Pediatric Respiratory Emergencies

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Pediatric Respiratory Emergencies

• DR.T.MOHAN KUMAR,MD,AB,DPPR,FCCP,
• CHIEF SENIOR CONSULTANT,
• DEPARTMENT OF PULMONOLOGY CRITICAL CARE ,
• SRI RAMAKRISHNA HOSPITAL,
• COIMBATORE.
• INDIA

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Emergency readiness of pediatric offices
(American academy of pediatrics survey 27(1999)

• 74 see acute severe asthma
• 60 see respiratory distress
• 50 see severe dehydration
• 45 other emergencies
• Only one third have their office staff to deal
  with emergencies
• Protocols for emergencies used in 37 only 27
  has pediatric CPR certificated staff 16 only
  has emergency equipment

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Access to pediatric emergency careAmerican
Academy of Pediatricians Pediatrics, vol105,
no3, March2000, pp647-649

• Lack of definition of emergency
• Lack of reasonable access in rural areas
• Lack of universal access to basic 911 service
• Variability in training programs
• Lack of pediatric emergency training to
  paramedics

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Pediatric life support

• Neonatal resuscitation remember Apgar score at
  1 minute of
• lt 5 indicates intrapartum asphyxia
• 5 to 7 mild asphyxia and
• gt 8 normal .
• Reassess every 5 minutes until gt7.

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Pediatric advanced life support A. Breathing
(remember positioning, suctioning airway)

• 1. Pediatric cardiac arrest is almost always
  secondary to respiratory insult
• 2. Treat any signs of respiratory distress such
  as tachypnea, retractions or stridor
• 3. Provide immediately humidified oxygen in
  highest possible concentration
• 4. In epiglottitis do not move the patient as
  any agitation can cause airway obstruction
• 5. Bag-valve mask with 100o2 usually adequate in
  epiglottitis

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Pediatric advanced life support B. Cardiac
assessment

• 1. Tachycardia usual response to stress.
• 2. Bradycardia is evidence of impending cardiac
  arrest.
• 3. BP may remain normal until cardiopulmonary
  arrest imminent.
• 4. Observe level of consciousness, urine output,
  capillary refill, color, as gauge of end organ
  perfusion.
• 5. For fluid resuscitation20ml/kg of NS or RL.
  May repeat twice or even more if needed.
• 6.efficacy of high dose epinephrine(0.1mg/kg) has
  still its uses.

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ET TUBE SIZES FOR CHILDREN

• Premature 2.5 ,3.0 uncuffed
• Newborn 3.0, 3.5 uncuffed
• 6 months 3.5 uncuffed
• 12 to 18 months 4.0, 4.5 uncuffed
• 2 years 4.5, 5.0 uncuffed
• 4 years 5.0, 5.5 uncuffed
• 6years 5.5 uncuffed , 8years 6.0 cuffed or
  uncuffed.10 years 6.5 cuffed,12 years 7.0
  cuffed
• TO CALCULATE APPROXIMATE SIZE (age/4)4.

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Pediatric life support

• Defibrillation energy dose 2 j / kg.If not
  effective use 4j / kg x 2.
• Dilutions for dopamine dobutamin 6 x body
  weight(kg) of mg in 100 ml D5W and then 1ml/hr
  1.0µg/kg/min.

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Acute upper airway obstruction

• Croup (acute laryngotracheobronchitis) viral
  origin (parainfluenzae) occurs predominantly in
  infants (1-3 years), relatively benign course
  characterized by subglottic inflammation
  narrowing which produces radiographic steeple
  appearance. Lungs are often hyper inflated with
  patchy atelectasis. Treatment with nebulized
  epinehrine 5ml of 11000, 95oxygen,
  dexamethasone 0.6 mg.kg/dose IM , in severe cases
  intubation

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ACUTE AIRWAY OBSTRUCTION

• Tonsillitis / Retropharyngeal cellulitis/abscess
• Epiglottitis infection (H. influenzae type B,
  staph strep) of the epiglottitis, aryepiglottic
  folds and surrounding soft tissues, may occur in
  children 2 to 7 years, child usually in sitting
  position high fever, respiratory distress, severe
  dysphagia. Thumb sign on x-ray. Treatment do
  not move, upset the child, use mask with O2, ET
  tube, emergency cricothyrotomy, cefataxime 50 to
  200 mg/kg/24 hr 7 to10 days.

