Pediatric Board Study Guide pp 197-245 | Cite as
Emergency Medicine
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Abstract
This chapter focuses on the clinical presentation of common pediatric emergencies, with an emphasis on recognition, initial management steps, and stabilization. Topics discussed include respiratory distress, anaphylaxis, trauma, burn care, status epilepticus, altered mental status, poisoning and toxic exposure, foreign body aspiration or ingestion, diabetic ketoacidosis, concussions, hypertensive crisis, and drowning, as outlined by the 2017 American Board of Pediatrics Content Specifications. Also covered is the initial first hour of emergency care management of sepsis and shock.
Keywords
Respiratory distress Acute abdomen Anaphylaxis Trauma/burns Status epilepticus Altered mental status Poisoning/toxic exposure Foreign body aspiration/ingestion Diabetic ketoacidosis Concussion/head injury Hypertensive crisis Drowning Sepsis and shockRespiratory Distress
- Definitions
- Respiratory distress
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Interruption of the respiratory tract or the systems that control respiration
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One of the most common pediatric complaints in the emergency room
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- Respiratory failure
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Inability of the respiratory system to meet metabolic demand for oxygenation or ventilation
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Prominent cause of pediatric deaths, particularly in infants
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Respiratory failure is a primary cause of pediatric cardiac arrest
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Special Considerations in the Anatomy of the Pediatric Airway
- Large occiput
Causes flexion of airway when supine
- Large tongue
May obstruct posterior pharynx when supine
- Obligate nose breathers (particularly < 4 months)
Nasal suctioning can significantly relieve respiratory distress due to nasal congestion
- Omega-shaped and floppy epiglottis
Structures easily collapse, and are not as rigid as adult airway structures
- Anterior airway with higher glottic opening at C2–C3 (versus C4–C5 in adults)
More difficult to visualize larynx during intubation
- Significant anatomic variation with age
- Shorter trachea
Technically difficult intubation
Easy to insert endotracheal tube too far (right mainstem intubation)
Easy to lose artificial airway (dislodged tube, esophageal intubation)
- Smaller tracheal diameter:
- Small increase in tracheal thickness causes disproportionately larger obstruction
- Poiseuille’s law: Resistance varies inversely with fourth power of the radius
Example: 1 mm thickening of trachea decreases tracheal diameter by 20% in an adult and 80% in a small child
- Narrowest portion of airway at cricoid ring (versus at vocal cords in adults)
Uncuffed endotracheal tubes may provide adequate seal at “natural” cuff
- Small cricothyroid membrane
Needle cricothyrotomy difficult
Surgical cricothyrotomy impossible in small children
- Localizing physical findings
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A careful physical can help rapidly localize the etiology of distress (Table 7.1)
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- Common causes of respiratory distress by anatomical location
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Many causes of respiratory distress in pediatric patients are commonly encountered and have well-defined clinical syndromes
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- Upper airway
- Upper airway obstruction
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Anaphylaxis (hives, angioedema, atopy, history of exposure to antigen, stridor, hoarseness)
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Nasal congestion/obstruction (congestion, rhinorrhea, concurrent upper respiratory infection [URI])
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Foreign body (history of coughing or choking event, stridor, drooling)
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Congenital/developmental airway anomalies (choanal atresia, adenotonsillar hypertrophy, laryngotracheomalacia, subglottic stenosis/web/hemangioma, branchial cleft abnormalities)
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- Upper airway infection
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Croup (URI symptoms, barky cough, fever, inspiratory stridor)
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Epiglottitis (toxic appearance, fever, dysphagia, drooling, inspiratory stridor)
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Peritonsillar abscess (fever, sore throat, trismus, dysphagia, drooling, vocal changes, uvular displacement)
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Retropharyngeal abscess (fever, dysphagia, drooling, vocal changes, neck stiffness/pain with extension, torticollis)
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Tracheitis (toxic appearance, fever, stridor—similar appearance to epiglottitis, usually will have risk factors)
-
-
- Lower airway
- Lower airway obstruction
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Anaphylaxis (hives, angioedema, atopy, history of exposure to antigen, wheezing)
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Asthma/reactive airway disease (atopy, history of bronchodilator use, expiratory wheezing, prolonged inspiratory to expiratory ratio)
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Bronchiolitis (previously healthy, no prior wheezing, concurrent URI symptoms)
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Foreign body
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Tracheobronchomalacia (recurrent stridor or noisy breathing, acute or chronic exacerbations with concurrent URI)
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- Lower airway infection
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Pneumonia (cough, tachypnea, fever)
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- Extrapulmonary
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Mediastinal masses (orthopnea, B symptoms, hoarseness, hemoptysis, lymphadenopathy)
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Pericardial tamponade (history of trauma, orthopnea, hypotension, jugular vein distention, pulsus paradoxus, muffled heart sounds)
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Pleural effusion (risk factors such as pneumonia/chemotherapy/autoimmune disorders, orthopnea, pleuritic pain)
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Pneumothorax/tension pneumothorax (possible history of trauma or spontaneous sudden onset, unilateral absent breath sounds, possible hypotension, deviated trachea with mediastinal shift if tension is present)
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An approach to the differential diagnosis by clinical syndrome
Respiratory distress with signs of upper airway obstruction (stridor, stertor, vocal change, dysphagia, drooling):- If acute onset with fever, consider infection
Croup, peritonsillar abscess, retropharyngeal abscess, tracheitis, epiglottitis
- If acute onset without fever, consider
Anaphylaxis, foreign body
- If chronic, consider
Masses, congenital/developmental abnormalities such as tonsillar hypertrophy, vocal cord dysfunction, laryngotracheomalacia, psychogenic causes
Respiratory distress with signs of lower airway pathology (wheezes, rales):- If acute onset with presence of fever, consider infection/inflammation
Bronchiolitis, pneumonia, subacute foreign body, myocarditis
- If acute onset without fever, consider
Asthma, bronchiolitis, viral/atypical pneumonia, foreign body aspiration, anaphylaxis
Respiratory distress with no signs of airway obstruction, with the presence of tachypnea:- If acute onset tachypnea with fever, broaden the differential to include a more systemic illness
Pneumonia, subacute foreign body, pulmonary embolism, myocarditis, pericarditis, sepsis
- If acute-onset tachypnea without fever and with concern for cardiac abnormality (arrhythmia, rubs, gallops, new murmurs, hepatomegaly, poor perfusion), consider
Congenital heart disease, myocarditis, pericarditis, pericardial effusion/tamponade, congestive heart failure, pleural effusion
- If acute-onset tachypnea without fever and no concern for cardiac abnormality:
- Very large differential diagnosis, obtain thorough history and physical
Respiratory disorder (pneumonia, atelectasis, pulmonary embolism, pulmonary deformity or mass)
Metabolic (acidosis, hyperammonemia, hyperglycemia, hepatic/renal disease)
Toxic (ingestions, methemoglobinemia)
CNS disorder (seizure, mass, encephalopathy, neuromuscular disease, anxiety, pain)
Intra-abdominal pathology (abdominal pain, distention, mass)
Hematologic (anemia, methemoglo-binemia)
Physical exam findings seen in pediatric patients in respiratory distress
Physical finding | Description | Physiology | Important notes |
---|---|---|---|
Retractions | Accessory muscle usage (supraclavicular, intercostal, abdominal) | Counteract high negative intrathoracic pressure via increased respiratory effort | Generalized finding of respiratory distress |
Head bobbing | Flexion–extension movement of head and neck during inspiration and expiration | Emerges due to severe accessory muscle use, seen particularly in small children and infants | Indicative of severe respiratory distress, potential impending respiratory failure |
Flaring | Widening of the lateral nares | Increases the upper airway diameter as an attempt to help relieve obstruction | Often a late finding of respiratory distress seen in small children and infants |
Stertor | Low pitched, loud, rumbling, snoring sound | Upper airway obstruction: may be due to large tongue, tonsils, or adenoids; poor muscle tone; or altered mental status | Can improve with repositioning (“sniffing position”) or jaw thrust |
“Hot potato” voice | Muffled, soft voice | Obstruction of upper airway, typically oropharynx or pharynx | May be seen in retropharyngeal abscess or peritonsillar abscess |
Hoarseness | Rough or harsh characteristic to voice | Obstruction or abnormality of vocal cords or larynx | Can indicate benign/minor pathology such as viral URI or concerning pathology such as injury to vagus or recurrent laryngeal nerve |
Barky cough | Loud, “seal-” or “dog-like” hacking cough | Pathology or obstruction of subglottic area | Commonly seen in acute viral croup |
Stridor | Harsh multiphonic, high-pitched upper airway noise, “noisy breathing” | Obstruction of upper airway results in turbulence and subsequent noise; inspiratory stridor most commonly glottic/subglottic in origin, expiratory stridor more likely lower airway, e.g., carina | Can indicate acute viral croup, or other concerning pathology such as aspirated foreign body or epiglottitis |
Grunting | Soft, quick “puffing” expiratory noise | Expiration against partly closed glottis, attempt to maintain lung volume and prevent atelectasis via “auto-PEEP” | Often late finding of respiratory distress, seen in small children and infants |
Wheezing | Musical, continuous noise | Expiratory wheezing indicates bronchi and bronchiolar obstruction | Expiratory wheezing commonly heard in asthma and bronchiolitis |
Rales (fine crackles) | Inspiratory, high-pitched, “Velcro-like” sounds | Opening of collapsed alveoli filled with secretions, indicate pathology at lung tissue level | Typically will not clear with repositioning and coughing |
Rhonchi (coarse crackles) | Inspiratory, mid- to low-pitched “popping” sounds | Turbulence and secretions from secretions or inflammation within bronchi and bronchioles | More likely to clear with repositioning and coughing |
Initial Emergency Care for Patient in Acute Respiratory Distress
- Airway management
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Leading cause of pediatric cardiac arrest is from respiratory failure
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Timely management of the pediatric airway is key to resuscitation of pediatric patients with acute respiratory distress
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- Categorize the airway
- Airway is clear: Airway is open and non-obstructed for normal breathing
Patient is able to vocalize clearly (speaking or loud crying)
- Airway is maintainable: Airway is obstructed but maintained with simple measures (Table 7.2)
Patient able to vocalize, but abnormally (stertor, stridor, choking, coughing, dysphonia, etc.)
- Airway is not maintainable: Airway is obstructed and requires advanced intervention such as intubation
Unable to speak or absence of cry (gurgling, gasping, cyanosis, loss of consciousness, extreme agitation, etc.)
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- Breathing management
- Pediatric patients are less tolerant of hypoxemia and hypercarbia
Higher metabolic rate means more metabolic demand
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Initial simple airway maneuvers for patients in acute respiratory distress
Airway maneuvers | Description |
---|---|
Airway clearing | Suctioning oro-/nasopharynx to remove secretions or debris |
Nasopharyngeal airway | |
Oral airway in patient with altered mental status | |
Airway positioning | Allow an awake child to assume position of comfort (e.g., tripoding) |
Head tilt and chin lift (“sniffing” position) to compensate for large occiput | |
Jaw thrust/chin lift to open airway and bring tongue forward | |
Shoulder roll to prevent forward flexion of cranium due to large occiput |
Initial interventions in resuscitation of patients in acute respiratory distress
Intervention | Common uses |
---|---|
Nasal cannula | Hypoxemia alone, will dry nasal mucosa over time |
Simple face mask | Hypoxemia alone, significant room air entrainment and mixing |
Non-rebreather face mask | Hypoxemia alone, allows for greater FIO2 via a reservoir |
Heated high flow nasal cannula | Hypoxemia and increased respiratory effort, allows humidification and heating, higher oxygen flow rates |
Noninvasive positive pressure ventilation | Hypoxemia and hypercarbia in select patients with respiratory failure but adequate airway protection and mentation; allows for positive pressure delivery via sealed mask |
Bag–valve–mask ventilation | Hypoxemia and hypercarbia, insufficient/absent respiratory effort, a temporizing but life-saving measure while definitive airway/ventilatory support is being planned |
Inhaled bronchodilators: albuterol and ipratropium | States of reversible bronchospasm (i.e., asthma exacerbation) |
Nebulized racemic epinephrine | Suspected upper airway obstruction and edema with stridor (i.e., acute infectious croup) |
Intramuscular epinephrine | Suspected anaphylaxis |
Summary
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Correction of respiratory distress ultimately needs identification of the underlying cause
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Any disorder that causes respiratory distress has the potential to be life-threatening
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Remember the unique characteristics of the pediatric airway
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Initial resuscitation of the patient in acute respiratory distress requires attention to airway, breathing, and circulation
The Acute Abdomen
The following section will focus on the presentation of the pediatric acute abdomen in the setting of emergency care, with a particular emphasis on the identification of surgical abdominal emergencies. Abdominal emergencies in the setting of pediatric abdominal trauma will be covered in the Trauma and Burns section.
