if the infant has a heart rate <100 bpm with poor muscle tone and respiratory effort).

Diagnostic Studies

Do not stop ventilation or chest compressions to obtain laboratory or diagnostic studies. Treat suspected pneumothorax with a needle thoracostomy based on clinical suspicion. If possible, resuscitation may be guided by arterial blood gas analysis, complete blood count, glucose and electrolytes, chest X-ray, or echocardiogram.

Subsequent Management

  • Maintain normothermia with radiant warming. If necessary, wrap preterm infants’ extremities in plastic wrap to prevent hypothermia. The larger body surface area and thin skin in the newborn may cause hypothermia to develop quickly.

  • If the patient has moderate or severe hypoxic ischemic encephalopathy, therapeutic hypothermia may be appropriate. Request a critical care consultation for neonatal therapeutic hypothermia.

  • After 10 minutes of adequate and uninterrupted resuscitation, discontinue efforts if no signs of life are present.

Risk Factors (for needing neonatal resuscitation)

  • Approximately 10% of newborns do not start breathing without assistance. (Less than 1% need extensive measures for resuscitation.)

  • Birth at less than <35 weeks postgestational age

  • Oligohydramnios

  • Chorioamnionitis or other infection

  • Maternal hypertension

  • Fetal factors: Breech, shoulder dystocia, nonreassuring fetal heart rate, meconium in the amniotic fluid

  • Use of opiates during otherwise normal labor

  • Risk is not increased by assisted delivery (forceps or vacuum) or by maternal anesthesia (regional OR general). Risk is decreased by elective caesarean section.

Special Considerations

  • The preductal SaO2 in a neonate is not expected to reach infant levels until 10 minutes after birth. Beginning resuscitation with room air and increasing FiO2 only if needed may lead to improved outcomes. Current guidelines state that not performing resuscitation is reasonable in patients with extreme prematurity (<23 weeks or birth weight <400 g), anencephaly, and chromosomal abnormalities that are incompatible with life (trisomy 13 or 18). Do not use naloxone to treat respiratory depression because it can cause sympathetic stimulation that can precipitate neonatal hemorrhagic stroke (intraventricular hemorrhage). If narcotic-induced respiratory depression is suspected, support ventilation with a bag and mask or endotracheal intubation (Table 9.3). If chronic opioid exposure has occurred, it may be necessary to gradually titrate a decreasing opioid dose over a period of days to weeks in order to avoid acute withdrawal.

Table 9.3 Endotracheal Tube Diameters and Lengths According to Gestation and Weight

50% weight by gestation

Tube diameter and length at the lip

Gestation (weeks)

Body weight (kg)

Diameter (mm)

Length (cm)

23/24

0.5

2.5

6

26

0.75

2.5

6.5

27

1

2.5

7

30

1.5

2.5

7.5

33

2

2.5–3

8

35

2.5

3

8.5

37

3

3–3.5

9

40

3.5

3.5

9.5

Further Reading

American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science: Part 15: Neonatal resuscitation. Circulation. 2010; 122: S909–S919.Find this resource:

Aziz K, Chadwick M, Baker M, Andrews W. Ante- and intra-partum factors that predict increased need for neonatal resuscitation. Resuscitation. 2008; 79(3): 444–452.Find this resource:

Pediatric Advanced Life Support: Outside the Operating Room

Definition

Guideline for cardiopulmonary resuscitation of a child or infant.

Presentation

  • No response or minimal response to stimulation (tapping shoulder, calling name).

Respiratory Failure

  • Apnea, cyanosis

  • Impending respiratory failure can present with tachypnea, gasping, grunting, nasal flaring, paradoxic or diminished chest movement, or retractions.

Cardiac Arrest

  • Pulseless: Electrocardiogram may show asystole, ventricular fibrillation, ventricular tachycardia, or may show a rhythm (pulseless electrical activity).

  • Impending cardiac arrest associated with decompensated shock can present with tachycardia and hypotension in older children.

Pathophysiology

Lack of end-organ oxygenation, most commonly due to either respiratory failure (no oxygenation) or uncompensated shock (organs are not perfused with oxygen-rich blood), causing acidosis. Acidosis and hypoxia lead to myocardial ischemia and reduced cardiac contractility, eventually causing bradycardia, arrhythmias, and asystole.