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Acute airway obstruction

• Foreign body aspiration Clinical presentation
  Majority 3 months to 6 years, triphasic history
  of
• 1. initial cough, choking, gagging, stridor,
  wheeze
• 2. FB then passes to smaller airways has a
  silent phase.
• 3. Recurrent pneumonia, wheezing, abscess,
  bronchiactasis. Radiograph showing air trapping
  on exhalation but ¼ have normal x-ray ,without
  respiratory distress bronchoscopy.

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Foreign Bodies

• When in distress
• In infants, 4 intrascapular back blows with
  childs head lower than the chest alternating
  with 4 chest compressions.
• In older children Heimlich maneuver. If
  unsuccessful, direct laryngoscopy removal with
  Magill forceps. Still problem, cricothyrotomy or
  intubation.

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Bronchiolitis

• Most serious in first 2 years of life.
  Respiratory syncytial virus principal agent. Also
  associated with Para influenza, adenovirus,
  rhinovirus influenza virus. Clinically
  sneezing, cough, low grade fever. Onset of rapid
  breathing and wheezing. Severe respiratory
  distress, nasal flaring, tachypnoea, retractions.

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BRONCHIOLITIS

• Treatment inhaled epinephrine, inhaled
  budesonide, ribavirin aerosol with patients of
  congenital heart disease, chronic lung disease,
  infantslt6 weeks of age, neurological disorders,
  immunosupressed. Intubation and ventilation when
  required. RSV immunoglobulin RSV-IGIV 750 mg/kg
  IV 30 days can prevent this in patients with
  bronchopulmonary dysplasia or prematurity.

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Differential Diagnosis of Stridor Dyspnea
epiglottitis
Retropharyngeal abscess
Bactrial trachietis
Viral laryngotracheitis
H.Influ/staph/strep
Beta-hemolytic strep/anaerobes
Viral/staph/strep/H. influ
Para/inflenza/RSV
cause
2to7y
6m to3y
3m to 3y
3m to3y
age
Sudden onset of fever, dysphagia,
stridor,drooligNO COUGH
Initial URI,dysphagia, refusal to feed, drooling,
toxic appearance, stridor
Improving croup then sudden increase,temperature,w
ork of breathing,stridor,NO DROOLING
Low grade fever,coryza, barking cough, hoarse
voice/ winter peak
clinical
Unnecessarythumb sign
Retropharyngeal soft tissue density air fluid
level
Detached pseudomembrane will show soft tissue
shadow
unnecessary
radiograph
Intubation,antibiotics
Surgical drainage ,antibiotics
Intubation,antibiotics
Cool mist,epinephrine,steroids
treatment
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Drowning Near Drowning

• Aspiration of fluid-wet drowning occurs in 90.
  Although less than 4 cc/kg of fluid enters the
  lungs , in most cases V/Q abnormalities do occur.
  Radiographs show pulmonary edema of variable
  severity. If no complicating pneumonia or ARDS,
  this clears within 24 to 48 hours
• Hydrocarbon pnemonia due to ingestion of
  kerosene, gasoline, furniture polish etc the low
  viscosity high volatility ensures rapid
  dissemination. Produces edema, atelectasis,
  vascular injury alveolar necrosis. Radiography
  shows perihilar edema, patchy consolidation.Resolv
  es within 3 to 5 days.

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Pneumothorax

• Spontaneous due to idiopathic pleural bleb or
  as a complication of diseases as asthma, cystic
  fibrosis, pneumonia. Most of idiopathic are small
  with no respiratory distress. Occasionally
  massive tension pneumothorax results in severe
  respiratory compromise.

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Pleural Effusions Empyema

• A large parapneumonic pleural effusion
  complicating pneumonia may be associated with
  severe respiratory distress. Most resolve with
  antibiotics. If not chest tube drainage.
• Pneumocystic carinii pneumonia seen in infants
  median age 5 months. Acute febrile onset
  tachypnoea, rapidly progressing to hypoxia
  respiratory failure. BAL isolaltion of PCP
  essential. Radiograph shows diffuse
  reticulo-nodular infiltrate / consolidation /
  pneumatoceles.

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GAS

• Invasive group A streptococcus GAS Rapidly
  invasive, necrotic mucosal cutaneous
  infections. GAS Pneumonia can spread rapidly to
  pleura chest wall. A toxic shock syndrome
  complicated with ARDS can occur with or without
  renal failure.