The Pediatric Acute Abdomen
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Abdominal complaints in pediatric patients are common and often benign
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Surgical abdominal emergencies must not be missed, due to high morbidity and mortality, and require prompt recognition and timely surgical evaluation
- Findings that may indicate a surgical abdomen
- Bilious emesis
Bilious emesis in infants is a surgical emergency
- Guarding
Active guarding
Passive guarding/rigidity
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Distention
- Bowel sounds
Absent bowel sounds may indicate ileus
- Tenderness
Rebound tenderness is indicative of peritonitis
- Associated symptoms
Fever can signify a systemic inflammatory response
Bloody diarrhea can signify bowel wall necrosis and malperfusion
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Age-dependent presentation
The age of the presentation can significantly shape the differential diagnosis- Infant: Maintain higher suspicion for congenital anomalies
Intussusception, malrotation with midgut volvulus, incarcerated hernias, Meckel diverticulum, pyloric stenosis
- School-aged child: Infectious causes become increasingly common
Acute appendicitis
- Adolescent:
Acute appendicitis, ectopic pregnancy, ovarian torsion, testicular torsion
General Principles of Management
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Definitive treatment must be targeted at the etiology of the acute abdomen
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There are general treatment principles that can be applicable in most cases
- Initial resuscitation
- Attend to the ABCs (airway, breathing, circulation)
Be alert for signs of shock and poor perfusion
Restore intravascular volume as clinically appropriate
- Pain control
Use an appropriate regimen to treat escalating degrees of pain
If warranted, opioids can be safely used in pediatric patients
- Nil per os (NPO) status
Do not allow the patient to eat or drink
- For active bilious emesis and abdominal distention, consider decompression
Nasogastric tube
- Early surgical consultation
In the presence of suspicion for an acute surgical abdomen, prompt and early surgical consultation is important and should not be delayed
- Imaging options
- Abdominal plain radiographs can be helpful in the evaluation of an acute abdominal obstruction, foreign body, bowel perforation, or constipation
Identification of free air
Air-fluid levels indicating ileus
Dilated loops of bowel in obstruction
Radiopaque ingested foreign body
Evaluation of stool burden
- Ultrasonography is the preferred first line in many cases
Acute appendicitis, intussusception, ovarian torsion, pyloric stenosis, cholecystitis, pancreatitis, nephrolithiasis, pregnancy
- Computed tomography (CT) imaging
CT of the abdomen/pelvis is the radiation exposure equivalent of more than 100 plain radiographs of the chest
CT of the abdomen/pelvis increases risk of radiation-induced solid cancers in children
- Due to radiation exposure risks:
CT is not recommended in the routine evaluation of abdominal pain
Ultrasound should be considered first in the evaluation of acute appendicitis in children
Magnetic resonance imaging (MRI) will typically not be obtained in the emergency setting for the evaluation of abdominal pain
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Select surgical abdominal emergencies (Table 7.4)
Selected surgical abdominal emergencies, clinical features, and management
Features | Disease process | Clinical pearls | Clinical pitfalls | Initial management |
---|---|---|---|---|
Periumbilical pain migrating to the right lower quadrant at McBurney’s point | Acute appendicitis | Most common abdominal emergency in children, with peak incidence between 9 and 12 years; many will have pain with walking or jumping; may also have anorexia, vomiting, diarrhea, and fever | The anatomic location of the appendix can vary, causing nonclassical sites of pain | Fluid resuscitation, pain control, appendix ultrasound, surgical consultation |
Suspected acute appendicitis followed by sudden relief of pain, then development of generalized peritonitis | Perforated appendicitis | More likely to occur if appendicitis present for > 72 h, will often present with increasing signs of peritonitis and toxicity | Although appendicitis in infants is rare, the young child is more likely to present with perforation due to difficulty in the abdominal exam early on | Fluid resuscitation, pain control, appendix ultrasound, surgical consultation |
Extreme colicky pain with periods of normalcy, currant jelly stools | Intussusception | Typically, 3 months to 6 years old, invagination of bowel at lead point, most common is ileocolic | Intussusception can present with emesis and altered mental status alone | Fluid resuscitation, ileocolic ultrasound, barium or air contrast enema, surgical consultation if unsuccessful, anticipatory guidance as intussusception can recur |
Tense inguinal bulge, vomiting | Incarcerated inguinal hernia | Common cause of intestinal obstruction in infants and children, 60% occurring within the 1st year of life | May not have known prior history of hernia; incarceration can progress to strangulation and bowel necrosis within 24 h | May need inguinal ultrasound or abdominal radiograph if unclear diagnosis; otherwise, attempt immediate manual reduction if no sign of bowel necrosis, and early surgical consultation |
Infant, projectile nonbilious emesis, hungry after emesis | Pyloric stenosis | Hypertrophied pylorus in infant 2–5 weeks old, occurs in 1 in 250 births, more common in first-born males, can cause hypokalemic, hypochloremic metabolic alkalosis | Does not present with acute abdomen, but due to potential for profound electrolyte disturbance, prompt diagnosis is important; alkalosis can be severe enough to cause apnea | Fluid resuscitation, careful electrolyte management, pyloric ultrasound, surgical consultation |
Acute-onset bilious emesis, abdominal pain | Malrotation with midgut volvulus | Most serious cause of intestinal obstruction; congenital malrotation with abnormal fixation of bowel predisposes it to volvulize and obstruct; usually presents neonatally; however, 25% present > 1 year | Variable presentation, from asymptomatic to failure to thrive; complete volvulus for > 1 h causes gut necrosis; a midgut volvulus can cause death of entire small bowel and ascending colon | Resuscitation in case of signs of shock, flat and upright radiographs of abdomen, upper GI series, immediate surgical consultation |
Bilious emesis, abdominal distention, significant abdominal surgical history | Surgical adhesions with obstruction | Any child with prior abdominal surgery or peritonitis can develop adhesions; requires low threshold of suspicion | Presentation can occur within days, or months to years after surgery | Fluid resuscitation, abdominal radiographs with more than one view (e.g., flat, upright, and decubitus), gastric decompression, early surgical consultation |
Abdominal distention with systemic signs of illness (lethargy, apnea, temperature instability) in neonate | Necrotizing enterocolitis | Typically presents in premature infants or neonates within 10 days of birth, may have history of birth asphyxia or stress | Although most common in premature infants, can occur in term infants | Resuscitation if signs of shock, radiographs of abdomen, prompt surgical and neonatal subspecialty consultation |
Nonsurgical Causes for an Acute Abdomen
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Due to the small size of pediatric patients and possibility for referred pain, many extraintestinal or nonsurgical diseases can present with an acute abdomen and acute abdominal pain
- Abdominal
Gastroenteritis, viral or bacterial
Constipation
Mesenteric adenitis
Gastritis/peptic ulcer disease
Pancreatitis
Gallbladder disease
Hepatitis
- Head, eyes, ears, nose, and throat (HEENT)
Streptococcal pharyngitis
Infectious mononucleosis
- Pulmonary
Pneumonia
- Cardiac
Pericarditis, myocarditis
- Renal
Spontaneous bacterial peritonitis (with peritoneal dialysis)
- Genitourinary
Testicular torsion
Ovarian torsion
Ectopic pregnancy
Pelvic inflammatory disease
Dysmenorrhea
- Urinary
Cystitis, pyelonephritis
Nephro-/urolithiasis
- Endocrine/metabolic
Diabetic ketoacidosis
- Autoimmune/inflammatory
Inflammatory bowel disease
Henoch–Schönlein purpura
Summary
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The differential diagnosis of the acute abdomen in pediatric patients is broad, ranging in nature from benign to life-threatening
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A careful history and physical are important to identify surgical emergencies
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Infants present a particularly diagnostic challenge due to difficulty of exam and nonspecific nature of presentation
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Maintain a low threshold for early surgical consultation
Anaphylaxis
- Definition
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Serious, systemic, rapid-onset allergic/hypersensitivity reaction
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Variable clinical presentation and severity
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Immunoglobulin E (IgE)-mediated, type I hypersensitivity reaction to antigen
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- Pathophysiology
- Antigen exposure leads to systemic mast cell and basophil degranulation with large histamine and cytokine release
Vasodilation
Smooth muscle spasm (can also cause coronary artery vasospasm)
Increased vascular permeability
End stage: Loss of intravascular volume and hypotension
- Common likely antigens
- Food allergies (most common in pediatrics)
Peanut
Tree nuts (cashews, pecans, walnuts, etc.)
Milk
Wheat
Soy
Seafood (crustaceans)
Fruit
- Other miscellaneous allergens
Antibiotics (penicillins, cephalosporins, sulfonamides)
Insect stings (Hymenoptera, fire ants)
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- Diagnosis
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Primarily a clinical diagnosis
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If the presentation is unclear, a serum tryptase can help assist future subspecialty management
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- Clinical criteria
- Anaphylaxis is highly likely with any of the three clinical syndromes, in the context of an exposure to a likely antigen:
- 1.Acute onset of illness with skin and/or mucosal symptom, and with one of the following symptoms:
Respiratory compromise (such as wheezing or stridor)
Hypotension or altered mental status (AMS)/syncope or
- 2.Two or more symptoms of the following occurring acutely after exposure to likely antigen:
Skin/mucosa (90%) (urticaria, angioedema, flushing)
Respiratory (50–70%) (rhinorrhea, oropharyngeal/laryngeal edema, hoarseness, stridor, wheezing, shortness of breath)
Gastrointestinal (40%) (nausea, abdominal pain, diarrhea, vomiting)
Circulatory (30%) (hypotension, tachycardia)
Neurologic (syncope, sense of impending doom, seizures, AMS) or
- 3.
Age-specific decrease in systolic blood pressure (BP) > 30% from normal or hypotension
- 1.
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- Biphasic presentation
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Immediate phase: Occurs within minutes to hours after exposure
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Delayed phase/recurrence: Occurs from hours to days after exposure (up to 72 h)
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- Differential diagnosis
- Anaphylactoid reaction
Non-IgE-mediated anaphylaxis
Most commonly caused by aspirin, nonsteroidal anti-inflammatory drugs (NSAIDS), or radiographic contrast
Clinically indistinguishable from anaphylaxis
Treatment is identical to anaphylaxis
-
- Treatment
-
Always attend to the ABCs
- Intramuscular epinephrine is the first-line treatment of choice in anaphylaxis and must be administered immediately
- Dosage: 0.01 mg/kg intramuscular
Maximum of 0.3 mg in prepubertal child
Maximum of 0.5 mg in adolescent
- Timing: Immediate
Repeat at 5- to 15-min intervals
Up to 19% of patients will need a second intramuscular dose
Location: Mid-lateral thigh (vastus lateralis)
- Autoinjector dosing options
Autoinjectors can come in 0.1 mg, 0.15 mg, and 0.3 mg forms:
0.1 mg (7.5–14 kg)
0.15 mg (15–30 kg)
0.3 mg (>30 kg)
- Pharmacokinetics
Alpha- and beta-adrenergic agonist induces bronchodilation, vasoconstriction, and decreased vascular permeability
Effectively treating upper airway edema, hypotension, and shock in addition to bronchodilator and positive cardiac inotropic and chronotropic effects
- Intramuscular epinephrine achieves peak concentration faster than subcutaneous injection
Intramuscular epinephrine is far safer than intravenous (IV) epinephrine
Serious adverse effects of appropriately dosed intramuscular epinephrine are rare
Side effects mimic signs of endogenous catecholamine release: Pallor, anxiety, tachycardia, tremor
- Adjuncts therapies: Do not prioritize administration of adjuncts over epinephrine
Diphenhydramine (H1 blockers)
Ranitidine (H-2 blockers)
Albuterol or racemic epinephrine
Glucocorticoids
-
- Patient disposition
-
Due to potential for rebound anaphylaxis and rapid deterioration, careful consideration of patient risk factors must be made at time of disposition from emergency care
- Risk factors that may necessitate admission to the hospital for observation:
First presentation
Infants
Concomitant asthma
Unknown antigen
-
- Home care after anaphylaxis
- Counseling and follow-up are key for safe disposition home after anaphylaxis
Avoidance of identified allergen
Discussion of signs and symptoms of anaphylaxis
- Epinephrine auto-injector instruction
Because anaphylaxis has highly variable clinical presentation between patients and between episodes, it is not possible to predict disease severity
All patients with anaphylaxis should be prescribed an epinephrine auto-injector
- High-risk patients:
Coexisting asthma
Reaction to trace amounts of food
Idiopathic anaphylaxis
Generalized urticaria from insect sting (higher risk of more severe reaction)
Patient lives in a remote or rural area
Referral to an allergy/immunology specialist
-
Trauma and Burns
- General principles of pediatric trauma
- Primary survey (identify and treat any life-threatening problems)
A Airway maintenance
B Breathing and ventilation
C Circulation with hemorrhage control
D Disability; neurologic status (Glasgow Coma Scale [GCS], pupils)
E Exposure/environment (remove clothing and keep normal body temperature)
- Secondary survey
Vital signs
