Presentation, diagnosis and management of severe status asthmaticus and complications in pediatric ICU

1. 18:40
9 y/o, 40 kg. male brought to ER by EMS
from home with difficulties of breathing for
about 3-4 hrs. Because of the history of
asthma and wheezes on PE paramedics
administered SQ. epinephrine and nebulized
albuterol x 2

2. Complaints
Difficulty of breathing
Feeling tired
Chest pain
Never felt so bad before

3. Complains
Difficulty of breathing
Feeling tired
Chest pain
Never felt so bad before

4. Differential Diagnosis of Severe Asthma
Congestive heart failure/myocardial infarction
Pulmonary embolism
Upper airway obstruction
Epiglottitis
Foreign body aspiration
Tumor
Anaphylaxis/angioedema
COPD
Bronchiolitis
Vocal cords dysfunction
Hyperventilation syndrome
Acute bronchitis/pneumonia

5. TRIAGE
Severe SOB
Drooling
Grunting
Wheezes on auscultation
HR 160
RR 36
O2Sat 95% on 15L
BP 123/57

6. TRIAGE
Severe SOB
Drooling
Grunting
Wheezes on auscultation
HR 160
RR 36
O2Sat 95% on 15L
BP 123/57

7. ABG in the ER
pH 7.34
PCO2 44
PO2 94
BICARBONATE 23.3

8. ABG in the ER
pH 7.34
PCO2 44
PO2 94
BICARBONATE 23.3

9. Patient received nebulized albuterol x 1 and xopenex
x 2
Prednisolone
Ceftriaxone and Azythromycin

10. PM History
Known asthmatic, used steroids in the past, uses
albuterol inhaler now
Immunization is UTD
Lives at home with the family
Family history is non-contributory
No previous admissions

11. History of PI
Cough, running nose, worsening SOB x 2 days
Frequent use of albuterol inhaler x 2 days

12. History of PI
Cough, running nose, worsening SOB x 2 days
Frequent use of albuterol inhaler x 2 days

13. PE
Alert, oriented, consolable, interactive
Afebrile
Able to speak in short phrases only
Grunting, drooling, retractions, bilateral wheezes
Well hydrated
HEENT normal
CV normal except tachycardia
Abdomen normal

14. PE
Alert, oriented, consolable, interactive
Afebrile
Able to speak in short phrases only
Grunting, drooling, retractions, bilateral wheezes
Well hydrated
HEENT normal
CV normal except tachycardia
Abdomen normal

15. 19:10
HR 160
RR 37
BP 130/70
O2Sat 84% on 15L non-rebreather

16. 19:10
HR 160
RR 37
BP 130/70
O2Sat 84% on 15L non-rebreather

17. What do we want to do?

18. Our choices
Continuous inhalation of beta agonists
Atrovent
IV MgSO4
Continuous infusion of beta agonists
Continuous infusion of aminophylline
Endotracheal intubation and mechanical ventilation

19. Continuous inhalation of beta
agonists
Titrate to effect
Tachycardia in children is well tolerated
The rule of thumb: allow HR to increase by 50%
over mean for the age

20. Ipratropium bromide
Work by blocking the irritant receptors and
inhibiting cGMP metabolism, which results in
bronchodilation.
Ipratropium bromide is poorly absorbed and does
not cross the blood-brain barrier, hence has fewer
side effects than atropine.
It is often an effective adjunct to beta-agonist
therapy.

21. Magnesium sulfate
Antagonizes calcium-induced smooth muscle contraction.
Inhibits the neuro-muscular release of acetylcholine and the
release of histamine.
Bronchodilation is proportional to blood levels.
It should be administered intravenously.
A serum magnesium level of 4 - 6 mg/DL is recommended.
Onset of bronchodilation should be noted after a few minutes
of infusion, and its total duration is approximately two hours.
Side effects include facial flushing and malaise.
Too rapid (>15 min.) intravenous infusion may induce
hypotension or bradycardia.
Magnesium levels > 6 mg/DL may result in absent reflexes,
muscle weakness and disturbances of cardiac conduction
Contraindicated in renal failure.

22. Continuous infusion of beta-agonists
Terbutaline is most commonly used in the United
States. Isoproterenol may lead to significant
tachycardia and inotropy, which has caused
myocardial infarction in adults.
The dose is 10mcg/kg slow bolus followed by
continuous infusion of 0.4-2.0 mcg/kg/min.
The dose should be titrated to effect and adverse
cardiac effects (tachycardia, arrhythmias, ECG
changes).
Some practitioners advocate monitoring cardiac
enzyme levels (not as important in children as in
adults).

