ARDS Management in

COVID-19

PRASENOHADI

• Perhimpunan Dokter Paru Indonesia

• Departemen Pulmonologi dan Kedokteran Respirasi FKUI
RSUP Persahabatan - Jakarta
INTRODUCTION

• Acute respiratory distress syndrome (ARDS) is a syndrome of acute

respiratory failure caused by non-cardiogenic pulmonary edema.
• The most common clinical disorders associated with the development
of ARDS are bacterial and viral pneumonia.
• ARDS is also commonly caused by sepsis due to non-pulmonary
sources, severe trauma, and aspiration of gastric contents, and less
commonly by pancreatitis and drug reactions.

Matthay MA, et al. J Clin Invest. 2012;122(08):2731–40.

Common Risk Factors for ARDS
Risk factor
• Pneumonia
• Non-pulmonary sepsis
• Aspiration of gastric contents
• Major trauma
• Pulmonary contusion
• Pancreatitis
• Inhalational injury
• Severe burns
• Non-cardiogenic shock
• Drug overdose
• Multiple transfusions or transfusion-associated acute lung injury (TRALI)
• Pulmonary vasculitis
• Drowning
The ARDS Definition Task Force. JAMA. 2012;307(23):2526-33.
Ferguson ND, et al. Intensive Care Med. 2012;38:1573–82.
The Berlin definition of ARDS
Acute respiratory distress syndrome
Timing
• Within 1 week of a known clinical insult or new/worsening respiratory
symptoms
Chest imaging
• Bilateral opacities—not fully explained by effusions, lobar/lung collapse,
or nodules
Origin of edema
• Respiratory failure not fully explained by cardiac failure or fluid overload;
• Need objective assessment (e.g., echocardiography) to exclude
hydrostatic edema if no risk factor present
The ARDS Definition Task Force. JAMA. 2012;307(23):2526-33.
Ferguson ND, et al. Intensive Care Med. 2012;38:1573–82.
The Berlin definition of ARDS
Oxygenation
Mild
• 200 < PaO2/FiO2  300 with PEEP or CPAP ≥ 5 cmH2O
Moderate
• 100 < PaO2/FiO2 ≤ 200 with PEEP ≥ 5 cmH2O
Severe
• PaO2/FiO2 ≤ 100 with PEEP ≥ 5 cmH2O
The ARDS Definition Task Force. JAMA. 2012;307(23):2526-33.
Ferguson ND, et al. Intensive Care Med. 2012;38:1573–82.
 Acute Respiratory Distress Syndrome (WHO)

Onset:
• new or worsening respiratory symptoms within one week of known clinical insult.

Chest imaging (radiograph, CT scan, or lung ultrasound):

• bilateral opacities, not fully explained by effusions, lobar or lung collapse, or
nodules.

Origin of edema:
• respiratory failure not fully explained by cardiac failure or fluid overload. Need
objective assessment (e.g. echocardiography) to exclude hydrostatic cause of
edema if no risk factor present.

ARDS Definition Task Force. JAMA. 2012;307:2526-33.

Riviello ED, et al. Am J Respir Crit Care Med. 2016;193:52-9.
Khemani RG, et al. Pediatr Crit Care Med. 2015;16:S23-40.
WHO. Clinical management of SARI when novel coronavirus (‎n ‎ CoV)‎‎infection is suspected. January 2010.
Acute Respiratory Distress Syndrome (WHO)

Oxygenation (adults)
• Mild ARDS: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg (with PEEP or CPAP ≥5 cmH2O, or non-
ventilated)
• Moderate ARDS: 100 mmHg < PaO2/FiO2 ≤200 mmHg with PEEP ≥5 cmH2O, or non-ventilated)
• Severe ARDS: PaO2/FiO2 ≤ 100 mmHg with PEEP ≥5 cmH2O, or non-ventilated)
• When PaO2 is not available, SpO2/FiO2 ≤315 suggests ARDS (including in non-ventilated
patients)

Oxygenation (children; note OI = Oxygenation Index and OSI = Oxygenation Index using SpO2)
• Bilevel NIV or CPAP ≥5 cmH2O via full face mask: PaO2/FiO2 ≤ 300 mmHg or SpO2/FiO2 ≤264
• Mild ARDS (invasively ventilated): 4 ≤ OI < 8 or 5 ≤ OSI < 7.5
• Moderate ARDS (invasively ventilated): 8 ≤ OI < 16 or 7.5 ≤ OSI < 12.3
• Severe ARDS (invasively ventilated): OI ≥ 16 or OSI ≥ 12.3

ARDS Definition Task Force. JAMA. 2012;307:2526-33.