Detailed head-to-toe examination
- History of traumatic event
AMPLE history: Allergies, medications, past illnesses, last meal, events or environment related to injury
-
Pediatric Head Trauma
-
Most pediatric head trauma is not serious and requires only observation
-
Identification of serious head trauma in pediatric patients requires careful physical examination and understanding of warning signs
- Red flags in pediatric head trauma
- Severe mechanisms of injury
- Motor vehicle collision (MVC) with
Patient ejection
Fatalities
Rollover
Motor vehicle vs. pedestrian crash (MPC) or cyclist injury in those without helmets
- Height of fall
Infants under 2 years with falls greater than 3 ft
Children 2 years and over with falls greater than 5 ft
High-impact or high-speed object striking head
- Patients at higher risk
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Infants in general, but particularly if < 3 months
-
Known bleeding disorder or anticoagulated
-
Multisystem injuries
-
Suspected nonaccidental trauma
-
- Patient with findings that are higher risk
- AMS or acute change in mental status
Lethargy
Irritability
Loss of consciousness
Persistent vomiting
Severe headache
Bulging fontanelle
Focal neurologic findings
Seizures
-
Presentation and Localizing Findings of Serious Injury
Basilar Skull Fracture
- Clinical presentation
-
Raccoon eyes (periorbital ecchymosis, bruising around eyes)
-
Battle sign (mastoid ecchymosis, bruising behind the ears)
-
Hemotympanum
-
Cerebrospinal fluid (CSF) otorrhea or rhinorrhea
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At increased risk for meningitis
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75% will have a temporal skull fracture
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- Evaluation and management
-
CT scan to evaluate for other fractures and bleeding
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If nondisplaced, then usually heals without intervention
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At higher risk for meningitis, but the utility of prophylactic antibiotics is unclear
-
Temporal Skull Fracture
- Clinical presentation
-
Bleeding from ear or hemotympanum
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Facial paralysis
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CSF otorrhea and rhinorrhea
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Vestibular symptoms, vertigo
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Leads to conductive, sensorineural, or both types of hearing loss
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- Evaluation and management
-
CT scan (evaluate for longitudinal or transverse type)
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MR angiography/venography (MRA/MRV), CT angiography/venography (CTA/CTV)
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Usually bedrest and raise head of bed initially
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Surgery if CSF still leaking after 1 week
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Facial paralysis, hearing loss, and vertigo are longer-term issues
-
Subdural Hematoma
- Bleeding between the inner layer of the dura mater and the arachnoid mater
Tearing of the bridging veins across the subdural space
Result of acceleration/deceleration mechanism (MVC, shaken babies)
Associated with cerebral contusion
If acute, the most lethal injury, but can be chronic, developing over days to weeks
- Clinical presentation
-
Gradually increasing headache and confusion
-
Ataxia, slurred speech
-
Loss of consciousness or fluctuating level of consciousness
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- Diagnosis and management
-
CT scan (concave, crescent-shaped hematoma)
-
Treatment ranges from monitoring to a small burr hole to drain the hematoma to an open craniotomy. Treatment depends on size and speed of growth
-
Epidural Hematoma
- Bleeding between the dura mater and the skull
Often occurs from a break in temporal bone with bleeding from the middle meningeal artery
- Clinical presentation
-
Classically causes loss of consciousness (LOC) after head injury, followed by brief regaining of consciousness (lucid period), and then LOC again
-
Headache, confusion, vomiting
-
With progression of bleed, pupils ipsilateral to injury become fixed and dilated (compression of CN III) and gaze is “down and out” (unopposed action of CN IV and VI)
-
Seizures and weakness on contralateral side due to compression of crossed pyramidal pathways
-
Final stage is tonsillar herniation and death
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- Diagnosis and management
-
CT scan (biconvex, lens-shaped hematoma)
-
Emergency burr hole and/or craniotomy
-
Subarachnoid Bleed
- Bleeding between the arachnoid membrane and pia mater
Result of head trauma or can occur spontaneously (e.g., ruptured cerebral aneurysm)
- Clinical presentation
-
Severe headache of rapid onset
-
Vomiting
-
Loss of consciousness
-
Fever
-
Seizures
-
- Diagnosis and management
-
CT scan
-
Support until neurosurgery
-
Retinal Hemorrhage
-
In an infant, this can indicate possible nonaccidental trauma
Considerations in the Use of Head Computed Tomography (CT)
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Children are at greater risk of developing malignancy as a result of radiation exposure
-
Because pediatric head trauma is common and often benign, the use of CT imaging should be applied judiciously and after careful consideration
-
The age of the patient, presence of other injuries, suspicion for nonaccidental trauma, and presence or absence of warning signs should all help guide the application of screening head CT (Table 7.5) [1]
Prediction rules for identification of children at low risk for clinically important traumatic brain injury found on computed tomography (CT) imaging of the head
Age is less than 2 years old | CT is not recommended if the following criteria are met (risk of clinically important TBI is low) | Observation vs. CT recommended if any of the following are present (risk of clinically important TBI is slightly elevated) | CT recommended if any of the following are present (risk of clinically important TBI is high) |
GCS 15 and no altered mental status | Occipital, parietal, or temporal hematoma | GCS less than 15 or altered mental status | |
No palpable skull fracture | History of loss of consciousness | Palpable skull fracture | |
Frontal hematoma only | Severe mechanism of injury | ||
No loss of consciousness | Not acting normally per caretaker | ||
Nonsevere mechanism of injury | |||
Acting normally per caretaker | |||
Age is equal to or greater than 2 years old | CT is not recommended if the following criteria are met (risk of clinically important TBI is low) | Observation versus CT recommended if any of the following are present (risk of clinically important TBI is slightly elevated) | CT recommended if any of the following are present (risk of clinically important TBI is high) |
GCS 15 and no altered mental status | History of loss of consciousness | GCS less than 15 or altered mental status | |
No signs of basilar skull fracture | History of vomiting | Signs of basilar skull fracture | |
No loss of consciousness | Severe mechanism of injury | ||
No vomiting | Severe headache | ||
Nonsevere mechanism of injury | |||
No severe headache |
Management of Clinically Significant Head Trauma
- Attention to the ABCs, with particularly focus on
- Protection and establishment of a secure airway
Particularly if unresponsive or GCS less than 8
Close hemodynamic monitoring and repeat neurologic assessments
Avoidance of hypothermia or hyperthermia
Monitoring for signs of hypovolemic or neurogenic shock
- Support to maintain cerebral perfusion pressure (CPP)
CPP = mean arterial pressure (MAP) – intracranial pressure (ICP) (or central venous pressure [CVP])
- Watch for clinical signs of increasing ICP
Unequal pupil dilation (pressure on cranial nerves)
Abnormal posturing
Cushing’s triad: Irregular, decreased respirations (caused by impaired brainstem function), bradycardia, and systolic hypertension (widening pulse pressure)
- Management of increasing ICP
Mild hyperventilation
Intravenous mannitol or hypertonic saline (3%) may be needed
Immediate consultation to neurosurgery can be life-saving for serious intracranial injuries
Neck/Cervical Spine Trauma
-
Penetrating neck injuries generally all need surgical evaluation
-
Blunt neck injury may warrant further evaluation for vessel injury and cervical spine injury
Cervical Spine Injury
-
Relatively uncommon
-
MVC, sports, and falls are most common etiologies
- Children have different injury patterns because of increased physiologic motion due to:
Larger size of head compared to trunk, which creates a larger fulcrum
Horizontally oriented facet joints
Elevated ligamentous laxity
Weaker muscles
-
Children < 8 years old 87% of spinal injuries are above C3
-
Children > 8 years old more commonly have lower cervical injury (adult injury pattern)
- Clinical presentation
-
Always suspect if head injury or facial fractures
-
Full neurologic exam, but note that > 20% with injuries will have normal exam
-
- Diagnosis and management
-
Cervical spine neck radiograph
-
CT
-
MRI
-
Proper cervical spine immobilization initially for all
-
Some may need longer-term immobilization (halo) or surgery
-
Abdominal Trauma
-
Children are smaller in size; organs are proportionally larger; less fatty tissue around major organs; weaker musculature; more compliant rib cage, all which increase risk of solid organ injury
-
Most are MVC, others are MPC, sports, falls, and nonaccidental trauma
-
Most common unrecognized fatal injury
- Clinical manifestation
-
Exams may be difficult due to age, verbal ability, and fear
-
Tachycardia can be the only sign (even with 45% circulating blood volume)
- Have high index of suspicion for abdominal injuries
Seatbelt sign (ecchymosis of abdominal wall) after MVC has increased risk of intra-abdominal injuries, primarily due to increased risk of gastrointestinal (GI) injuries
Handlebar mark (handlebar-shaped ecchymosis over abdominal wall) at increased risk of small bowel hematoma and others
-
- Diagnosis and management
-
Complete blood count (CBC), lipase, aspartate transaminase (AST)/alanine transaminase (ALT) coagulation studies, uric acid (elevated AST/ALT combined with positive physical exam has good sensitivity)
-
Abdominal radiograph to evaluate for free air
-
CT scan (without contrast, with IV contrast, with IV and oral contrast)
-
Focused assessment with sonography in trauma (FAST) exam is of unproven utility in pediatrics but combined either with physical exam or serial exams can have good sensitivity and specificity
-
Conservative management for most, laparoscopy for some
-
Laparotomy for significant injuries
-
Pediatric Wounds and Lacerations
Laceration
-
A laceration is a traumatic disruption to the dermis layer of the skin.
-
Common locations are the face (~60%) and upper extremities (~25%)
-
Most lacerations in pediatric patients are non-life-threatening but require appropriate management
- Severe and life-threatening lacerations must be evaluated and treated promptly
Hemostasis: Apply pressure or tourniquet as necessary
Injury to deeper structures: Especially at high-risk areas like the neck (carotid) arteries, jugular veins, trachea, and esophagus must be considered
- Management and treatment
- Repair may be more difficult in pediatrics due to fear, anxiety, and lack of cooperativity
- Anesthetic and anxiolytic options
- Topical anesthetic LET (4% lidocaine, 1:2000 epinephrine, 0.5% tetracaine)
Effective 20–30 min after application
Blanching of the site after application most often indicates achievement of effective anesthesia
- Local anesthetic may be used to prepare for placement of sutures
Injectable lidocaine alone or with epinephrine
- Distraction and soothing techniques
Child life experts, toys, movies, music, etc.
Oral/intranasal pharmacologic options
Inhaled and IV pharmacologic options for procedural sedation
- Wound preparation
-
Wound irrigation is the standard of care
-
Evaluation for possible foreign bodies or complications
-
Suspicion for foreign body or associated bony fracture should prompt radiographs of the affected site
- Tissue adhesive
With selection of appropriate type of laceration, tissue adhesive has good cosmetic outcome with benefit of no need for suture or suture removal
-
- Suture and staples
-
Selection of suture material (absorbable versus nonabsorbable) will depend upon the location and depth of the injury
-
As a general rule, sutures should be evenly spaced
-
- Wound aftercare
-
All patients should be given follow-up instructions for local wound care, cleansing, timing (if necessary) of removal of suture, monitoring for infection, and use of sunscreen to decrease scar formation
-
- Consider the need for tetanus prophylaxis
- Prophylactic antibiotics not recommended with simple, uncontaminated lacerations
Lacerations due to bites will typically require antibiotics
Lacerations to hands and fingers with associated distal fingertip fracture
-
Specialized Scenarios
- Lip lacerations
-
An injury crossing the vermilion border will likely require subspecialist repair
-
Failure to align the vermilion border can result in a poor cosmetic outcome and permanent lip deformity
-
Young and uncooperative patients may additionally require varying degrees of anxiolysis and possibly sedation to repair well
-
- Nail bed lacerations
-
Repair of nail bed lacerations can be particularly painful and anxiety-provoking and may require a higher level of care
- Approximately half of all nail bed injuries are associated with a fracture of the distal phalanx and will likely require subspecialist repair
Low threshold for obtaining plain radiographs of the digit to evaluate for associated fracture
- Nail bed laceration with associated distal phalanx fracture may be an open fracture
Open fractures require antibiotic therapy
-
- Ear lacerations
-
Significant ear lacerations will likely require subspecialty repair
-
Lacerations of the ear have the potential to involve the avascular cartilaginous support
- Timely repair of ear laceration and close follow-up are important to avoid complications
Auricular hematoma: Disruption to cartilage and underlying perichondrium can lead to a hematoma, which, if untreated, can cause cosmetic deformity of the ear (“cauliflower ear”)
-
- Timing of suture removal
Timely removal of sutures reduces likelihood of suture tracks; better cosmetic outcome
Face: 3–5 days
Scalp: 5–7 days
Trunk: 5–7 days
Extremities: 7–10 days
Animal and Human Bites
- Dog bites
-
Typically causes a crushing-type wound
-
The extreme pressure of a dog bite may damage deeper structures such as bones, vessels, tendons, muscles, and nerves