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CHEST TRAUMA

• Flail chest paradoxical chest wall motion
  secondary to mutiple fractured ribs. Treatment
  by intubation and chest tube on the affected
  side. Never give positive pressure ventilation.
• Pneumothorax / hemothorax chest tube

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PNEUMONIA IN CHILDREN

• Neonatal perinatally (lt5 days) or prenatally
  acquired, caused by maternal vaginal flora, group
  A,B,C Strep, E.Coli, C.Trachomatis, T.Pallidum,
  TB, genital mycoplasma
• Treatment amp/genta/3rd generation cephalosporin
  with antipseudomonal activity like ceftazidime

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Pneumonias-2

• Infantlt1 month ,Group AB strep, staph, E.Coli,
  pseudomonas, chlamydia, pneumocytis. Treatment
  pencillinase resistantsynthetic
  penicillinnaficillin / genta / vancomycin if
  methicillin resistant staph for clamydia,
  erythromycin
• Children 1month to5 years viral common RSV,
  para influenza, influenza, strep, H.influenzae,
  chlamidia, mycoplasma. Treatment clarithromycin
  /amp / ceftriaxone / cefataxime
• Above 5 years pnemo / m.pneumoniae /
  anerobes/ pneumocytis / staph/viral TB, strep.
  Treatment erythromycin

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Pnemonias-atypical

• Clamydia pneumoniae 10 of all pneumonias
  macrolide
• Fungal itraconazole / ketokonazole /
  amphoterocin
• Hanta virus getting common in India (rats mice
  vectors) rapid respiratory failure ribavrin
  useful
• Legionnaires urine antigen erythromycin / clar
  /azi
• Mycoplasma epidemics, macrolides

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Acute severe asthma

• Risk factors associated with asthma death
  1.intubation 2. hospitalizations 3. hypoxemia
  seizure 4. steroid dependence 5. increased use
  of beta2 agonists
• Look for silent chest, persistant non productive
  cough, tachypnea / tachycardia, retractions,
  nasal flaring, accessory muscle use, cyanosis,
  altered mental status, somnolence respiratory
  failure. Bradycardia shock herald impending
  cardiac arrest

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Treatment of ASA

• Oxygen when SaO2lt93
• Salbutamol continuous nebulization 0.5mg/kg/hour
• Steroids prednisolone 1 to2 mg/kg/day Or
  solumedrol 4mg/kg/day
• Terbutalin aerosol nebulization dose 1 mg of 0.1
  solution in 2ml of saline for children lt1 yr of
  age 2mg for those over 1 year of age every 15
  to 20 minute. SC dose 0.01ml/kg every 15 to 20
  min max dose 0.25 ml. IV dose0.4ug/kg/min
  titrated to 2ug/kg/min
• SC epinephrine 0.01 ml/kg every 15 to 20 min max
  dose.0.3ml can be used through ET tube

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Treatment of ASA

• Aminophylin infusion
• 1-6 months 0.5mg/kg/hour
• 6months to 9 years 0.8 to 1.5mg/kg/hour
• 10 to 12 years 0.8 to 1.2 mg/kg/hour
• Mechanical ventilation volume ventilation ideal,
  larger TV 18-24ml/kg with long expiratory
  times. Ketamine 1 to 2 mg/kg/IV is used for its
  bronchodilator property for intubation. No
  morphine/demerol/atacurium which produce
  bronchospasm due to histamin release. Ketamin for
  sedation dose 0.5 to 1.0 mg/kg/hour

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ASA

• Magnesium sulphate 25 to 100mg/kg iv over 20 min
• Ipratropium bromide nebulisation 0.5 mg in 2.5
  ml of NS every 4 to 6 hours
• Frusemide nebulized 10 to 40 mg in 2 to 4 ml of
  0.9NS
• Extracorporal life support arterial venous or
  veno-venous
• Heliox (O2 20plus helium 80)
• Halothane, enflurane, isoflurane

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DIAGNOSTIC CRITERIA

• ARDS
• Acute
• PaO2/Fio2lt200 mmHg
• Bilateral interstitial
• or alveolar infiltrates
• Pcwp lt15-18 mmHg

• ALI
• Acute
• lt300 mm Hg
• Same
• same

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Clinical diagnosis

• Rapid
• Within 12 to 48 hr of the predisposing event
• Awake patients become anxious, agitated
• dyspnoeic
• Dyspnoea on exertion proceeding to severe when
  hypoxemia intervenes
• Stiffening of lung leads to increase work of
  breathing, small tidal volumes, rapid respiratory
  rate
• Initially respiratory alkalosis
• Respiratory failure

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Laboratory studies

• To date no lab findings pathognomonic of ARDS
• X-ray chest shows bilateral infiltrates
  consistent with pulmonary edema, may be mild or
  dense, interstitial or alveolar, patchy or
  confluent
• ABG shows hypoxemia with respiratory alkalosis.
  In late stages hypoxemia, acidosis, hypercarbia
  may be seen.