23. Aminophylline
The mechanism of bronchodilatation is likely
explained by PDE inhibition, resulting in an increase
in cAMP (different from beta agonists)
A relatively weak bronchodilator
Anti-inflammatory effect
Reverses diaphragm fatigue

24. Risk Factors for Near-Fatal Asthma
Prior severe attacks
Nonadherence to therapy
Poor asthma self-management skills
High baseline peak-flow variability
Frequent b-agonist use
Inadequate use of inhaled corticosteroids
Age < 40 yr
Cigarette smoking
Prior barotrauma
Hospitalization despite chronic oral corticosteroid use
Psychiatric illness
Recreational drug and alcohol abuse
Diminished ability to sense and respond to airway obstruction
Female sex
Poor socioeconomic status

25. 19:15
Patient is intubated
Receives manual ventilation

27. Foley catheter
NG tube
Radial arterial line

28. Mechanical ventilation strategies in
status asthmaticus
Provide adequate oxygenation
Avoid dynamic hyperinflation and autoPEEP
(intrinsic PEEP)
Avoid high inflating pressure

30. autoPEEP
Measurements of autoPEEP are frequently used to
assess DHI.
AutoPEEP is measured by occluding the airway
during an end-expiratory breath hold.
In normal individuals exhaling to FRC, this
pressure should be 0. However, in patients unable
to exhale fully between breaths, expiratory flow
continues and a persistent positive driving
pressure can be detected

31. Effects of DHI
1 Hemodynamic compromise, caused by high
intrathoracic pressure, which leads to:
 Decreased venous return.
 Pulmonary vascular compression and increased right
ventricular afterload.
 Decreased left ventricular preload caused by right
ventricular dilation and shift of the intraventricular septum
towards the left ventricle.
 External compression of the heart by the hyperinflated
lungs.
2 Barotrauma

32. When airways become entirely occluded (mucus
plugs), measured autoPEEP may significantly
underestimate the pressures present in the distal
airways and alveoli in lung units that do not
communicate with the airway opening

33. High inflating pressures
PIP (Peak Inspiratory Pressure)
Ppl (Plateau Pressure)

35. High level of measured PIP may greatly
exceed pressure in the distal airways and
alveoli due to pressure drops across areas of
obstruction

36. Ventilator settings in status
asthmaticus
Mode PC, PRVC, VC
TV low to “normal”
RR slow
FiO2 keep O2Sat above 90% if
possible
I:E ratio no less than 1:3, preferably 1:4 or higher

37. Age 0-12 m 1-5 y 5-12y adults
Mode PC, PRVC, VC
FiO2 100%, or to keep sats above 90%
TV (ml/kg) 10-15 10-12 8-12 6-10
Rate 20-30 15-25 10-20 <10
I. time 0.3-0.6 0.6-0.7 0.7-0.9 >0.9
PEEP 0-7

38. Ventilator settings in our patient:
TV 400 ml, RR12, Fi02 1.0
ABG: pH 7.04 / PCO2 109 / PO2 403
PIP > 45 cm H2O; Ppl 35 cm H20
PEEP 0

39. Permissive hypercapnea
Deliberate induction of alveolar hypoventilation
and acceptance of hypercapnea.
Hypercapnea is not the goal of this approach;
rather, it is a secondary effect of the attempt to
limit airway pressures.

40. Acidosis in PH
Intracellular buffering is rapid, reaching 90 percent
completion within three hours after the onset of
hypercapnia.
It is advised that hypercapnia be achieved in steps
not exceeding 10 mmHg; smaller increments should
be used when the PCO2 exceeds 80 mmHg

41. Oxygenation in PH
The reduction in minute ventilation associated with
PH has the potential to lower the arterial PO2.
This may be compounded by increased
intrapulmonary shunt (increased PVR) in patients
with ARDS

42. Hemodynamic effects of PH
Increases plasma levels of epinephrine and
norepinephrine.
Increases heart rate, mean pulmonary artery
pressure, right atrial pressure, pulmonary capillary
wedge pressure, right ventricular work (bad)
Increases cardiac output, oxygen delivery, and mixed
venous PO2 (good)

43. Contraindications for PH
Acute cerebrovascular disease (vascular tone)
Seizure disorder (seizure threshold)
Severe pulmonary hypertension with right heart
failure

44. Neurological effects of PH
Hypercapnia leads to cerebral vasodilation,
increased intracranial pressure, and lowering of the
seizure threshold.

