Resp E-P Flashcards
What is acute epiglottitis?
Life threatening emergency due to inflammation of epiglottis and supraepiglottis structures leading to upper airway obstruction
What is the background of acute epiglottitis?
Very rare since Hib vaccine introduction. 2-4yo.
Used to be mainly due to Hib, but due to vaccine development now it is more commonly associated with StaphA and GAS.
DDx: Croup (less toxic, more gradual stridor onset), foreign body, EBV, measles, diphtheria.
Path: epiglottis looks cherry red and swollen, this may involve surrpunding tissues (aryepiglottis folds, arytenoid soft tissue and uvula).
What would you find in history and examination of acute epiglottitis?
Sudden onset drooling, stridor and inability to swallow. Pyrexia, very unwell. Voice is NOT hoarse and does NOT have a cough (distinguish from croup).
General: unwell, toxic, pyrexia, tachycardia.
Specific:
· Breathing: difficult and stridor
· Throat: unable to talk and swallow
· Drooling – with sitting posture (upright with throat thrust forward to prevent drooling)
What investigations do you do for acute epiglottitis?
INTUBATE FIRST – to avoid shock causing obstruction of airway
Bloods: high WCC, neutrophilia, CRP high
Cultures: if toxic
ABG: determine severity of resp compromise
What is the management for acute epiglottitis?
EMERGENCY:
· Admit and transfer to PICU – with ENT surgeon to preform emergency tracheostomy if necessary
· Call for senior anaesthetist to make diagnosis by laryngoscopy and then intubate
· Give 3rd gen cephalosphorin (cefotaxime) and continue for 5d.
· ?Hydrocortosone sometimes given but unclear value.
Prophylaxis: rifampicin offered to close house contacts
What are the complications and prognosis for acute epiglottitis?
Acute airway obstruction causing death or ischaemia
With prompt Dx and Tx it’s good, recovery 3-5d. Extubate after 1-2d. Mortality 10% without tx. .
What is Meconium aspiration syndrome?
Respiratory distress in the neonate secondary of aspiration of meconium (fetal intestinal continents) stained amniotic fluid.
What is the background of Meconium aspiration syndrome?
Meconium staining in 10% live births, of these 1-10% experience aspiration
Meconium passage into the amniotic fluid occurs as a response to fetal stress/hypoxia. Further trauma, smoking/alcohol, maternal HTN or pre eclampsia and placental insufficiency may cause it. These lead to peristalsis and relaxation of the anal sphincter -> meconium passage.
More common in post term infants, low BW, cord compression and oligohydramnios.
Pathophysiology:
· Aspiration -> obstruction lung -> air trapping -> PPH
· Aspiration -> chemical pneumonitis -> cytokines -> pneumonia -> PPH
· Aspiration -> surfactant dysfunction -> low surface tension -> PP
What would you find in history and examination of Meconium aspiration syndrome?
High risk children identified: in utero tachy or bradycardia and absence of fetal accelerations on cardiotocography.
At birth, affected children have:
· Signs of postmaturity, weight loss, yellow nails / skin / umbilical cord.
· Respiratory distress: tachypnea/tachycardia, recession, grunting, nasal flaring, diminished breath sounds, hyperinflation
What investigations do you do for Meconium aspiration syndrome?
CXR: hyperinflation, flat diaphragm, cardiomegaly if PPH, patchy shadowing
Gas: low pO2 (right=left shunt of blood via PFO as pressure differential does not reach threshold for closure).
What is the management for Meconium aspiration syndrome?
Children with MEA require assessment by pediatrician ASAP after birth.
Good condition: no need for further treatment
Bad condition: suction via ET tube, +/- intermittent PPV.
NICU tx: supportive therapy with Abio, ventilation, surfactant therapy, inhaled NO and ECMO.
What are the complications and prognosis for Meconium aspiration syndrome?
Pneumothorax, pneumoperitoneum from obstruction and work of breathing
Infection leading to pneumonia
Low surface tension leading to alectasis due to surfactant deficiency
Likely to have PPH as a result of above three
Depends on extent of hypoxia, relating to other possible injuries sustained.
What is Persistent pulmonary hypertension (PPH)?
Persistently raised vascular resistance, leading to shunting of blood away form the lungs through the ductus arteriosus and foramen ovale.
What is the background of Persistent pulmonary hypertension (PPH)?
1/500-700 births. More common in Downs and IUGR, fetal distress.
May be primary (idiopathic) or secondary to:
· Surfactant deficiency
· Meconium aspiration
· Pulmonary hypoplasia
· Diaphragmatic hernia
· Congenital pneumonia
· HIE
Pathology: After birth infant lung is supposed to undergo vasodilation due to pressure form breathing, increased pO2 and pH and decreased CO2. However, this can fail in the case of
a. Maladaptation of the pulmonary circulation to injury,
b. Following chronic fetal hypoxia that caused chronic inflammation in the lung,
c. Obstruction of the vasculature secondary to polycythaemia.
What would you find in history and examination of Persistent pulmonary hypertension (PPH)?
Suspect: when infant has low O2 sats that are not responsive to 100% O2 treatment (hyperoxia test) and are disproportionate to CXR parenchymal pathology.
Respiratory distress: grunting, nasal flaring, recession (costal/ intercostal/ sternal/ substernal) and cyanosis.
Cardiogenic shock: secondary to myocardial ischaemia and papillary muscle dysfunction leading to mitral and tricuspid regurg. Presents with low end organ perfusion.