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Respiratory Support
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Spontaneously Breathing Patient

• In the early stages of ARDS the hypoxia may be
  corrected by 40 to 60 inspired oxygen with CPAP
• Peak inspiratory flow rates of gt 70 ltrs / min
  require a tight-fitting face mask with a large
  reservoir bag or a high flow generator
• If the patient is well oxygenated on lt 60
  inspired oxygen and without CO2 retention and
  apparently stable, then ward monitoring may be
  feasible but close observation (15 to 30 Min),
  continuous oximetry, and regular blood gases are
  required

Contd..
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Indications for mechanical ventilation

• Inadequate Oxygenation (PaO2 lt 8k Pa on FiO2 gt
  0.6)
• Rising or elevated PaCO2(gt 6k Pa)
• Clinical signs of incipient respiratory failure

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Mechanical Ventilation
The Aims are to increase PaO2 while minimizing
the risk of further lung injury (Oxygen toxicity,
Barotrauma). This is the realm of the IRCU
Physician seek specialist advice early to
prevent complications. The general principles are
the following
Contd..
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• Invasive monitoring is mandatory (Arterial line,
  PA catheter (Swan-Ganz) to measure cardiac
  outputs and if available, continuous mixed venous
  oxygen saturation)
• In order to minimize pulmonary oedema, aim to
  keep PCWP low (8 to 10 mm Hg) and support the
  circulation with inotropes if necessary
• The role of colloids and albumin is relatively
  minor the increased capillary permeability
  allows these molecules to equilibrate with the
  alveolar fluid with little increase in net plasma
  oncotic pressure

Contd..
36

• Renal failure is common and may require
  haemofiltration to achieve a negative fluid
  balance and normalize blood chemistry.
• Oxygen consumption (VO2) in patients with ARDS
  appears to be delivery dependent. The current
  trend is to aim for target levels of oxygen
  delivery (DO2 Cardiac Index (HbXSao2X1.34) X10)
  as guided by tissue perfusion (clinically and
  serum lactate, pHi from a gastric tonometer). DO2
  may be increased by blood transfusion, inotropes
  and vasodilators including prostacyclin).

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Cardiovascular Support
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• Look for a precipitant
• In general prevention (example of aspiration of
  gastric acid) is more effective than trying to
  treat ARDS. However there are no effective
  measures for prophylaxis in patients at risk ( Eg
  from Trauma)
• Steroids there is no benefit from treatment
  early in the disease. Treatment later (gt 7
  to 14 days from onset) especially in patients
  with peripheral blood eosinophilia or eosinophils
  in bronchoalveolar lavage, improves prognosis

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• Leukocytosis/Leukopenia/anemia are common
• Renal function abnormalities/or liver function
• Von Willebrands factor or complement in serum
  may be high
• Acute phase reactants like ceruloplasmin or
  cytokine (TNF,IL-1,IL-6,IL-8)may be high.

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BRONCHOALVEOLAR LAVAGE

• Inflammatory mediators like cytokines, reactive
  oxygen species, leukotrienes activated
  complement fragments are found in the fluid
• Cellular analysis shows more than 60 of
  neutrophils.
• As ARDS resolves neutrophils are replaced with
  alveolar macrophages.
• Another interesting finding is the presence of a
  marker of pulmonary fibrosis called procollagen
  peptide III (PCPIII) and this correlates with
  mortality.
• Presence of more eosinophils suggest eosinophilic
  pneumonia, high lymphocyte counts may be seen in
  hypersensitivity pneumonitis, sarcoidosis, BOOP,
  or other acute forms of interstitial lung disease.

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Therapy -goals

• Treatment of the underlying precipitating event
• Cardio-respiratory support
• Specific therapies targeted at the lung injury
• Supportive therapies