- Dog bites are contaminated and require antibiotic therapy
Staphylococcus species, Eikenella species, Pasteurella species
-
- Cat bites
-
The sharp pointed teeth of cats usually cause puncture wounds and lacerations that may inoculate bacteria deep into the tissues
-
Infections caused by cat bites generally develop faster than those of dogs
- Cat bites are contaminated and require antibiotic therapy
Pasteurella species, Bacteroides species
-
- Other animals
Foxes, raccoons, skunks, and bats carry a high risk for rabies
- Bat bites may be asymptomatic
If a bat is discovered within a patient’s sleeping quarters, rabies treatment should be given regardless of history of a known bite
- Human bites
- Three general types of injuries can lead to complications:
Closed-fist injury
Chomping injury to the finger
Puncture-type wounds about the head caused by clashing with a tooth
- Human bites are contaminated and require antibiotic therapy
Eikenella corrodens, Staphylococcus species, Streptococcus species
Human bites can also transmit the following organisms: Hepatitis B, hepatitis C, herpes simplex virus (HSV), and syphilis
-
- General evaluation
-
Time and location of event
-
Type of animal and its status (i.e., health, rabies vaccination history, behavior)
-
Circumstances surrounding the bite (i.e., provoked or defensive bite versus unprovoked bite)
-
Location of bites
-
- Laboratory
-
Fresh bite wounds without signs of infection do not need to be cultured
-
Infected bite wounds should be cultured to guide antibiotic therapy
-
- Imaging studies
-
Radiography is indicated if any concerns exist that deep structures are at risk (e.g., hand wounds, deep punctures, crushing bites, especially over joints)
-
- Antibiotic therapy
-
All human and animal bites should be treated with antibiotics
-
The choice between oral and parenteral antimicrobial agents should be based on the severity of the wound and on the clinical status of the victim
-
Oral amoxicillin–clavulanate is the initial drug of choice for empiric oral therapy
-
Amoxicillin alone does not provide adequate coverage
-
Parenteral ampicillin–sulbactam is the drug of choice in severe cases
-
Clindamycin in combination with trimethoprim/sulfamethoxazole can be given if penicillin allergic
-
- Wound care
-
Debridement and removal of devitalized tissue
-
Irrigation is key to prevention of infection
-
100 ml of irrigation solution per centimeter of wound
-
Primary closure may be considered in limited bite wounds that can be cleansed effectively (this excludes puncture wounds, i.e., cat bites)
-
Other wounds are best treated by delayed primary closure
-
Indications for tetanus vaccine and tetanus immune globulin in the United States
Vaccine status | Clean and minor wounds | Contaminated wounds (soil, dirt, feces, saliva) |
---|---|---|
Unknown or not up to date (< 3 doses) | Tetanus vaccine only | Tetanus vaccine and tetanus immune globulin |
Series completed (> 3 doses) less than 5 years ago | No tetanus vaccine or immune globulin | No tetanus vaccine or immune globulin |
Series completed but > 5 years since final dose | If > 10 years since final dose, tetanus vaccine only | If > 5 years since final dose, tetanus vaccine only |
Indications for rabies prophylaxis and treatment in the United States
Vaccination status | Intervention | Description |
---|---|---|
No prior vaccine | Human rabies vaccine | Human rabies vaccine (human diploid cell vaccine) should be administered IM on days 0, 3, 7, and 14 |
Human rabies immune globulin (HRIG) | Immune globulin (20 IU/kg) should be administered via direct infiltration around the wound, with any remaining volume administered IM at an anatomical site distant from the vaccine site (e.g., the opposite deltoid or lateral thigh) | |
Previously vaccinated | Human rabies vaccine | Human rabies vaccine (human diploid cell vaccine) should be administered IM on days 0 and 3 |
Human rabies immune globulin (HRIG) | Not indicated |
Snake Bites
-
Most are nonpoisonous and are delivered by nonpoisonous species
-
North America is home to 25 species of poisonous snakes
- Characteristics of most poisonous snakes:
Triangular head
Elliptical eyes
Pit between the eyes and nose
Examples: Rattlesnakes, cottonmouth and copperheads
- Few snakes with round head are venomous
Example: Coral snakes (“red on yellow—kill a fellow”)
- Clinical presentation
- Local manifestations
Local swelling, pain, and paresthesias may be present
Soft pitting edema that generally develops over 6–12 h but may start within 5 min
Bullae
Streaking
Erythema or discoloration
Contusions
- Signs of systemic toxicity
Hypotension
Petechiae, epistaxis, hemoptysis
Paresthesias and dysesthesias—Indicate neuromuscular blockade and should be aware of possible respiratory distress (more common with coral snakes)
- The time elapsed since the bite is a necessary component of the history
Determine history of prior exposure to antivenin or snakebite (this increases risk and severity of anaphylaxis)
Assessment of vital signs, airway, breathing, and circulation
-
- Evaluation and management
- Laboratory
CBC with differential and peripheral blood smear
Coagulation profile, fibrinogen and split products
Blood chemistry, including electrolytes, blood urea nitrogen (BUN), creatinine
Urinalysis for myoglobinuria
- Management
-
Support and transfer to definitive care
-
Bitten extremities should be marked proximal and distal to the bite, and the circumference at this location should be monitored every 15 min for progressive edema and compartment syndrome
- Antivenom
Hemodynamic or respiratory instability
Abnormal coagulation studies
Neurotoxicity, e.g., paralysis of the diaphragm
Evidence of local toxicity with progressive soft tissue swelling
Antivenom is relatively specific for the snake species against which they are designed to protect
There is no benefit to administer antivenom to unrelated species due to risk of anaphylaxis and expense
-
Surgical assessment focuses on the injury site and concern for the development of compartment syndrome
-
Fasciotomy is indicated only for those patients with objective evidence of elevated compartment pressure
-
-
Black Widow Spider Bite
-
Black spider with bright-red or orange abdomen
-
Neurotoxin acts at the presynaptic membrane of the neuromuscular junction; decreased reuptake of acetylcholine and severe muscle cramping
- Clinical presentation
-
Pricking sensation that fades almost immediately
-
Uncomfortable sensation in the bitten extremity and regional lymph node tenderness
-
A “target” or “halo” lesion may appear at the bite site
-
Proximal muscle cramping, including pain in the back, chest, or abdomen, depending on the site of the bite
-
Dysautonomia that can include nausea, vomiting, malaise, sweating, hypertension, tachycardia, and a vague feeling of dysphoria
-
- Management
- Analgesics should be administered in doses sufficient to relieve all pain
Oral or IV opioid analgesics
Benzodiazepines are adjunctive for cramping
-
Hydration
-
Management of severe hypertension
-
Brown Recluse Spider Bite
-
Dark, violin-shaped mark on the thorax
-
Venom causes significant local skin necrosis
- Clinical presentation
-
Typically, initially painless bite
-
Rarely is the spider found or recovered
-
Erythema, itching, and swelling begin one to several hours after the bite
-
Central ischemic pallor to a blue/gray irregular macule to the development of a vesicle
-
The central area may necrose, forming an eschar
-
Induration of the surrounding tissue peaks at 48–96 h
-
Lymphadenopathy may be present
-
The entire lesion resolves slowly, often over weeks to months
-
- Management
-
Tetanus status should be assessed and updated
-
Signs of cellulitis treated with an antibiotic that is active against skin flora
-
Treatment is directed at the symptoms
-
Scorpion Stings
-
The only scorpion species of medical importance in the United States is the Arizona bark scorpion (Centruroides sculpturatus)
-
Toxins in its venom interfere with activation of sodium channels and enhance firing of axons
- Clinical presentation
-
Local pain is the most frequent symptom
-
Small children may have more severe symptoms
-
Peripheral muscle fasciculation, tongue fasciculation, facial twitching, and rapid disconjugate eye movements, which may be misdiagnosed as experiencing seizures
-
Agitation
-
Extreme tachycardia
-
Salivation
-
Respiratory distress
-
- Management
- Supportive care
Airway support and ventilation in severe cases
Analgesia and sedation
-
Antivenom therapy also may obviate or reduce the need for airway and ventilatory support
-
Burns
Pediatric Burn Classification
- Superficial burn (formerly first degree)
Epidermal injury, intact dermis
Erythematous, dry, and painful
Minor injuries that heal within 1 week without scarring
- Partial thickness burn (formerly second degree)
Partial injury of the dermis, often with edema and blistering
Commonly are caused by scald injuries and result from brief exposure to the heat source
Blanchable pink or mottled red, often with blisters and moist appearance
Typically, painful
Healed within 1–3 weeks with minimal scarring
- Deep partial thickness burn (formerly second degree)
Injury to epidermis and dermis
Dry, pale appearance, non-blanchable, may have speckled appearance
Less painful than partial thickness, although some sensation preserved
Heals after many weeks, often with significant scarring requiring surgical subspecialty care for optimal cosmetic outcomes
- Full thickness burn (formerly third degree)
Most serious and deepest type of burn
Destruction of epidermis and entire dermis with necrosis
Pearly white, charred, hard, or parchment-like appearance
Destruction of cutaneous nerves makes the burn typically nonpainful
- Loss of tissue elasticity makes the skin scar-like and unable to expand
Circumferential or near-circumferential burns can cause compartment syndrome, vascular compromise of distal extremity, respiratory distress if present on the chest
Burn cannot re-epithelialize and requires surgical subspecialty care and often skin grafting
Inhalation Injury
-
A large percentage of burn-related deaths are due to associated smoke and inhalation injuries
- Evaluate all burn victims for potential for inhalational injury:
Signs of respiratory compromise: Coughing, stridor, wheezing, hoarseness
Signs of neurologic compromise: Irritability or lethargy
Facial burns
Black (carbonaceous) sputum
Burned nasal hair and eyebrows
- Early and aggressive airway management prior to onset of airway obstruction
Suspected inhalation injury with signs of airway compromise will need intubation and bronchoscopy
Electrical Burns
-
Electrical current can cause significant internal damage via the arc of current through the body
-
External visible injury may be minimal
- Depending upon the arc of the electrical current, multiple complications can arise
Cardiac arrhythmia (ventricular fibrillation) and myocardial damage
Rhabdomyolysis and renal failure
-
Neurologic damage can develop in the years following an electrical burn
-
Oral electrical burns affecting the commissure of the lips can be very scarring and at risk of bleeding from the labial artery
Description of Burn
-
The percent body surface area is an important calculation in the classification of burns
- Palmar method
-
Surface of palm of hand can be used to approximate 1% body surface area in older children
-
Not useful in small children and infants
-
Rule of nines: Infants versus children over 9 years old. (From Suguitan [4]), with permission)
Management of Burns
- Supportive home therapy for minor burns
- Superficial burns (< 10% total body surface area) can typically be treated on an outpatient basis with supportive care, unless abuse is suspected
- Cotton gauze occlusive dressing to protect the damaged skin from bacterial contamination:
Eliminate air movement over the wound (thus reducing pain)
Decrease water loss
Change dressings daily
- Topical antimicrobial agent should be applied to the wound prior to the dressing for prophylaxis
Silver sulfadiazine or bacitracin
Application of various wound membrane dressings can promote healing and lessen pain of dressing changes
- Pain control
Alternating over-the-counter medications
- Opioid-containing medications for breakthrough pain
Caution in overreliance on opioids due to risk for dependence, withdrawal, and opioid-induced hyperalgesia
-
- Initial treatment of extensive burns
-
Extensive burns (> 10% total body surface area) and burns to high-risk areas (face, hands, neck, genitalia) will often require subspecialty care
- Identification of airway involvement due to risk for concomitant inhalation injury
Early and aggressive airway management recommended
-
Fluid resuscitation to prevent shock
-
Early excision and grafting of the burn wound coupled with early nutrition support
-
Measures to treat sepsis
- Fluid administration
Once the nature and extent of injury are assessed, fluid resuscitation is begun
Two large-bore IV catheters
- Parkland formula for fluid requirements:
4 ml/kg/day for each percent of body surface area (BSA) burned
The first half of the fluid load is infused over the first 8 h post-burn
The remainder is infused over the ensuing 16 h
The infusion rates should be adjusted to maintain a urine flow of 1 ml/kg per hour
During the second 24 h, fluid administration is reduced 25–50%
-
Status Epilepticus
- Definitions
-
A seizure that lasts more than 30 min or
-
Multiple seizures that occur without return of the individual to baseline, for a duration of not less than 30 min
-
- Causes and risk factors
- Many conditions can cause status epilepticus
Infection (viral, bacterial, fungal, parasitic)
Trauma (intracranial hemorrhage, diffuse axonal injury, cerebral contusion)
Subtherapeutic anticonvulsant levels (patients with known epilepsy)
Congenital abnormality
Metabolic (hypoglycemia, hyponatremia, hypocalcemia, hypomagnesemia, hypercarbia, inborn errors of metabolism, pyridoxine deficiency in neonates)
Vascular (hypoxic ischemic injury, cerebrovascular accident, hypertensive encephalopathy)
Toxicologic (tricyclic antidepressants, isoniazid, pesticides (organophosphates), heavy metals (lead), topical anesthetic overdose)
Endocrine (hyper-/hypothyroidism, Addison’s disease)
-
- Management
-
Treatment should be based on an institutional protocol
-
- General principles of management
- Attend to the ABCs before starting any pharmacologic intervention
- Airway
Place patient in the lateral decubitus position to avoid aspiration of emesis and to prevent epiglottis closure over the glottis
Make further adjustments of the head and neck if necessary to improve airway patency
Suction secretions
Immobilize the cervical spine if trauma is suspected
