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

Complaints

Difficulty of breathingFeeling tiredChest painNever felt so bad before

Complains

Difficulty of breathingFeeling tiredChest painNever felt so bad before

Differential Diagnosis of Severe AsthmaCongestive heart failure/myocardial infarctionPulmonary embolismUpper airway obstructionEpiglottitisForeign body aspirationTumorAnaphylaxis/angioedemaCOPDBronchiolitisVocal cords dysfunctionHyperventilation syndromeAcute bronchitis/pneumonia

TRIAGE

Severe SOBDroolingGruntingWheezes on auscultationHR 160RR 36O2Sat 95% on 15LBP 123/57

TRIAGE

Severe SOBDroolingGruntingWheezes on auscultationHR 160RR 36O2Sat 95% on 15LBP 123/57

ABG in the ER

pH 7.34

PCO2 44

PO2 94

BICARBONATE 23.3

ABG in the ER

pH 7.34

PCO2 44

PO2 94

BICARBONATE 23.3

Patient received nebulized albuterol x 1 and xopenex x 2

PrednisoloneCeftriaxone and Azythromycin

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

History of PI

Cough, running nose, worsening SOB x 2 daysFrequent use of albuterol inhaler x 2 days

History of PI

Cough, running nose, worsening SOB x 2 daysFrequent use of albuterol inhaler x 2 days

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

19:10

HR 160RR 37BP 130/70O2Sat 84% on 15L non-rebreather

19:10

HR 160RR 37BP 130/70O2Sat 84% on 15L non-rebreather

What do we want to do?

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

19:15

Patient is intubatedReceives manual ventilation

Foley catheter

NG tube

Radial arterial line

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 inflating pressures

PIP (Peak Inspiratory Pressure)Ppl (Plateau Pressure)

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.

Patient is receiving continuously nebulized xopenex

Other meds

MethylprednisoloneFamotidineMorphine, versedRocuroniumCeftriaxone, azythromycin

Exotic therapies

Ketamine infusionInhalation of general anestheticsVentilation with helioxECMO

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.

ABG

pH 7.15

PCO2 78

PO2 90

pH 7.15

PCO2 78

PO2 90

ABG

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

Normal BMPFluid balance is +1900 mlPupils 5 mm, equal and reactive

Fluid intake is restricted to provide maintenance amount

Ketamine is replaced with propofolContinue fentanylBP is still around 150-160/100

Enalapril started on day 4BP is nearly normal

What is this?

PneumoniaAtelectasis

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

Our selection

Bronchial lavages with NSCPT

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?

Post-paralytic myopathy?

steroids, NMB, aminoglycosides Central hypoventilation?

Respiratory depression was reversed with one dose of naloxone

New issues

Bibasilar atelectasisHyperglycemia: serum glucose level

Day 1 149 mg%

Day 2 368 mg%

Day 3 186 mg%

Upper GI bleeding

What now?

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%

Stress ulcer

Danger of life threatening bleedingTreatment: maintain gastric pH at >4.5

Antacids

H2 blockers

Proton pump inhibitors