Differential Diagnosis

  • Look for and treat reversible causes. Hypoxia is the most common cause of cardiac arrest in children.

  • “Hs and Ts”—a mnemonic for common causes—REVIEW EARLY IN RESUSCITATION.

    • Hs: Hypoxia (airway obstruction, asphyxiation), H+ (acidosis), Hyper/Hypokalemia, Hypothermia, Hypovolemia (e.g., hemorrhage leading to shock), Hypoglycemia, Hypothermia

    • Ts: Trauma, Toxins, Tension pneumothorax (or hemothorax), Thrombosis (e.g., coronary artery, air embolus), Tamponade (cardiac)

  • Arteriosclerotic myocardial infarction is an adult disease. Consider likely pediatric etiologies: anaphylaxis, congenital heart disease, foreign body aspiration, or ingestion of poisons (e.g., prescription medications!).

Immediate Management

  • CAB: Circulation, airway, breathing

  • Call for help.

  • Call for a defibrillator/monitor.

For cardiac arrest:

  • Circulation: Begin chest compressions at least 100 per minute. Minimum depth should be 1½ inches (4 cm) in infants and 2 inches (5 cm) in children, corresponding to one-third of the anterioposterior diameter of the chest. Allow full chest recoil between compressions. Continue compressions during other steps: No end-organ perfusion occurs when compressions are stopped (e.g., continue compressions while attaching defibrillator pads and establishing intravenous access).

  • Breathing: Begin bag-mask ventilation if the patient is not intubated, looking for adequate chest rise. Single rescuers should give two breaths for every 30 chest compressions. If two rescuers are present, the second rescuer should give two breaths for every 15 compressions during a brief pause. Inspiratory time should be 1 second. Administer 100% FiO2. Caution: Do not overventilate. If ventilation is difficult, consider two-person mask ventilation, with one provider using both hands on the mask, and the other provider squeezing the bag.

If the patient is intubated, ventilate without stopping chest compressions at a rate of 8–10 breaths/minute.

  • Establish intravenous access.

  • Attach defibrillator pads or paddles immediately, analyze for a rhythm, and shock if indicated (VF or VT). Many defibrillation units will automatically calculate the dose; if manual, use 2 J/kg for the first shock. Use the largest paddles or pads that can fit on the patient’s chest without touching.

  • Resume chest compressions and ventilation immediately after each shock is given or if the defibrillator indicates “no shock.” Recheck the rhythm every five cycles (2 minutes) of CPR. The second and subsequent shocks should be 4 J/kg minimum (maximum dose is 10 J/kg or maximum dose for adults).

  • Drug therapy: Administer epinephrine 0.01 mg/kg IV/IO every 3–5 minutes during resuscitation. Administer amiodarone 5 mg/kg IV/IO for ventricular fibrillation or ventricular tachycardia (may repeat twice if needed). Administer magnesium (25–50 mg/kg IV/IO: 25–50 mg/kg) for torsades de pointes (polymorphic VT with prolonged QT interval).

  • Consider intubating the trachea if bag-mask ventilation is inadequate. Minimize interruptions in chest compressions. Attempt to measure end tidal CO2, but absence may be caused by either esophageal intubation or lack of circulation (i.e., inadequate chest compressions). Note: Gastric inflation from overventilation can make ventilation difficult or impossible, especially in younger children. If ventilation becomes difficult, suction the stomach with an orogastric tube or a long suction catheter.

  • Call for ECMO early if return of spontaneous circulation does not occur within the first 6 minutes of CPR

For respiratory arrest only:

  • Bag-mask ventilation, give one breath every 3–5 seconds “squeeze-release-release.”

  • Prepare for the possibility that cardiac arrest may be imminent.

For bradycardia (slow pulse causing decreased perfusion):

  • Support the airway and breathing. Begin high-flow O2. Initiate cardiopulmonary monitoring and establish intravenous or intraosseous access. Obtain a 12-lead ECG. Assess for and treat underlying causes (Hs and Ts). If decreased perfusion does not resolve by improving ventilation and oxygenation, begin CPR without delay.