- Breathing
Administer 100% oxygen by face mask
Assist ventilation
Use artificial airways (e.g., endotracheal intubation) as needed
Decompress the stomach as needed with a nasogastric tube
- Circulation
Carefully monitor vital signs, including BP
Carefully monitor the temperature, as hyperthermia may worsen brain damage
In the first 5 min of seizure activity, before starting any medications, try to establish IV access and obtain samples for laboratory tests
Infuse isotonic IV fluids plus glucose. In children younger than 6 years, use intraosseous (IO) infusion if IV access cannot be established within 5–10 min
-
- Laboratory studies
- Finger-stick blood glucose
If serum glucose is low or cannot be measured, give children 2 ml/kg of D25% glucose
-
Obtain basic metabolic panel, antiepileptic drug levels, and other labs, depending on the history and physical examination
-
If the seizure fails to stop within 4–5 min, prompt administration of anticonvulsants may be indicated
-
- Potential anticonvulsant medication options
- Anticonvulsant medication—selection can be based on seizure duration as follows:
- Initial seizure activity (5–15 min):
- Benzodiazepines are first-line GABA receptor blocker
Preferred options: Lorazepam IV or diazepam IV/rectal gel
Others: Midazolam IM or intranasal
- Prolonged seizures (> 15 min), if refractory to benzodiazepines:
Many options exist with no clear literature to support a particular therapy
Selection should be made in consultation with a pediatric neurologist
- Some options:
Phenytoin or fosphenytoin IV
Levetiracetam IV
Valproic acid IV
- Continued seizure activity despite second- and third-line agents
General anesthesia may be required
- Options include inhalational agents, pentobarbital anesthesia, continuous benzodiazepines
Anesthesia is titrated to achieve electroencephalogram (EE with burst suppression or flat line
By this point, advanced airway must be established, if not already
- Other specific treatments may be indicated if the clinical evaluation identifies precipitants of seizures
- Pyridoxine—IV/IM for possible dependence/deficiency or isoniazid toxicity
Pyridoxine-dependent seizures are a rare but reversible cause of refractory seizures in neonates: Consider administration of pyridoxine for neonatal status epilepticus
Naloxone: IV preferably (if needed may administer IM or subcutaneous) for narcotic overdose
Antibiotics: If meningitis is strongly suspected, initiate treatment with antibiotics prior to CSF analysis or CNS imaging
-
- Anticipatory guidance
- Patients with history of status epilepticus will need:
Rescue abortive benzodiazepine (e.g., rectal diazepam) for prolonged seizures for home administration prior to arrival of emergency medical services
Seizure first aid teaching
-
Consideration of additional benzodiazepine to raise seizure threshold during times of illness
-
Altered Mental Status (AMS)
- Definitions
-
AMS is a state of abnormally activated or abnormally suppressed awareness/consciousness
-
It is a symptom and not a diagnosis—caused by an underlying disease or by trauma
-
Altered level of consciousness or cognition—varying degrees of alteration of awareness
-
Coma—the most severe form of altered level of consciousness in which an individual is not aware of his or her surroundings and cannot be easily aroused. A state lacking consciousness (both wakefulness and awareness) that cannot be overcome by stimulation
-
Lethargy—state of altered level of consciousness that resembles deep sleep, from which a person can be aroused but immediately returns to that state. Depressed consciousness that, with adequate stimulation, can be overcome
-
Obtunded—state of altered level of consciousness in which a person has greatly decreased responses and/ or is slow to respond
-
Delirium (agitation)—abnormally activated consciousness with decreased awareness of environment from fluctuating global cerebral dysfunction, with inability or decreased ability to focus, shift, or sustain attention
- Consciousness
-
State of being awake and aware
- Result of complex interplay of system controls
Ascending reticular activating system (ARAS) in brainstem and pons regulate wakefulness
Connections from the ARAS project out to the cortex and regulate awareness
- Function is dependent on many factors
Requires adequate perfusion; adequate perfusion pressure; energy substrate (oxygen, glucose, hydration); electrolyte and acid-base balance (glucose, carbon dioxide, blood pH); removal of toxins (waste products); body temperature; absence of neuronal excitation/irritation (seizures)
-
-
- Etiology of AMS
-
The differential diagnosis of AMS is extremely broad and spans all possible organ systems
- Many possible causes of AMS have the potential to be life-threatening
- Trauma
Head trauma (subdural hematoma, epidural hematoma, cerebral edema, severe concussions)
- Infection
Meningitis, encephalitis, sepsis, brain abscess, subdural empyema
Sepsis with hypotension
- Neoplasm
Primary brain neoplasms or secondary brain involvement, blockage of CSF
- Vascular disease
Cerebral hemorrhage vs. infarct (arteriovenous malformation, aneurysm, hemangioma, thrombotic stroke), hypertensive emergency
- Obstruction to CSF
Malfunctioning ventriculoperitoneal (CSF) shunt
Hydrocephalus
- Metabolic anomalies
Hypoglycemia, hyponatremia, hypocalcemia, hypo-/hypermagnesemia, hypophosphatemia, metabolic acidosis and metabolic alkalosis, Reye syndrome
- Toxic ingestions
Many kinds of ingestions can cause AMS (e.g., severe aspirin ingestion, carbon monoxide poisoning, salicylates, barbiturates, alcohol, antihistamines, narcotics, phenothiazines, GHB [gamma hydroxybutyrate])
- Advanced stages of medical illnesses
Liver failure, kidney failure, heart failure, respiratory failure
- Specific disease states
Dehydration
Hypoxemia or hypercarbia
Hypothermia or hyperthermia
Hemolytic uremic syndrome: CNS infarction in basal ganglia
Intussusception: Infants can present initially with lethargy
Seizures: Postictal state, subclinical status epilepticus
Psychiatric disorders (pseudoseizure, conversion disorder)
-
- Glasgow Coma Scale
- The Glasgow Coma Scale (GCS) score can be used to help convey the level of AMS (Table 7.8) [5, 6]
GCS is 15 for individuals with normal level of mentation
- GCS < 15 indicates an altered mental state
The subcategory including the lowest number should be indicated, e.g., a GCS of 13 (−2 M) indicates −2 from the motor subcategory
-
- Management
-
Treatment of AMS requires identification and treatment of the underlying cause
- In all patients, attend to ABCs promptly
- Vital signs
- Blood pressure
Attend to hypotension or severe hypertension
Fluid resuscitation
- Heart rate
Attend to severe bradycardia or tachycardia
- Hypothermia or hyperthermia
Thermoregulate patient
- Pulse oximetry
Administer supplemental oxygen
Assess risk for methemoglobinemia or carboxyhemoglobinemia
- Inadequate respiratory effort
Assist ventilation
- Point-of-care glucose
Correction of hypoglycemia
Point-of-care blood gas
Consider empiric naloxone if clinical concern for opioid exposure
-
- Specific disease categories:
- Trauma
-
This may be related to single system trauma (e.g., involving injury to the head/brain alone) or multisystem trauma
-
Decreased GCS with head trauma is presumed to be increased ICP until proven to be otherwise
-
May not have a history of a traumatic event if nonaccidental trauma is involved or injury was unwitnessed
- Initial steps
Attend to airway, breathing, and circulation
Maintain cervical-spine immobilization
Obtain emergent noncontrast head CT and prompt neurosurgical consultation
Neuroprotective measures: May need 3% saline or mannitol, elevation of head to 30°, midline positioning of head
Other ongoing resuscitation measures may also be indicated
-
- Infection
-
In the presence of fever with meningismus, presume CNS infection
-
Attend to airway, breathing, and circulation promptly
-
Attempt diagnostic lumbar puncture if patient is stable enough to tolerate it
- Order broad-spectrum IV antibiotics or antifungal medications if suspected fungal process, and do not delay administration
Order additional broad-spectrum IV antivirals for febrile neonate with risk factors for HSV encephalitis
-
If focal neurologic deficit or seizures are present, obtain noncontrast head CT prior to lumbar puncture
-
- Neoplasm
-
Space-occupying mass lesions in the brain can predispose to rapid decompensation
-
Attention to airway, breathing, circulation, and neuroprotective maneuvers and interventions
-
Requires prompt consultation with appropriate subspecialties (neurosurgery, oncology)
-
- Metabolic abnormalities
-
May be determined from results of testing or if adequate history is obtained, can help aid diagnosis
- Therapy is directed at the specific abnormal electrolyte abnormality
Examples: Administration of glucose in the form of dextrose for hypoglycemia, or calcium for hypocalcemia
-
- Toxic ingestions
-
Attention to airway, breathing, circulation, and neuroprotective maneuvers and interventions
-
For specific antidotes, see Table 7.10
-
- Suspected CSF shunt malfunction
Attention to airway, breathing, circulation, and neuroprotective maneuvers
Emergent head CT and radiographs to confirm shunt continuity (“shunt series”)
Timely neurosurgical consultation
-
Score | Infant | Child | Adult |
---|---|---|---|
Eye opening | |||
4 | Spontaneous | Spontaneous | Spontaneous |
3 | Opens to speech | Opens to speech | Opens to sound |
2 | Opens to pain | Opens to pressure | Opens to pressure |
1 | None | None | None |
Best verbal response | |||
5 | Coos and babbles | Oriented, appropriate | Oriented, appropriate |
4 | Irritable or cries | Confused | Confused |
3 | Cries in response to pain | Words | Words |
2 | Moans in response to pain | Sounds | Sounds |
1 | None | None | None |
Best motor response | |||
6 | Moves spontaneously and purposefully | Obeys commands | Obeys commands |
5 | Withdraws to touch | Localizing | Localizing |
4 | Withdraws to pain | Normal flexion | Normal flexion |
3 | Abnormal flexion to pain | Abnormal flexion | Abnormal flexion |
2 | Abnormal extension to pain | Extension | Extension |
1 | None | None | None |
Poisoning and Toxic Exposure
- Background
-
Children less than 6 years have the greatest risk
-
Adolescent exposure either intentional or occupational
-
- Prevention of poisoning
-
Child-resistant packaging
- Anticipatory guidance in well childcare
Best provided at 6 months well child visit prior to the onset of mobility
- Poison-proofing child’s environment
Labeling all hazardous material
Locking medicine cabinets and securing cleaning products
Securing all medications in purses and handbags
-
- Evaluation of a potentially toxic exposure
-
Call the poison control center, describe the toxin, read the label, and follow the instructions
-
Determine amount of exposure, number of pills, number of the remaining pills, and/or amount of liquid remaining
-
Determine time of exposure
-
Evaluate for progression of symptoms (any pattern of toxidromes)
-
Consider associated ingestions and underlying medical conditions
-
- General measures for toxic exposures
-
For external exposures, remove clothes and wash the skin with soap and water
- For ingestions, can use activated charcoal if within 60 min of ingestion
Absorbs substances and decreases bioavailability
- It is ineffective in the following (mnemonic CHEMICaL)
Caustics
Hydrocarbons
Ethanol (alcohols)
Metals
Iron
Cyanide
Lithium
- Ipecac
-
No longer recommended
-
Induction of emesis is particularly contraindicated with ingestions of hydrocarbons and caustics
-
- Gastric lavage
-
Contraindicated in hydrocarbons, alcohols, and caustics
-
Not recommended in most ingestions
-
May be considered with careful consideration if life-threatening ingestion occurred within 30–60 min of seeking medical attention
-
- Whole bowel irrigation
-
Reduces drug absorption by decontaminating the entire GI tract via large amounts of an osmotically balanced polyethylene glycol-electrolyte solution (PEG-ES) to induce a liquid stool and empty the bowel
-
Conclusive evidence that it improves outcomes is lacking
-
May cause vomiting and abdominal distention and lead to risk of aspiration
- Should not be performed routinely, but may be considered for
Potentially toxic ingestions of sustained-release or enteric-coated drugs
Drugs not adsorbed by activated charcoal (e.g., lithium, potassium, and iron)
Removal of illicit drugs in the body (e.g., “packers” or “stuffers”)
-
-
Specific Ingestions (Tables 7.9, 7.10, and 7.11) [7, 8]
Acetaminophen
-
Responsible for one-third of all pediatric emergency department visits for ingestions
-
The single toxic acute dose is generally considered to be > 200 mg/kg in children, and more than 7.5–10 g in adults and can cause hepatic injury or liver failure
-
Any child with history of acute ingestion of > 150 mg/kg of acetaminophen should be referred for assessment and measurement of acetaminophen level
- Clinical presentation (4 phases)
- First 24 h
Asymptomatic or nonspecific signs
Nausea, vomiting, dehydration, diaphoresis, pallor
Elevation of liver enzymes
- 24 to 72 h post-ingestion
Tachycardia and hypotension
Right upper quadrant pain with or without hepatomegaly
Liver enzyme is more elevated
Elevated prothrombin time (PT) and bilirubin in severe cases
- 3 to 4 days post-ingestion
Liver failure
Encephalopathy, with or without renal failure
Possible death from multiorgan failure or cerebral edema
- 4 to 14 days post-ingestion
Complete recovery or death
-
- Management
-
Measure serum acetaminophen level 4 h after the reported time of ingestion
-
Acetaminophen level obtained < 4 h after ingestion cannot be used to estimate potential toxicity
-
Check acetaminophen level 6–8 h if it is co-ingested with other substance that slows GI motility, e.g., diphenhydramine
-
Check liver function AST/ALT/coagulation parameters, renal function
- Start N-acetylcysteine (NAC)
If acetaminophen level is above the treatment line on Rumack-Matthew nomogram (4 h and after) (Fig.7.2) [6]
If acetaminophen level is low or undetectable with abnormal liver function
Patients with a history of potentially toxic ingestion more than 8 h after ingestion (single dose > 200 mg/kg in children and more than 7.5–10 g in adults)
-
Liver transplant for liver failure
-
Toxidromes
Group | Vital signs | Mental status | Pupils | Other |
---|---|---|---|---|
Anticholinergics | Increased P, T | Delirium | Mydriasis | “Dry as a bone, red as a beet” … a |
Cholinergics | Varies | Normal to depressed | Varies | “Drowning in secretions” |
DUMBBELLSa | ||||
Opioids | Decrease BP, P, R, T | Depressed | Miosis | Hyporeflexia |
Withdrawal from opioids | Increase BP, P | Normal to anxious | Mydriasis | Vomiting, diarrhea, rhinorrhea |