Riviello ED, et al. Am J Respir Crit Care Med. 2016;193:52-9.
Khemani RG, et al. Pediatr Crit Care Med. 2015;16:S23-40.
WHO. Clinical management of SARI when novel coronavirus (‎n ‎ CoV)‎‎infection is suspected. January 2010.
Case-Fatality Rate by Age Group in Italy and China

Onder G, et al. JAMA. March 2020.

 Patogenesis ARDS

• Levy BD, Shapiro SD. Acute respiratory distress syndrome. In: Loscalzo J, editor.
Harrison’s pulmonary and critical care medicine. New York: The McGraw-Hill; 2010.p.290–6.
• N Engl J Med 2000;342:1334-49.
 Fase Proliperatif Alveolus Normal

Fase Fibrotik Fase Eksudatif

Lancet, April 2016.
Hubungan Antara Fase Eksudatif, Fase Proliferatif
dan Fase Fibrosis pada Pasien ARDS

Lancet, July 2013.

Aligning Therapeutic Options of ARDS

Ferguson ND, et al. Intensive Care Med. 2012;38:1573–82.

 Prinsip Tatalaksana ARDS
• Penilaian klinis awal  kegagalan respirasi.
• Terapi O2, monitor saturasi dan mencari faktor risiko
ARDS.
• Penilaian objektif  analisis gas darah dan foto toraks
• Pertimbangkan  intubasi dan ventilasi mechanis.
• Low tidal volume, low plateau pressure, lung-protective
ventilator strategies.
• Terapi cairan, nutrisi, pencegahan infeksi dan mengatasi
komplikasi.
• Pertimbangkan  rujuk layanan tersier (uji klinis dan
teknik canggih).
Am Fam Physician. 2003;67:315-22.
 Rekomendasi Tatalaksana ARDS Berbasis Bukti
Tatalaksana Rekomendasi
Ventilasi mekanis :
• Low tidal volume A
• High-PEEP atau “open-lung” C
• Prone position C
• Recruitment maneuvers C
• High-frequency ventilation dan ECMO D

Minimalisasi tekanan atrium kiri B

Glukokortikoid C
Surfactant replacement, inhalasi nitrit oksida D
dan terapi anti-inflamasi lain (ketokonazol,
PGE1, NSAIDs)

Levy BD, Shapiro SD. Acute respiratory distress syndrome. In: Loscalzo J, editor.
Harrison’s pulmonary and critical care medicine. New York: The McGraw-Hill; 2010.p.290–6.
Computed tomography (CT) scans showing the shift of densities from
the dorsal to the ventral regions of the lung during the prone
position, and the complete reversal when the patient is turned to the
supine position. This led to the idea of the “sponge model.”

Gattinoni L, et al. Semin Respir Crit Care Med. 2019;40:94–100.

 The original explanation (panel A) for the
improvement of oxygenation was that the
ventral regions that were thought to be not
affected by ARDS when the patient was
pronated may receive more blood flow
maximizing the V/Q ratio.

The confirmed hypothesis is instead the one

showed in panel B. The amount of tissue in
the dorsal regions of the lung is actually
greater than the one in the ventral part.

Hypothesizing a superimposed pressure

capable of making the lung collapse below
50% of its height, it is clear that if the dorsal
50% becomes nondependent, the amount of
tissue recruited is greater than the one
derecruited in the ventral part (now
dependent) (panel B: U, upper; L, lower).

Gattinoni L, et al. Semin Respir Crit Care Med. 2019;40:94–100.

Int. J. Care Injured 2013;44:1700–9.
Management of Patients with ARDS
Grasselli G, et al. JAMA. April 2020.
Patients were admitted between 2/20/2020 and 3/18/2020, with follow-up through 3/25/2020

Grasselli G, et al. JAMA. April 2020.

Grasselli G, et al. JAMA. April 2020.
Persahabatan Hospital

COVID meninggal PDP, meninggal Bukan covid, meninggal

• Venti : 32 /43 : 74.4% • Ventilator : 6 / 20 : 30% • Ventilator : 3 / 5 : 60%
• HNFC : 3 /43 : 6.9% • HFNC : 3 / 20 : 15% • HFNC : 0
• NRM : 8 / 43 : 18.6% • NRM : 6 / 20 : 30% • NRM : 2 / 5 : 40%

• HNFC -> venti : 6 / 32 : 18.8% • HFNC -> venti : 1/6 = 16%

Case 1 (Male) with MV (12-3, 13-3, 16-3-2020)
Case 1 (18-3, 25-3, 30-3-2020)
Case 1 (3-4, 25-3, 7-4-2020)
Case 2 (Male) with HFNC (5-3, 7-3, 9-3-2020)
Case 2 (9-3, 12-3, 16-3-2020)
Case 3
(Female)