  • Drug therapy: After 2 minutes of chest compressions, give epinephrine IV/IO 10 MICROgrams/kg or endotracheally 100 MICROgrams/kg if needed. Administer atropine 20 MICROgrams/kg only if the primary cause is suspected to be AV block or vagal.

  • Consider transthoracic or transvenous pacing, especially if a primary cardiac cause is suspected. Request an emergency consultation from a pediatric cardiologist.

For tachycardia (with a pulse):

  • Support airway, breathing, and circulation, administer high flow oxygen. Initiate cardiopulmonary monitoring, and establish intravenous or intraosseous access. Obtain a 12-lead ECG. Assess for and treat underlying causes (Hs and Ts).

  • Narrow complex tachycardia (QRS <0.09 seconds):

    • Sinus tachycardia: look for and treat reversible causes.

    • Stable supraventricular tachycardia (SVT): Perform a vagal maneuver (place a bag of ice wrapped in a towel on the forehead in infants and toddlers, have older children blow through a straw, or perform a unilateral carotid sinus massage). Drug therapy (if vagal maneuvers ineffective): Administer adenosine 0.1 mg/kg IV/IO, flushed rapidly. In older children only, can considering administering verapamil 0.1–0.3 mg/kg.

  • Unstable supraventricular tachycardia (SVT):

    • Sedate the patient (consider midazolam at least 0.1–0.2 mg/kg IV), administer synchronized cardioversion (administer 0.5–1 J/kg for the first shock, 2 J/kg for subsequent shocks if needed). If the rhythm does not convert or SVT occurs again quickly, administer amiodarone 5 mg/kg IV/IO or procainamide then give a third shock.

  • Wide complex tachycardia (QRS >0.09 seconds):

    • This may be ventricular tachycardia. If unstable, administer synchronized cardioversion (0.5–1 J/kg for the first shock, 2 J/kg for subsequent shocks if needed). If stable, request an emergency consultation from a pediatric cardiologist.

Diagnostic Studies

  • Do not interrupt CPR unnecessarily for blood draws or delay treatment of reversible causes while waiting for laboratory values. Consider arterial blood gas analysis, serum electrolytes, glucose, and calcium, as well as a carboxyhemoglobin level and toxicology screen. If a toxic ingestion is suspected, contact a toxicologist or poison control!

  • Echocardiography can identify cardiac tamponade, massive embolus, poor cardiac contraction, and decreased preload. Do not delay treatment for an echocardiogram if one of these causes is suspected.

Subsequent Management (After Successful Resuscitation from Cardiac Arrest)

  • Decrease the FiO2 while maintaining a SaO2 >94%.

  • Monitor for adequate perfusion and O2 delivery. Over time, acid-base status will normalize and lactate will decrease if resuscitation is successful.

  • Consider administering a vasopressor (e.g., dopamine) for cardiac output caused by myocardial dysfunction.

  • Therapeutic hypothermia (core temperature 32° C to 34° C for 12–24 hours) may improve neurologic outcome in children who remain unconscious following successful resuscitation.

  • Treat hyperthermia (core temperature >38° C) to improve neurologic outcome.

Risk Factors

  • Insufficient supervision leading to trauma or drowning

  • Congenital disease: Down syndrome (bradycardia and cardiac arrest can occur even in the absence of structural heart disease), long QT syndrome, family history of sudden cardiac arrest

  • Children who were born prematurely

Special Considerations

  • The American Heart Association changed its guidelines for the management of cardiac arrest in children and adults in 2010 to prioritize chest compressions. The mnemonic has changed from “ABC” to “CAB”—circulation, airway, breathing. Although the most likely cause of cardiac arrest in children is a respiratory event, mobilizing supplies for airway management (bag, mask) typically requires at least several seconds, whereas chest compressions can be started immediately.

  • Minimize interruptions in chest compressions, even when checking the pulse or securing the airway. It is difficult to maintain high-quality compressions for long; the rescuer performing compressions should rotate every 2 minutes.

  • Patients receiving CPR are commonly overventilated, which decreases the likelihood of successful resuscitation. Overinflation of the lungs decreases venous return, decreasing the amount of blood that the heart can then pump to the brain, end-organs, and coronary arteries. Inflation of the stomach during overventilation also increases the risk of aspiration of stomach contents into the lungs.