Sympathomimetics | Increase BP, P, R, T | Agitated | Mydriasis | Tremor and seizures |
Ethanol or sedatives/hypnotics | Decrease BP, P, R, T | Depressed, agitated | Varies | Hyporeflexia and ataxia |
Withdrawal from ethanol or sedatives/hypnotics | Increase BP, P, R, T | Agitated, disoriented | Mydriasis | Tremor and seizures |
Common antidotes for poisoning
Poison | Antidote |
---|---|
Acetaminophen | N-acetylcysteine (Mucomyst) |
Anticholinergics | Physostigmine |
Benzodiazepines | Flumazenil |
β-blockers | Glucagon; insulin/glucose |
Calcium channel blockers | Insulin and calcium salts |
Carbon monoxide | Oxygen |
Cyanide | Hydroxocobalamin (B12), Nitrites |
Digitalis | Digoxin-specific fragments antigen-binding (Fab) antibodies |
Ethylene glycol and methanol | Fomepizole |
Iron | Deferoxamine |
Isoniazid (INH) | Pyridoxine |
Lead and other heavy metals, e.g., mercury and arsenic | British anti-Lewisite (BAL) (dimercaprol) |
Methemoglobinemia | Methylene blue |
Opioids | Naloxone |
Organophosphates | Atropine and pralidoxime |
Salicylates | Sodium bicarbonate |
Sulfonylureas | Octreotide |
Tricyclic antidepressants | Sodium bicarbonate |
Differential of toxic related findings (with mnemonic devices)
Finding | Differential diagnosis | |
---|---|---|
Anion gap metabolic acidosis | C | Carbon monoxide, cyanide |
(Anion gap = Na – (HCO3 + Cl) | A | Aminoglycosides |
T | Theophylline, toluene (glue sniffing) | |
M | Methanol, metformin | |
U | Uremia | |
D | Diabetic ketoacidosis, starvation | |
P | Paraldehyde, paracetamol/acetaminophen, propylene glycol | |
I | Iron, isoniazid, ibuprofen, inborn errors of metabolism | |
L | Lactic acidosis | |
E | Ethylene glycol | |
S | Salicylates/aspirin | |
Widened QRS | Bupivacaine, bupropion, carbamazepine, class I (quinidine, amiodarone, procainamide) antiarrhythmics, class Ic (flecainide, propafenone, moricizine) antiarrhythmics, cocaine, diphenhydramine, lamotrigine, tricyclic antidepressants | |
Prolonged QTc | T | Thiazides |
O | Ondansetron (antiemetics), opioids (methadone) | |
Q | Quinidine (class Ia), quinolones (antibiotics) | |
R | Risperidone (antipsychotics) | |
S | Sotalol (class III) | |
A | Antihistamines | |
D | antiDepressants (TCA) | |
E | Erythromycin and other macrolides | |
S | SSRI (fluoxetine, sertraline) | |
Hypoglycemia | H | Hypoglycemic (sulfonylureas not metformin) |
O | Others (quinine, quinolones, pentamidine) | |
BB | β Blockers, Bactrim | |
I | Insulin | |
E | Ethanol | |
S | Salicylates | |
Bradycardia and hypotension | C | Calcium channel blockers (diltiazem, verapamil, amlodipine) |
O | Opiates | |
P | Propranolol and other beta-blockers (metoprolol, esmolol) | |
A | Anticholinergics (organophosphates, carbamates, neostigmine, sarin, VX) | |
C | Clonidine and other central α-2 receptor agonist (guanfacine, dexmedetomidine, oxymetazoline) | |
E | Ethanol | |
D | Digoxin and cardiac glycosides (oleander, foxglove, lily of the valley) |
Rumack-Matthew nomogram for acetaminophen poisoning [6]
Ibuprofen
-
Inhibit prostaglandin synthesis
- Clinical presentation
-
Nausea, vomiting, and epigastric pain
-
Drowsiness, lethargy, and ataxia may occur
-
Anion gap metabolic acidosis, renal failure, seizure, and coma may occur in severe cases (usually > 400 mg/kg)
-
May cause GI irritation, ulcers, decrease renal blood flow, and platelet dysfunction
-
- Management
-
Activated charcoal
-
Supportive care
-
Salicylic Acid
-
Aspirin, certain antidiarrheal medications, topical agents, e.g., keratolytics and sports creams
-
Refer to an emergency department for ingestions > 150 mg/kg
-
Ingestion of > 200 mg/kg is generally considered toxic; > 300 mg/kg is more significant toxicity; > 500 mg/kg is potentially fatal
- Clinical presentation
- Acute salicylism
Nausea, vomiting, diaphoresis, and tinnitus
- Moderate toxicity
Tachypnea, hyperpnea, tachycardia, and AMS
- Severe toxicity
Hyperthermia and coma
-
- Management
-
Consider activated charcoal
-
Check blood gas (respiratory alkalosis, metabolic acidosis, and high anion gap)
-
Check serum level every 2 h until it is consistently down trending
-
IV fluids
-
Sodium bicarbonate therapy in the symptomatic patients
-
Goal of therapy includes a urine pH of 7.5–8.0, a serum pH of 7.5–7.55, and decreasing salicylate levels
-
Anticholinergics
-
Diphenhydramine, atropine, scopolamine, hyoscyamine, jimsonweed (Datura stramonium), and deadly nightshade (Atropa belladonna)
- Clinical presentation (anticholinergic symptoms)
Dry as a bone: Dry mouth, decreased sweating, and urination
Red as a beet: Flushing
Blind as a bat: Mydriasis, blurred vision
Mad as a hatter: Agitation, seizures, hallucinations
Hot as a hare: Hyperthermia
Bloated as a toad: Ileus, urinary retention
Heart runs alone: Tachycardia
- Management
-
Consider activated charcoal
-
Supportive care
-
Physostigmine can be considered for severe or persistent symptoms
-
Beta-Blockers
-
Acebutolol, atenolol, bisoprolol, metoprolol, nadolol, sotalol, and propranolol
- Clinical presentation
-
Hypotension, bradycardia, atrioventricular (AV) block, heart failure
-
Bronchospasm
-
Hypoglycemia, hyperkalemia
-
Stupor, coma, seizures
-
- Management tailored to the symptoms
-
Consider dose of activated charcoal
-
Hypotension/bradycardia/AV block: Fluid boluses, beta-agonists, vasopressors, atropine, possibly pacing
-
Hypoglycemia: Glucose
-
Hyperkalemia: Calcium gluconate, dextrose and insulin, sodium bicarbonate, possibly dialysis
- Two special cases
Propranolol → causes sodium channel blockade → QRS widening → treat with sodium bicarbonate
Sotalol → causes potassium efflux blockade → prolonged QT → monitor for torsades
-
Carbamazepine
- Clinical presentation
- Mild ingestion:
CNS depression
Drowsiness
Vomiting
Ataxia
Slurred speech
Nystagmus
- Severe intoxication:
Seizures
Coma
Respiratory depression
-
- Management
-
Activated charcoal
-
Supportive measures
-
Charcoal hemoperfusion for severe intoxication
-
Cardiac Glycosides (Digitalis)
-
Digoxin, foxglove plants, oleander, lily of the valley (Convallaria)
- Clinical presentation
-
Nausea and vomiting
-
CNS depression (confusion)
-
Blurry vision
-
Cardiac conduction abnormalities (irregular pulse, bradycardia or tachycardia)
-
- Management
-
Electrocardiogram (ECG) and digoxin levels
-
Activated charcoal
-
Atropine, cardiac pacing (for severe bradycardia)
-
Magnesium sulfate (for premature ventricular contractions [PVCs])
-
Management of hyperkalemia, hypokalemia, hypomagnesemia
-
If severe, digoxin-specific antibody fragments
-
Clonidine
-
Antihypertensive medication with α-2 adrenergic receptor blocking ability
-
Commonly used in children with attention-deficit hyperactivity disorder (ADHD)
-
Dose as small as 0.1 mg can cause toxicity in children
- Clinical presentation
-
Lethargy
-
Miosis
-
Bradycardia
- Hypotension
Can cause transient initial hypertension
-
Apnea
-
- Management
-
Supportive care, e.g., intubation, atropine, dopamine as needed
-
Charcoal usually not recommended due to CNS depression
-
Opiates
-
Morphine, heroin, methadone, propoxyphene, codeine, meperidine
-
Most cases are drug abuse
- Clinical presentation
- Common triad of opiate poisoning:
Pinpoint pupil
Mental depression (lethargy to coma)
Respiratory depression
-
Hypotension with no change in heart rate
-
Decreased GI motility, nausea, vomiting, abdominal pain
-
- Management
-
Supportive care, e.g., airway, breathing, and circulation; intubation; fluids as necessary
- Naloxone as needed
Half-life of naloxone is short
Repeat doses and continuous infusions may be necessary
- Cautious use in known opioid-dependent patients
Can induce withdrawal
-
Phenothiazines
-
Promethazine, prochlorperazine, and chlorpromazine
- Clinical presentation
-
Hypertension
-
Cogwheel rigidity
-
Dystonic reaction (spasm of the neck, tongue thrusting, oculogyric crisis)
-
CNS depression
-
- Management
-
Activated charcoal
-
Manage high BP
-
Diphenhydramine for dystonic reaction
-
Tricyclic Antidepressants (TCAs)
-
TCAs can cause significant toxicity in children even with ingestion of 1–2 pills (10–20 mg/kg)
- Clinical presentation
-
Anticholinergic toxidrome: Delirium, mydriasis, dry mucous membrane, tachycardia, hyperthermia, hypotension, and urinary retention
-
Cardiovascular and CNS symptoms dominate the clinical presentation
-
Most common cardiac manifestations: Widening of QRS complex, PVCs, ventricular arrhythmia
-
Refractory hypotension is poor prognostic indicator and is the most common cause of death in TCA toxicity
-
- Management
-
Supportive measures, ABCs
- ECG:
A QRS duration > 100 ms identifies patients at risk for seizures and cardiac arrhythmia
An R wave in lead aVR of > 3 mm is an independent predictor of toxicity
-
Start sodium bicarbonate therapy: QRS duration > 100 ms, ventricular dysrhythmias, hypotension, and seizures
-
Carbon Monoxide (CO)
-
Wood-burning stove, old furnaces, and automobiles
- Prevention of CO poisoning
-
CO detectors
-
Maintenance of fuel-burning appliances
-
Yearly inspection of furnaces, gas pipes, and chimneys
-
Car inspection for exhaust system
-
No running engine in a closed garage
-
Avoid indoor use of charcoal and fire sources
-
- Clinical presentation
-
Headache, malaise, nausea, and vomiting are the most common flu- or food poisoning-like early symptoms
-
Confusion, ataxia, syncope, tachycardia, and tachypnea at higher exposure
-
Coma, seizure, myocardial ischemia, acidosis, cardiovascular collapse, and potentially death in severe cases
-
- Management
-
Evaluate for COHb level in symptomatic patients
-
Arterial blood gas with CO level
-
Check creatine kinase in severe cases
-
ECG in any patient with cardiac symptoms
-
100% oxygen to enhance elimination of CO, use until CO < 10% and symptoms resolve
-
Severely poisoned patient may benefit from hyperbaric oxygen especially if COHb > 25%, significant CNS symptoms, or cardiac dysfunction
-
Cyanide
-
Seeds (cherries, apricots, peaches, apples, plums); cassava; burning plastics (nitrile-containing products); nitroprusside; some pesticides
-
Amygdalin is contained in seeds and produces hydrogen cyanide, which is a potent toxin
-
Inhibition of cellular respiration (cytochrome c oxidase) stops ATP production
- Clinical presentation
-
Decreased level of consciousness
-
Low exposures—weakness, headache, dizziness, confusion
-
Severe exposures—seizure, apnea, cardiac arrest
-
Cherry red skin
-
- Management
-
Supportive measures
-
Hydroxocobalamin (vitamin B12), nitrites
-
Ethylene Glycol Ingestion (Antifreeze)
- Clinical presentation
-
Nausea, vomiting, CNS depression, anion gap metabolic acidosis
-
Hypocalcemia, renal failure due to deposition of calcium oxalate crystals in the renal tubules
-
- Management
-
Osmolar gap can be used to estimate ethylene glycol level
-
IV fluids, glucose, and bicarbonate as needed for electrolyte imbalances and dehydration
-
Fomepizole
-
Ethanol can be used if fomepizole is unavailable
-
Methanol
-
Toxicity primarily caused by formic acid
- Clinical presentation
-
Drowsiness, nausea, and vomiting
-
Metabolic acidosis
-
Visual disturbances: blurred and cloudy vision, feeling of being in a snowstorm, and untreated cases can lead to blindness
-
- Management
-
Osmolar gap (may be used as surrogate marker until methanol blood level is available)
-
IV fluids, glucose and bicarbonate as needed for electrolyte imbalances and dehydration
-
Fomepizole
-
Ethanol can be used if fomepizole is unavailable
-
Hemodialysis (consider if > 30 ml methanol ingested)
-
Iron
-
Ingestion of > 60 mg/kg/dose is toxic
- Clinical presentation
- Gastrointestinal stage (30 min−6 h)
Nausea, vomiting, and abdominal pain
Hematemesis and bloody diarrhea in severe cases
- Stability stage (6–24 h)
No symptoms: Patient must be observed during this stage
- Systemic toxicity within (48 h)
Cardiovascular collapse
Severe metabolic acidosis
-
Hepatotoxicity and liver failure (2–3 days)
-
Gastrointestinal and pyloric scarring (2–6 weeks)
-
- Management
-
Abdominal radiograph (may show pills and need for GI decontamination)
-
Serum iron < 300 mcg/dl is nontoxic
-
Chelation with IV deferoxamine if serum iron > 500 mcg/dl
-
Mushrooms
-
Ingestion of mushrooms can have fatal consequences in species that harbor amatoxins (e.g., Amanita) and related compounds
- Clinical presentation
-
Nausea, vomiting, and diarrhea; delayed onset (6 h)
-
A second latent period is followed by acute and possibly fulminant hepatitis beginning 48–72 h after ingestion
-
- Management
-
Activated charcoal
-
Whole bowel irrigation
-
Supportive care, including liver transplant, if necessary, is the mainstay of therapy
-
Caustic Ingestion
-
Strong acid and alkalis < 2 or > 12 pH can produce severe injury even in small-volume ingestion
-
Patient can have significant esophageal injury without visible oral burns
- Clinical presentation
-
Pain, drooling, vomiting, and abdominal pain
-
Difficulty in swallowing, or refusal to swallow
-
Stridor and respiratory distress are common presenting symptoms
-
Esophageal stricture caused by circumferential burn; requires repeated dilation or surgical correction
-
- Management
- Supportive measures, ABCs
Inducing emesis and lavage are contraindicated
Endoscopy should be performed within 12–24 h in symptomatic patients, or on basis of history and characteristics of ingested products
-
Hydrocarbons
-
Products contain hydrocarbon substances, mineral spirits, kerosene, gasoline, turpentine, and others
-
Aspiration of even small amount can be serious and potentially life-threatening
-
Pneumonitis is the most important manifestation of hydrocarbon toxicity
-
Benzene is known to cause cancer
-
Inhalants, including toluene, propellants, and volatile nitrite, can cause dysrhythmias and sudden death
- Clinical presentation
-
Cough, tachypnea, respiratory distress
-
- Management
-
Emesis and lavage are contraindicated
-
Activated charcoal should be avoided due to risk of inducing vomiting
-
Observation and supportive care
-
Organophosphate and Carbamate Insecticides (Nerve Gas Agents)
-
Inhibit anticholinesterase
- Clinical presentation
- (DUMBBELLS) “Drowning in your own secretions”
Diarrhea
Urination
Miosis
Bradycardia
Bronchospasm
Emesis
Lacrimation
Lethargy
Salivation and Seizures
-
- Management
-
Wash all exposed skin with soap and water and immediately remove all exposed clothing
-
Fluid and electrolyte replacement, intubation, and ventilation if necessary
-
Atropine and pralidoxime
-
Foreign Body Aspiration and Ingestion
Foreign Body Aspiration
-
Occurs in the context of child’s play/exploration of environment
-
Foreign bodies may lodge in the upper or lower respiratory tract
- Upper airway
- The most commonly implicated foods are
Candy, meat, hot dogs, grapes