45. Patient is receiving continuously nebulized xopenex

46. Other meds
Methylprednisolone
Famotidine
Morphine, versed
Rocuronium
Ceftriaxone, azythromycin

47. Exotic therapies
Ketamine infusion
Inhalation of general anesthetics
Ventilation with heliox
ECMO

48. Ketamine
 Ketamine is a dissociative anesthetic which can
produce bronchodilation.
 Less respiratory depression than most other
anesthetics.
 Produces increased sympathetic tone (BP)
 Other side effects include myocardial depression,
increased secretions and emergence reaction.
 Used most frequently for induction of anesthesia
when intubating asthmatics.
 Usual dose is 0.5-1.0 mg/kg. Continuous infusion
2-4 mg/kg/hour, titrated to effect (sedation and
bronchodilation).

49. Inhaled anesthetic agents
Are known to relieve bronchospasm.
Halogenated gases (isoflurane, enflurane) are most
commonly used
Require mechanical ventilation.
Effects in asthma are attributed to sustained
bronchodilation, possibly by airway reflex blockade
and a direct effect on smooth muscle
Cumbersome, requires presence of
anesthesiologist at the bedside

50. Helium
Helium is an inert gas; less dense than nitrogen.
The administration of a helium-oxygen mixture
(heliox) reduces turbulence of airflow, and helps to
reduce the work of breathing, improves gas
exchange, PCO2 and clinical symptoms.
Nebulized-size particles may be more uniformly
distributed in the airways when administered via
heliox.
The effectiveness of heliox is dependent on the
helium concentration.
Heliox when used in mechanical ventilation will
lower PIP.

53. ABG
pH 7.15
PCO2 78
PO2 90

54. pH 7.15
PCO2 78
PO2 90
ABG

55. Multiple boluses failed to bring serum Mg level to
“therapeutic” range
On continuous xopenex aerosol
Sedation changed to ketamine drip
Condition is essentially unchanged for the next 2-3
days.

56. On day 2 Patient develops
hypertension. Arterial BP is up to
190/120 on day 4
Our choices:
Increase doses of sedatives
Change sedative meds
Give antihypertensive drugs
Vasodilators
Beta blockers
ACE inhibitors
Ca channel blockers

57. Normal BMP
Fluid balance is +1900 ml
Pupils 5 mm, equal and reactive

58. Fluid intake is restricted to provide
maintenance amount
Ketamine is replaced with propofol
Continue fentanyl
BP is still around 150-160/100

59. Enalapril started on day 4
BP is nearly normal

61. What is this?
Pneumonia
Atelectasis

63. This condition is called “plastic
bronchitis”
Not uncommon in life threatening asthma
Treatment is either bronchoscopy to remove
bronchial casts, or ECMO if bronchoscopy fails.

64. Our choices
CPT
Vigorous suction
Bronchial lavage with NS
Bronchial lavage with 2% Na bicarbonte
Pulmozime inhalations
Bronchoscopy

65. Our selection
Bronchial lavages with NS
CPT

67. Ventilator support was weaned during the 3d day. Patient
Continues to receive:
Steroids
Aerosols of bronchodilators
Antibiotics
PPN
Antacids
Sedations stopped and patient is extubated on the 4th
day.
O2 sats immediately after extubation below 80%.

68. RR is <10. Patient is obtunded, good air exchange, no
retractions, mild wheezes, pupils 2mm, equal,
reactive.
What is wrong?

69. Post-paralytic myopathy?
steroids, NMB, aminoglycosides
Central hypoventilation?

70. Respiratory depression was reversed with one dose
of naloxone

72. New issues
Bibasilar atelectasis
Hyperglycemia: serum glucose level
Day 1 149 mg%
Day 2 368 mg%
Day 3 186 mg%
Upper GI bleeding

73. What now?

74. Glucose intolerance
Stress
Steroids
Beta-agonists
Ketamine (epinephrine release)
regular sq insulin started on day 2,
changed to lantus on day 4 ,
PPN, despite hyperglycemia, started on day 3
Serum glucose on day 5 123 mg%

75. Stress ulcer
Danger of life threatening bleeding
Treatment: maintain gastric pH at >4.5
Antacids
H2 blockers
Proton pump inhibitors