  • ETCO2 and arterial blood pressure indicate adequate chest compressions and return of spontaneous circulation. ETCO2 consistently >10–15 mm Hg indicates high-quality CPR (adequate chest compressions and recoil, absence of overventilation). A sudden and sustained increase in ETCO2 may indicate the return of spontaneous circulation. Caution: For 60–120 seconds following intravenous vasoconstrictors (e.g., epinephrine, vasopressin), ETCO2 may decrease due to the concomitant decrease in pulmonary blood flow; this is usually an artifact.

  • Pulse oximetery is not accurate in patients with decreased perfusion, and may appear normal in patients with carbon monoxide poisoning.

  • If intravenous access cannot be secured, obtain intraosseus access promptly. Intraosseus access can be used to administer all medications, fluids, and blood products. Intraosseus administration is preferable to endotracheal administration of medications, although if absolutely necessary, naloxone, epinephrine, atropine, and lidocaine (NEAL) can be administered through the endotracheal tube. The endotracheal dose is two to three times the intravenous dose for naloxone, atropine, and lidocaine, and 10 times the intravenous dose for epinephrine.

  • Parents should be given the option of being present during the resuscitation, Class I evidence shows that being there will help families to later process this traumatic experience.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care: Part 13: Pediatric basic life support. Circulation. Circulation. 2010; 122: S862–S875.Find this resource:

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care: Part 14: Pediatric advanced life support. Circulation. 2010; 126: e1361.Find this resource:

Stridor, Postextubation

Definition

Upper airway narrowing (proximal trachea or above) that reduces airflow and may lead to respiratory failure.

Presentation

  • Typically seen after extubation, especially if the endotracheal tube was too large (no leak at a pressure of 20–25 mm Hg) or after prolonged intubation.

  • A high-pitched, “squeaking” sound may be heard on auscultation over the anterior neck, and will be associated with tachypnea, hypoxemia, and hypercarbia. Sternal retractions and nasal flaring are caused by increased work of breathing.

Pathophysiology

Stridor is caused by fast, turbulent airflow in the oropharynx, larynx, or upper trachea. It occurs during inspiration because abnormal or inflamed upper airway tissue is pulled inward, generating turbulence and noise. Poiseuille’s law dictates that airway obstruction increases 16 times for each 50% reduction in the airway radius.

Immediate Management

  • Administer humidified 100% O2 via blow-by or face mask, as tolerated.

  • Administer nebulized racemic epinephrine 0.5 mL of 2.25% solution, diluted in 2 cc normal saline, 0.25 mL for infants.

  • Administer dexamethasone 0.5–1 mg/kg (airway dose) if not already given during the surgical procedure. This will decrease airway inflammation after 4–6 hours.

  • In severe cases: Continuous positive airway pressure, consider reintubation (may need a smaller endotracheal tube).

  • In severe cases: Consider administering helium-oxygen mixture (Heliox) to decrease turbulent airflow.

Differential Diagnosis

  • Bronchospasm

  • Laryngospasm

  • Acute allergic reaction (often accompanied by rash and hypotension)

  • Vocal cord dysfunction caused by recurrent laryngeal nerve injury

  • Foreign body aspiration (e.g., tooth dislodged during laryngoscopy)

  • Tracheomalacia or laryngomalacia (prematurity, prior tracheostomy) Caution: Sedation will exacerbate airway obstruction in these patients.

Diagnostic Studies

  • Clinical diagnosis

Subsequent Management

  • Reintubation and/or pediatric intensive care unit management may be needed for severe cases.

Risk Factor

Further Reading

da Silva PS, Fonseca MC, Iglesias SB, Junior EL, de Aguiar VE, de Carvalho WB. Nebulized 0.5, 2.5 and 5 ml L-epinephrine for post-extubation stridor in children: a prospective, randomized, double-blind clinical trial. Int Care Med. 2012; 38(2): 286–293.Find this resource:

Trauma

Definition

Mechanical injury, often involving multiple organ systems, and which may cause rapid deterioration. Associated injuries, sometimes remote in location from the primary injury, can increase morbidity and mortality. Requires simultaneous evaluation and implementation utilizing advanced cardiac life support—ACLS (to maintain end-organ perfusion) and advanced trauma life support—ATLS (for injury management).