- Associated symptoms include
Choking, coughing, stridor, respiratory distress
May result in complete airway obstruction
- In patients with complete airway obstruction, emergency procedures may be life-saving
Back blows in infants
Heimlich maneuvers in older children
- If patient becomes unconscious, may need to initiate cardiopulmonary resuscitation (CPR)
Convert to rescue breaths and chest compressions
If all of the above are unsuccessful, then advanced airway techniques may be necessary
-
- Lower airway
-
More common in younger children
-
Foreign body may lodge in the right or left lung
-
Symptoms may involve coughing, choking, wheezing, or may be asymptomatic
-
Diagnosis may be delayed due to lack of symptoms
-
- Management
- If the patient is stable and not in respiratory distress, neck and/or chest radiographs may help with diagnosis
Not all inhaled foreign bodies are radiopaque and may not be visualized on radiographs even if present
-
Bilateral decubitus views may aid in diagnosis: Bilateral to compare which lung exhibits air trapping, which may be where the foreign body is lodged
-
The presence of normal chest radiographs does not exclude this diagnosis in the presence of a compelling history
-
For patients in severe respiratory distress, immediate bronchoscopy to remove the foreign body emergently is key to treatment
-
Foreign Body Ingestion
-
Most children will have a history of ingested foreign body, often reported by a caregiver or playmate/sibling
- Most commonly ingested foreign bodies are
Food (meat)
Followed by coins, pins, toy parts, button batteries, magnets
-
Most will pass harmlessly through the GI tract
- Foreign bodies may lodge in areas where there is physiological/anatomic narrowing of the lumen of the GI tract
Lodging may occur secondary to pathological narrowing of the lumen of the GI tract (e.g., from previous surgeries such as in tracheoesophageal fistula, esophageal/duodenal webs)
-
Symptoms, if present, may include coughing, choking, foreign body sensation, throat pain, drooling, vomiting, refusal or inability to tolerate fluids/food
-
Children may also be completely asymptomatic
-
Esophagus
-
The esophagus is the most common site for ingested foreign bodies to become lodged
- Ingested foreign bodies typically become lodged in one of three sites:
At the thoracic inlet
Mid-esophagus, at the level of the carina and aortic arch
Esophago-gastric junction
- Management
-
If the patient is asymptomatic and there is no airway compromise, may do neck and/or chest radiographs
-
If foreign body is not visualized and patient is asymptomatic, then can do an esophagram
-
If foreign body is lodged in the esophagus, may need removal by esophagoscopy
-
Some authorities report the use of glucagon with varying degrees of success
-
Emergent removal is indicated for two or more magnets, button batteries, lodged sharp objects
-
Stomach and Lower Gastrointestinal Tract
-
Most foreign bodies in the stomach will pass harmlessly through the remaining portion of the GI tract
-
Single, not sharp foreign bodies may be managed conservatively and observed
-
Parents may be advised to watch patient stools, or have repeat abdominal radiographs within 1 week to assess if foreign body has been eliminated
- If two or more button batteries or magnets are located in any portion/part of the GI tract, consultation with a gastroenterologist to facilitate removal is necessary
If not removed, the magnets may “adhere” together across tissues/tissue planes and cause necrosis with ensuing perforation
-
Sharp objects (particularly if longer than 5 cm) in the stomach and lower GI tract require consultation with a gastroenterologist
-
-
-
Diabetic Ketoacidosis (DKA)
DKA in Pediatric Patients
-
DKA is a severe complication of type 1 diabetes
-
Occurs in 25–40% of new-onset type 1 diabetes
-
Inadequate relative or absolute deficit of insulin leads to starvation of insulin-dependent tissue (muscle, liver, fat) with resultant hyperglycemia
-
Starvation state triggers a cascade of hormonal release such as glucagon, catecholamines, cortisol, cytokines
-
Results in a catabolic state with lipolysis, proteolysis, adipose tissue metabolism into free fatty acids, hepatic conversion of fatty acid to keto-acids, and anion gap metabolic acidosis
-
Hyperglycemia causes osmotic diuresis with hypovolemia and dehydration
- Diagnostic laboratory findings
-
Acidosis (venous pH < 7.3, serum bicarbonate < 15 mEq/L)
-
Serum glucose > 200 mg/dL
-
Glucosuria, ketonemia, and ketonuria
-
- Degrees of severity of DKA
-
Mild: pH > 7.2 and < 7.3, bicarbonate < 15 mEq/L
-
Moderate: pH > 7.1 and < 7.2, bicarbonate < 10 mEq/L
-
Severe: pH < 7.1, bicarbonate < 5 mEq/L
-
- Review of pathophysiology
- Inadequate insulin secretion
Decrease in cell uptake of glucose, leading to hyperglycemia
Hyperglycemia causes osmotic diuresis, leading to dehydration
Compounded by stress response with activation of gluconeogenesis, glycogenolysis, and increased insulin resistance
- Protein catabolism
Adipose tissue broken down into fatty acids
Fatty acids converted to keto-acids in the liver
- Dehydration
Osmotic diuresis from hyperglycemia
Compounded by acidosis with nausea, vomiting, and oral intolerance
Typically occurs in setting of several weeks of polyuria, polydipsia, and weight loss
Dehydration can be profound and lead to shock state
- Acidosis
Keto-acids from protein catabolism cause anion gap acidosis
Poor tissue perfusion in setting of severe dehydration causes lactic acidosis
- Electrolyte abnormalities
- Potassium
Acidosis causes extracellular shift of potassium with hyperkalemia
Excess serum potassium is cleared by kidney
Hypovolemia stimulates secondary hyperaldosteronism and further urinary potassium excretion
Factors leads to total body potassium depletion in all patients with DKA
Measured serum potassium levels are highly variable at presentation (hypokalemia, normal, or hyperkalemia) and do not correlate with degree of total body potassium losses
- Phosphate
Acidosis stimulates phosphate depletion due to renal phosphate excretion
- Sodium
Hyperglycemia and osmotic diuresis lead to renal sodium losses and typically hyponatremia
-
Cerebral Edema
-
Most serious immediate risk to child in DKA with mortality rate of 40–90%
-
Occurs in 1/100 pediatric cases during the first 24 h of DKA
-
Causes 50–60% of diabetes-related pediatric deaths
-
Pathophysiology of cerebral edema is controversial
- Risk factors for cerebral edema continue to be studied
New-onset diabetes
Age < 3 years
High BUN at presentation
Low PCO2
Treatment with bicarbonate
Failure of serum sodium to correct with therapy
- Signs
-
AMS, from agitation to frank coma
-
Severe headache
-
Heart rate deceleration
-
Focal neurologic deficit
-
- Treatment
-
Immediate recognition
-
Immediate mannitol 1 g/kg over 10–20 min
-
Cerebral edema is a reversible condition with prompt treatment
-
- Principles of initial resuscitation of DKA in the emergency department
-
Treatment of DKA is often based on institutional protocol
- General concepts are
- Initial rehydration with isotonic fluid
10–20 ml/kg of 0.9% normal saline over 1–2 h
Goals: adequate tissue perfusion, not normovolemia
- Administration of insulin as continuous IV infusion
Regular insulin 0.1 unit/kg/h via IV line
- Addition of dextrose in fluid after serum glucose begins to fall
Varying concentrations of dextrose from 5% up to 12.5% via IV line
Plasma glucose target range 200–300 mg/dL
- Careful correction of electrolyte disturbances
Addition of potassium once serum K < 5.0 mEq/L
Addition of phosphate as potassium phosphate as serum phosphate allows
Prompt subspecialty consultation
Frequent laboratory monitoring
Frequent neurologic assessments to monitor for cerebral edema
-
Life-Threatening Complications to Consider in the Emergency Department
-
Cerebral edema
- Shock/cardiovascular collapse
Dehydration can be profound
Requires prompt restoration of intravascular volume
Consider infection/sepsis as trigger for stress response and hyperglycemia if clinically warranted
- Hyperkalemia or hypokalemia
Obtain ECG in critically ill child
May cause life-threatening arrhythmias or cardiovascular collapse
- Profound metabolic acidosis
Insulin infusion is necessary to stop primary ketoacidosis
Insulin infusion should never be stopped in DKA: If hypoglycemia occurs, adjust dextrose in fluids or rate of fluids to maintain plasma glucose levels
- Hypophosphatemia
Caution with replacement of phosphate is advised due to risk of precipitating hypocalcemia, renal failure, and arrhythmias
- Ongoing management
-
Children with DKA typically require subspecialty monitoring
-
Admission frequently required to specialized unit or to the intensive care unit
- Continued monitoring
Hourly plasma glucose
Hourly neurologic assessments
Hourly intake and output
Serial measurements of serum potassium, calcium, phosphate, magnesium
Serial venous blood gas
-
- Goals of treatment
- These goals are typically achieved in the inpatient setting
Resolution of hyperglycemia
Correction of dehydration
Closure of anion gap acidosis (anion gap normalized between 10 and 12)
Oral tolerance to feeds
Resolution of other symptoms
-
Concussion/Head Injury
- Definition
- Concussion can be defined as
An acute injury to the brain from an external physical force
Resultant confusion, disorientation, brief loss of consciousness, self-limited posttraumatic amnesia and/or other transient neurologic abnormalities
GCS score of 13–15 after 30 min following the injury
-
Also known as a mild traumatic brain injury
-
- Epidemiology and mechanism of pediatric concussions
-
Major cause across all age groups for pediatric visits to emergency care
-
Arises from either a direct or transmitted blow to the head, face, or neck
-
Subsequent injury to the brain is the result of an interplay of pathophysiologic processes, induced by biomechanical forces, without evidence of structural brain injury on standard neuroimaging
-
- Risk factors for a concussion
- An individual’s risk for a concussion is multifactorial with no single element being absolutely predictive
Boys reportedly affected more than girls due to predilection for more injuries/inclusion in more sports-related activities
Girls more likely to report symptoms of concussion
History of ADHD or learning problems raises lifetime risk
History of prior concussion raises risk for future concussion
-
- Risk factors for prolonged concussion symptoms
- An individual’s risk for prolonged symptoms is multifactorial with no single element being absolutely predictive
Prior history of concussion-like symptoms
Known history of intracranial abnormalities
Psychiatric disorders, headache disorders
Family and social stressors
Female sex predictive of symptoms lasting more than 4 weeks
Older age
-
- Signs and symptoms
- The signs and symptoms of pediatric concussions are variable
- Cognitive
Amnesia—may be retrograde or anterograde
Confusion
Difficulty concentrating
Disorientation
Persistent crying
- Neurologic
Headache
Dizziness
Gait abnormalities
Sensitivity to light/noise
Slurred speech
Fatigue
- Behavioral
Increased sleep
Emotional lability
- Gastrointestinal
Nausea
Vomiting
Refusal to feed
-
- Management
- Conservative management is the mainstay of treatment for pediatric concussions
Antiemetics may be used for nausea and/or vomiting
Pain control with nonopioid medications (e.g., ibuprofen and acetaminophen)
- Stepwise approach to cognitive and physical rest (see Chap. 14 “Sports Medicine”)
Complete bed rest may be required for a variable length of time (typically no more than 2–3 days)
Additional avoidance of activities that have high cognitive load is based upon the patient’s individual risk factors and developmental stage
Gradual return to daily activities and increasing cognitive and noncontact physical activity in a manner that does not exacerbate symptoms
Return to full activities only if patient is asymptomatic and has passed prior stages of recovery
- Anticipatory guidance is important to manage expectations and promote recovery
Inadequately treated concussions can prolong symptomatology and place patient at risk for reinjury
Warnings signs and symptoms to watch for that could indicate more severe injury
Recovery time is unique to each patient and for each incidence of head trauma
Concussions can cause physical, cognitive, and psychological impairments
Drowning
- Definition
- Drowning is defined as
The process of experiencing respiratory impairment from submersion in a liquid
Avoid using confusing older terms: Near drowning, secondary drowning, and wet drowning
- Classification of drowning
Fatal
Nonfatal with no morbidity
Nonfatal with morbidity (moderate, severe, vegetative state, brain death)
-
- Epidemiology
- Drowning is a major cause of injuries and death
Seasonal variation, with increasing incidence in summer months
- Incidence follows a bimodal distribution
- First peak occurs in children < 5 years of age
- Children < 1 year
Often drown in bathtubs, buckets, and toilets
Over half of infants in bathtubs
- Children 1–4 years of age
Over half of young children drown in swimming pools where they have been unsupervised temporarily (usually for < 5 min)
Typical incidents involve a toddler left unattended temporarily or under the supervision of an older sibling
- Second peak: Occurs at ages 15–24 years
Primarily male adolescents and young adults
Most incidents occur in natural water
-
- Mechanism of injury
- Initial progression of injury
- Swallowing of water
Laryngospasm
Loss of consciousness due to hypoxemia
Hypoxia
Loss of circulation
Tissue ischemia
CNS injury (the most common cause of death)
- Secondary progression of injury
After nonfatal drowning, further complications can develop:
- Pulmonary
Aspiration pneumonia
Acute respiratory distress syndrome (ARDS)
- Cardiac
Myocardial depression, arrhythmias
- Neurologic
Cerebral edema, increased ICP
- Metabolic
Metabolic and respiratory acidosis
- Hematologic
Hemolysis, coagulopathy
- Renal
Acute tubular necrosis
-
- Management
- At the scene
Immediate cardiopulmonary resuscitation (CPR) once a submersion has occurred is the most important initial step
-
Prompt attention to airway, breathing, and circulation
- Early intubation if
Signs of neurologic deterioration
Inability to protect airway
- Inability to maintain adequate oxygenation or ventilation despite supplemental oxygen
Remember orogastric tube for gastric decompression if intubated
- Administer 100% oxygen immediately to maintain SpO2 > 94%
Prevent further hypoxemia and acidosis
- Support work of breathing
If patient does not require intubation but has signs of impaired gas exchange, can elect to use noninvasive positive pressure ventilation such as continuous positive airway pressure (CPAP).
