Status asthmaticus
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Transcript of Status asthmaticus
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
Differential Diagnosis of Severe AsthmaCongestive heart failure/myocardial infarctionPulmonary embolismUpper airway obstructionEpiglottitisForeign body aspirationTumorAnaphylaxis/angioedemaCOPDBronchiolitisVocal cords dysfunctionHyperventilation syndromeAcute bronchitis/pneumonia
PM History
Known asthmatic, used steroids in the past, uses albuterol inhaler now
Immunization is UTDLives at home with the familyFamily history is non-contributoryNo previous admissions
PE
Alert, oriented, consolable, interactiveAfebrileAble to speak in short phrases onlyGrunting, drooling, retractions, bilateral wheezes Well hydratedHEENT normalCV normal except tachycardiaAbdomen normal
PE
Alert, oriented, consolable, interactiveAfebrileAble to speak in short phrases onlyGrunting, drooling, retractions, bilateral wheezes Well hydratedHEENT normalCV normal except tachycardiaAbdomen normal
Our choices
Continuous inhalation of beta agonistsAtroventIV MgSO4Continuous infusion of beta agonistsContinuous infusion of aminophyllineEndotracheal intubation and mechanical ventilation
Continuous inhalation of beta agonists
Titrate to effectTachycardia in children is well toleratedThe rule of thumb: allow HR to increase by 50%
over mean for the age
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.
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.
Continuous infusion of beta-agonistsTerbutaline 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).
Aminophylline
The mechanism of bronchodilatation is likely explained by PDE inhibition, resulting in an increase in cAMP (different from beta agonists)
A relatively weak bronchodilatorAnti-inflammatory effect Reverses diaphragm fatigue
Risk Factors for Near-Fatal AsthmaPrior 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 sexPoor socioeconomic status
Mechanical ventilation strategies in status asthmaticus
Provide adequate oxygenationAvoid dynamic hyperinflation and autoPEEP
(intrinsic PEEP)Avoid high inflating pressure
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
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
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
High level of measured PIP may greatly exceed pressure in the distal airways and
alveoli due to pressure drops across areas of obstruction
Ventilator settings in status asthmaticus
Mode PC, PRVC, VCTV low to “normal”RR slowFiO2 keep O2Sat above 90% if
possibleI:E ratio no less than 1:3, preferably 1:4 or higher
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
Ventilator settings in our patient:TV 400 ml, RR12, Fi02 1.0ABG: pH 7.04 / PCO2 109 / PO2 403PIP > 45 cm H2O; Ppl 35 cm H20PEEP 0
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.
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
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
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)
Contraindications for PH
Acute cerebrovascular disease (vascular tone)Seizure disorder (seizure threshold)Severe pulmonary hypertension with right heart
failure
Neurological effects of PH
Hypercapnia leads to cerebral vasodilation, increased intracranial pressure, and lowering of the seizure threshold.
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).
Inhaled anesthetic agents
Are known to relieve bronchospasm. Halogenated gases (isoflurane, enflurane) are most
commonly usedRequire 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
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.
Multiple boluses failed to bring serum Mg level to “therapeutic” range
On continuous xopenex aerosolSedation changed to ketamine drip
Condition is essentially unchanged for the next 2-3 days.
On day 2 Patient develops
hypertension. Arterial BP is up to 190/120 on day 4
Our choices:Increase doses of sedativesChange sedative medsGive antihypertensive drugs Vasodilators
Beta blockers
ACE inhibitors
Ca channel blockers
Fluid intake is restricted to provide maintenance amount
Ketamine is replaced with propofolContinue fentanylBP is still around 150-160/100
This condition is called “plastic bronchitis”
Not uncommon in life threatening asthmaTreatment is either bronchoscopy to remove
bronchial casts, or ECMO if bronchoscopy fails.
Our choices
CPTVigorous suctionBronchial lavage with NSBronchial lavage with 2% Na bicarbontePulmozime inhalationsBronchoscopy
Ventilator support was weaned during the 3d day. Patient Continues to receive:
SteroidsAerosols of bronchodilatorsAntibioticsPPNAntacids
Sedations stopped and patient is extubated on the 4th day. O2 sats immediately after extubation below 80%.
RR is <10. Patient is obtunded, good air exchange, no retractions, mild wheezes, pupils 2mm, equal, reactive.
What is wrong?
New issues
Bibasilar atelectasisHyperglycemia: serum glucose level
Day 1 149 mg%
Day 2 368 mg%
Day 3 186 mg%
Upper GI bleeding
Glucose intolerance
StressSteroidsBeta-agonistsKetamine (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%