Presentation

Advanced Trauma Life Support (ATLS) evaluation begins with the primary survey (ABCDE—Airway and cervical Spine, Breathing and ventilation, Circulation and hemorrhage management, Disability and neurologic status, Exposure and environment). Ignoring or delaying any of these components may cause serious morbidity; therefore, these steps are taken simultaneously, guided by a team leader. This is followed by the secondary survey, which is an assessment from head-to-toe and re-evaluation of vital signs. The components of the primary survey must be constantly re-assessed due to the potential for a worsening of the patient’s condition.

Airway and Cervical Spine

  • If talking or crying, the patient is able to exchange air. Stridor may indicate imminent airway obstruction. Chest rise can be misleading, especially in children, as it can be seen in the absence of air movement (i.e., if patient has respiratory effort but complete airway obstruction).

  • Unconscious patients are at high risk for aspiration and airway obstruction.

  • Obtunded or unconscious patients, or those with a distracting injury, cannot be evaluated clinically for a cervical spine injury.

Breathing and Ventilation

  • Hypoxia and cyanosis (from hypopnea, pulmonary contusions, flail chest, pneumothorax, hemothorax, or aspiration)

  • Tachypnea and respiratory distress, including paradoxic chest movement, retractions, nasal flaring, gasping, grunting

  • Imminent airway loss and need for intubation if the patient is hypopnic, if mask ventilation is impossible, or if the patient has signs of respiratory distress, a C1/C2 injury, a Glasgow Coma Scale (GCS) <9, penetrating neck injury, is hemodynamically unstable, or has a major pulmonary or chest wall injury.

  • Visible tracheal deviation or penetrating injury. Subcutaneous emphysema or unilateral breath sounds (pneumothorax, hemothorax) may also be present.

Circulation and Hemorrhage Management

  • In children, blood pressure will not decrease until >25%–30% of blood volume has been lost. The first sign of hypovolemia in children is an increase in heart rate.

  • Can have hidden blood loss into the intrathoracic, intraperitoneal, or retroperitoneal spaces, or into the pelvis or long bones.

Disability

  • Assess neurologic status with the mnemnoic AVPU—alert, verbal stimuli response, painful stimuli response, unresponsive.

Exposure and Environment

  • Examine completely by undressing the patient.

  • Take steps to prevent hypothermia.

Secondary Survey

  • AMPLE—Allergies, Medications, Past medical problems and surgery, Last Meal, Events related to the injury

  • Glasgow Coma Scale

  • Head-to-toe evaluation

Pathophysiology

Due to a child’s small size, internal organ and multiple system injuries are common in major trauma, as force is transmitted quickly through the more elastic skeleton and connective tissue. Hemorrhage can be can cause rapid decompensation because of the smaller total blood volume. Hypothermia occurs quickly in these patients with a large body surface area relative to total body mass. Coagulopathy is a concern in patients who are transfused more than one blood volume.

Differential Diagnosis

  • Toxins (ingestion of household chemicals, unsecured medications, or drug or alcohol abuse).

  • Child abuse (story inconsistent with injuries, multiple healing fractures of varying age, detached retina).

Immediate Management

Airway and Cervical Spine

  • In an awake patient, provide supplemental oxygen by face mask or nasal cannula as needed to maintain SaO2 >90%.

  • Use of a correctly sized cervical spinal collar is required after blunt trauma injuries for immobilization if the C-spine cannot be immediately cleared. Clearance requires five clinical criteria: no midline cervical tenderness, no focal neurologic deficit, normal alertness, no intoxication, and no painful distracting injury.

  • If the patient appears unconscious or has a severely altered mental status, keep the C-spine immobile while performing a chin lift and jaw thrust and suctioning any obstructing airway secretions and blood. If the patient “wakes up” when suctioned and can protect his airway, intubation might not be needed.

  • Intubate if minimal consciousness, severe injury, or imminent loss of airway. If the patient was intubated pre-hospital, confirm proper ETT size and placement. Utilize a “rapid-sequence” induction, with the c-collar removed and one person keeping the C-spine immobile throughout the time the collar is off with manual in-line stabilization.