If advanced airway is established, mechanical ventilation with positive end-expiratory pressure (PEEP)
- Judicious fluid and shock resuscitation
Especially important with high levels of positive airway pressure required for adequate ventilation with poor lung compliance, with resultant increased intrathoracic pressure and decreased venous return to the heart
Vasopressors as indicated
After hemodynamic stability achieved, severe drowning may require fluid restriction and diuretic therapy due to pulmonary edema
- Cervical spine immobilization if suspected head/neck trauma is present
Classic example: Dive into shallow water
- Serial measurements
- Cardiopulmonary monitoring, temperature, and neurologic assessments
Pediatric drowning victims typically are hypothermic even if the water is warm
Abrupt change in mental status can reflect worsening lung function and hypoxemia
- Initial laboratory studies
Point-of-care glucose, complete blood cell count, electrolytes, urinalysis
- Initial imaging
Chest radiograph: indicated for all patients
Head CT: may be indicated for patients presenting with AMS
-
- Disposition
-
If CPR is required at the scene, recommend admission regardless of clinical status upon presentation
-
If patients with mild symptoms on arrival, recommend admission for monitoring
- If patient is asymptomatic with the following criteria, the patient may be monitored for 6–8 h prior to discharge home with close follow-up instructions
GCS 15
Normal chest radiograph
Normal lung exam
Normal oxygen saturations
Safe home
-
- Prevention and guidance
- Prevention is the key intervention in pediatric drowning
- Installation of 4-sided fencing
Completely prevents direct access to the pool from the house and yard
At least 4 ft high (or higher if required by local ordinance) and climb-resistant
Distance from bottom to ground less than 4 in.
Gate should be self-latching and self-closing, with the latch placed at least 54 in. above the bottom of the gate, open away from the pool, and should be checked often
Effective in preventing more than 50% of swimming-pool drownings of young children
- Supervision needs to be close, constant, and capable
Never—even for a moment—leave small children alone or in the care of another young child while in bathtubs, pools, spas, or wading pools or near irrigation ditches or other open standing water
A supervising adult with swimming skills should be in the water, within an arm’s length, providing “touch supervision”
With older children and better swimmers, the eyes and attention of the supervising adult should be constantly focused on the child
The adult should not be engaged in other distracting activities that can compromise this attention, such as talking on the telephone, socializing, tending chores, or drinking alcohol
Children should never swim alone without an adult
-
- Swim lessons
-
Swim lessons for children > 4 years: Recommended
-
Swim lessons for children 1–4 years: Insufficient data to recommend at this time
-
- Equipment
-
Personal flotation devices (PFDs or life jackets) are recommended
-
Air-filled swimming aids (inflatable arm bands, floaties) are not recommended
-
Do not use air-filled swimming aids in place of PFDs
-
Hypertensive Crisis
- Definitions
- Hypertensive urgency
Significantly elevated BP with potential for harm but without findings of end-organ damage
Develops over days to weeks
- Hypertensive emergency
Significantly elevated BP with evidence of secondary organ damage (e.g., encephalopathy or left ventricular failure)
Develops over hours
- Essential (primary) hypertension
Hypertension in which no underlying disease is discovered
Multifactorial causes
Increasingly common due to increasing obesity, sedentary lifestyle, and poor diet
Diagnosis of exclusion
- Secondary hypertension
Result of underlying pathology
Many causes: cardiac, endocrine, toxic, renal, CNS
- Blood pressure (BP) measurement in pediatrics
- Manual BP with auscultation is ideal
If initial BP via automated BP cuff is abnormal, must repeat with manual reading
- Appropriately sized BP cuff
Circumference completely encircles arm with overlap
- Bladder width ~40% of arm circumference
Small cuff size can falsely elevate BP readings
- Attempt to obtain when patient is calm and cooperative
Crying, fear, pain, anxiety, fever, and hunger can all falsely elevate BP readings
If initial BP is elevated and patient shows no sign of end-organ failure, repeat measurement when patient has calmed
- Secondary causes of hypertension
- Kidney disease
Chronic kidney disease, nephritis, renal artery stenosis, obstructive uropathy, Wilms tumor, etc.
More frequent < 6 years of age
- Cardiac disease
- Coarctation of the aorta (most common)
BP in right arm > 20 mmHg above lower extremity BP
Others: Abdominal aortic obstruction (abdominal masses), inflammatory arteritis (e.g., Takayasu arteritis, vasculitis)
- Endocrine disease
Rare but highly treatable, with many potential causes
Examples: Congenital adrenal hyperplasia, familial hyperaldosteronism, hyperthyroidism, hyperparathyroidism, pheochromocytoma, Cushing syndrome, etc.
- Special note on neurofibromatosis type 1 (NF1)
NF1 is particularly known to have multiple potential causes for hypertension
Association with renal artery stenosis, coarctation of the aorta, middle aortic syndrome, pheochromocytoma
- Neurologic disease
Many causes, including any intracranial process with increased ICP
Examples: Familial dysautonomia, Guillain–Barré syndrome, neuroblastoma
- Environmental/drug exposures
Many drugs, prescription and otherwise, can elevated BP
Common sources: Stimulants (pseudoephedrine, caffeine, cocaine, amphetamines), oral contraceptives, corticosteroids, anabolic steroids
- Medication withdrawal can also induce hypertension
Clonidine withdrawal
- Approach to severe hypertension presenting to emergency care
History and physical to evaluate for secondary causes of hypertension
- Careful attention to signs of end-organ failure
Cardiac exam: Signs of congestive heart failure, pulmonary edema, absent or decreased femoral pulses, peripheral edema
Abdominal exam: Palpable mass, audible bruit
Neurologic exam: Mental status, cerebellar function
Ophthalmologic exam: Disc edema, hemorrhage or infarct, visual acuity
- Laboratory investigations
Initial investigations should be limited to basic interventions
CBC, electrolytes, BUN, serum creatinine, urinalysis and urine culture
Four-limb manual BP
ECG
- Further investigations must be targeted to the suspected secondary source of the hypertension
Example: Echocardiogram to evaluate for left ventricular hypertrophy and coarctation; Doppler renal ultrasound to evaluate for renal artery stenosis
- Initial interventions
Attention to airway, breathing, and circulation
Establish IV access
- Careful selection of a short-acting IV antihypertensive medication
The choice of antihypertensive must be tailored to patient need, with consideration of underlying disease process, potential drug–drug interactions, and medication side effects
Avoidance of long-acting antihypertensives to avoid overaggressive drop in BP and allow for tighter control of therapy
- Avoidance of enteral medications due to variable effect and longer half-lives
Enteral medications may be considered in some cases of hypertensive urgency
- Examples of IV pharmacologic options
- Nicardipine
Calcium channel blockade
Reduces peripheral vascular resistance
Caution with intracranial processes, as can increase ICP
- Labetalol
Alpha-1 and beta-blockade
Reduces peripheral vascular resistance
Contraindicated in asthma, congestive heart failure, heart block, or in pheochromocytoma or cocaine overdose (unopposed alpha effects)
- Sodium nitroprusside
Potent and direct vasodilator
Strong arterial and venous smooth muscle relaxant with instant onset
Black box warning: Can cause cyanide toxicity (metabolized to thiocyanate and cyanide), must monitor thiocyanate levels
- Esmolol
Beta-1-blockade
Metabolism is independent of liver/kidney
Contraindicated in asthma, heart block, congestive heart failure
- Hydralazine
Arterial vasodilator
Can cause increased ICP and fluid retention
- Phentolamine
Alpha-adrenergic antagonist
Reserved for hypertension from catecholamine excess, e.g., pheochromocytoma or cocaine toxicity
- Goals of therapy
- Reduction of BP by < 25% in first 6–8 h
Cautious approach is warranted due to cerebrovascular autoregulation
Overaggressive drop in BP can put patient at risk for brain ischemia
- Further management
Patients with hypertensive urgencies typically require admission for further evaluation and management
Patients with hypertensive emergencies typically require intensive care monitoring and resuscitation
Sepsis and Shock
- First-hour management of septic shock
Early recognition and resuscitation is key, although recognition is challenging
Institutions benefit from implementing a sepsis screening tool and a sepsis intervention protocol (Table 7.12)
Clinician assessment within 15 min
Resuscitation begins within 30 min
Timeline for first hour management of pediatric septic shock
Timeline (min) | Intervention |
---|---|
0–15 | ABCs, cardiorespiratory monitoring, supplemental oxygen, frequent blood pressure monitoring, strict intake and output, order intravenous access and labs |
5–15 | Obtain IV access, escalate to IO if unable to obtain IV |
Labs: Blood culture, venous blood gas, glucose, lactate, electrolytes, complete blood count | |
0–20 | Initial rapid fluid resuscitation of 20 mL/kg normal saline fluid bolus |
0–60 | Up to 3 fluid boluses with maximum 60 mL/kg, reassessments after each additional bolus for attainment of clinical goals, have vasopressor of choice ready for infusion, monitor for need for intubation and development of pulmonary edema |
0–60 | Administer intravenous antibiotics within 1 h |
60 | Initiation of vasopressor of choice if fluid-refractory shock, consideration of need for stress dose steroids, continual reassessments |
> 60 | Prompt transfer to pediatric ICU within 1 h |
Pearls and Pitfalls
- Respiratory distress
-
In the search for a localizing problem for respiratory distress, remember to carefully consider disorders external to the lung.
-
A significant amount of non-airway disease can cause respiratory distress via derangement of either the respiratory system controls or acid-base status causing a secondary respiratory compensation.
- Be alert for abnormal breathing patterns in the absence of abnormal auscultatory findings.
Bradypnea/tachypnea may signify increased ICP or CNS depression, as in hypothermia, narcotic overdose, mass lesion, meningitis, encephalitis, spinal cord injury or neuromuscular disease, or anxiety or pain.
Kussmaul respirations: acidosis (diabetic ketoacidosis).
-
“Not all that wheezes is asthma.”
- For patients with atypical or unexpectedly severe clinical presentations of what appears to be an asthma exacerbation, always consider less common intrathoracic pathology:
Intrinsic lung disease (bronchopulmonary dysplasia, cystic fibrosis, pneumonitis, lung malformations), heart failure, mediastinal masses, and GERD.
- Be alert for “red flag” warning signs that can indicate imminent respiratory failure:
Upper airway: tripoding, drooling, gurgling, inspiratory and expiratory stridor.
Lower airway: grunting, head bobbing, see-saw abdominal retractions.
Neurologic: AMS, lethargy, extreme irritability.
-
- The acute abdomen
-
See Table 7.4 for Pearls and Pitfalls.
-
- Anaphylaxis
- The absence of skin findings does not rule out anaphylaxis.
Many children will have only transient skin changes or rash.
-
Anaphylaxis can present with primarily neurologic symptoms such as syncope.
-
Prompt administration of intramuscular epinephrine is associated with lower risk of hospitalization and fatality.
-
Delayed administration of epinephrine is associated with increased risk of hospitalization and worsened outcomes such as hypoxic-ischemic encephalopathy and death.
-
Antihistamines such as diphenhydramine relieve itching through H1-blocker effects but do not help with airway or respiratory symptoms, hypotension, or shock.
- Inhaled bronchodilator therapy with albuterol can reverse bronchospasm but does not help with angioedema, hypotension, or shock.
Keep in mind that epinephrine is also a potent bronchodilator and will help relieve acute wheezing from anaphylaxis.
-
- Head trauma
-
Infants are at higher risk from mortality and morbidity due to head trauma from nonaccidental trauma and may not have many signs or symptoms due to limited neurologic exams.
-
Always maintain a low threshold of suspicion for nonaccidental trauma.
-
- Burns
-
Always maintain a low threshold of suspicion for nonaccidental trauma.
- “Red flag” warning signs that should raise suspicion for abuse:
“Stocking and glove” distribution of burn: Suggest forceful immersion of extremity in hot liquid.
Full thickness burns: Children typically will retract extremity before this degree of injury can occur.
-
- Inhalation injury
-
Severe airway injury from smoke inhalation can occur in the absence of external burn findings.
-
Risks for smoke inhalation injury include young age and exposure within a closed space.
-
Due to risk for CO poisoning, early application of 100% oxygen, blood gas analysis, and carboxyhemoglobin level are important.
-
- Altered mental status
-
Broad differential diagnosis can make management of AMS a challenging diagnostic puzzle.
-
Careful attention to history and physical clues and low index of suspicion for life-threatening disorders can help guide the differential diagnosis.
- Many of the more common causes of AMS are reversible if discovered promptly
Promptly identify and correct hypoglycemia, hypoxia, hypothermia, hypercarbia, and hypotension.
-
- Foreign body ingestion and aspiration
-
Unwitnessed foreign bodies within the airway have the potential to masquerade as more common diseases such as croup and bronchiolitis/asthma.
-
Esophageal foreign bodies have the potential to cause significant airway compromise.
-
Impaction is often to underlying pathology such as eosinophilic esophagitis, GERD, and known prior strictures.
-
- Drowning
-
Conduct careful assessment of all end-organ function in drowning victim.
-
Underlying disease can be the precipitating cause for or a coexisting risk factor in a drowning event, e.g., toxic ingestion, intentional overdose, recreational drug use, seizure disorder, cardiac arrhythmia, hypoglycemia.
-
Prevention of drowning is key.
-
- Hypertensive crisis
-
Hypertension in a young child or infant is more likely to represent secondary hypertension with identifiable cause.
-
Unless there are signs of acute end-organ dysfunction, treatment of hypertension in pediatric patients is conservative.
-
- Sepsis and shock
-
Pediatric sepsis requires prompt recognition and treatment.
- Emphasis on first-hour fluid resuscitation and inotropic therapy with the following clinical goals:
Improvement in heart rate.
Normalization of BP.
Restoration of perfusion and pulses.
Reassessments after each bolus for signs of fluid overload.
Antibiotic administration within first hour of recognition,
Prompt transfer to the intensive care unit for further support.
-
References
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