  • Have suction and emergency airway equipment immediately available. Visualization of the airway may be difficult due to distortion and bleeding. A supraglottic airway, such as a LMA, may be life-saving in cases of difficult ventilation and difficult intubation. If a difficult airway is anticipated, have equipment and a surgeon qualified to perform a surgical airway immediately available.

Breathing and Ventilation

  • Dependent on injury: pneumothorax may require immediate needle decompression and a chest tube; lung injury may require immediate operative management.

Circulation and Hemorrhage Management

  • Establish two large-bore intravenous lines in major trauma. In infants and small children, can often only obtain 22–24g IVs. Consider intraosseus access if intravenous access is not feasible.

  • Assess and control bleeding, external and internal. Emergency surgery may be required.

  • If the patient is hypotensive, begin fluid resuscitation with normal saline or lactated Ringers; administer a bolus of 20 mL/kg. May need to be repeated.

  • For major bleeding, begin transfusion with blood products as early as possible. May need to activate the massive transfusion protocol.

  • In patients with severe injury, consider invasive monitoring (intra-arterial catheter, central venous catheter), orogastric tube, and bladder catheter.

Disability and Neurologic Status

  • Patients with altered neurologic status may have a brain injury.

Exposure and Environment

  • After major trauma, remove all clothing to assess for associated injuries.

  • Monitor temperature and maintain normothermia by warming the room, utilizing forced air warming devices, and warming intravenous fluids and blood products.

Diagnostic Studies

  • Chest radiograph

  • If the patient is stable, advanced imaging such as a CT scan may be indicated.

  • Serial hemoglobin and hematocrit, toxicology screen, electrolytes, coagulation panel. A thromboelastogram may be useful to quickly obtain information about coagulation and qualitative platelet function.

Subsequent Management

  • In patients with acute head injury: avoid steroids for increased intracranial pressure, avoid prolonged hyperventilation, do not routinely give anticonvulsants to patients who have not had a seizure.

  • Maintain oxygenation and perfusion. (Cerebral and spinal cord perfusion pressures are particularly important if these structures are injured.)

  • Only use glucose-containing intravenous fluids if patient is hypoglycemic, especially for traumatic brain injury or spinal cord injuries.

  • Do not give steroids for spinal cord injury (Level I evidence in adults), pediatric evidence pending.

  • Manage acute pain with opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, low-dose ketamine infusions for NMDA blockade (e.g., 0.1 mg/kg/h), or regional anesthetic techniques (particularly for orthopedic injuries). Patient-controlled analgesia (PCA) may be appropriate for children 5 years or older.

Risk Factors

  • Riding in the car without a car seat or safety belt (as appropriate for age)

  • Not wearing a helmet for high-speed activities (e.g., bike riding, skiing, ATV riding)

  • Child abuse

Prevention

Prenatal, postpartum, and infant/toddler home visits by nurses for disadvantaged children through the nurse–family home partnership significantly decrease mortality from both accidental and intentional injury.

Special Considerations

  • Patients suffering from massive hemorrhage quickly become coagulopathic and acidotic. These factors can be made worse with the administration of large amounts of crystalloid fluid and packed red blood cells, which can cause hemodilution and hypothermia. Increasing evidence has been found for “damage-control resuscitation,” which involves early blood product administration (platelets, fresh-frozen plasma, and PRBCs in a 1:1:1 ratio) and limited crystalloid infusion, as well as accepting a slightly lower blood pressure in settings of uncontrolled hemorrhage.

Further Reading

Greene N, Bhananker S, Ramaiah R. Vascular access, fluid resuscitation, and blood transfusion in pediatric trauma. Int J Crit Illn Inj Sci. 2012; 2(3): 135–142.Find this resource:

Hughes NT, Burd RS, Teach SJ. Damage control resuscitation: permissive hypotension and massive transfusion protocols. Pediatr Emerg Care. 2014; 30(9): 651–656.Find this resource:

McFadyen, JG, et al. Initial assessment and management of pediatric trauma patients. Int J Crit Illn Inj Sci. 2012; 2(3): 121–127.Find this resource:

Olds DL, Kitzman H, Knudtson MD, Anson E, Smith JA, Cole R. Effect of home visiting by nurses on maternal and child mortality: results of a 2-decade follow-up of a randomized clinical trial. JAMA Pediatr. 2014. http://www.nursefamilypartnership.orgFind this resource: