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PRONE VENTILATION
Dr Raman Ghimire
Department of anesthesiology
& Intensive Care
OBJECTIVES
• Case presentation
• Discussion on Prone Ventilation
HISTORY
• SAMBHA SHAH (W/O H/C BIRENDRA SHAH )
• 36yrs/F ; Bara ( currently Kathmandu),housewife
• Presented to NPH ER in (2075/11/15)@ 7;30 am
C/O :
Cough X 5days ;dry
SOB X 3 days ; increased 1 day : MMRC GR IV
Fever X 3 days ;not documented ,chills-,rigors-, sorethroat+
No H/O chest pain, hemoptysis ,swelling of limbs ,LOC ,pain abdomen ,
burning micturation
No H/O similar illness in family members
No H/O recent visit to terai
Taking medication for cough from local medical shop ;4days
H/O visit to Kathmandu model hospital before arrival, managed for RD in ER
nebulization ,inj solumedrol, inj durataz,inj hydrocort ,inj lasix
MH: regular LMP: 2075/11/08
OH: G4 P3+1 L3
P1=12yrs/F ;home delivery
P2=10yrs /F ;NVD @ Hospital
A1=Medical termination after sex determination
P3= 6months /M ;Elective LSCS for GHTN @39WOG
PMH: H/O Gestational HTN ;Tab amlodipine 10mg BD was started;
took for 3months then left
EXAMINATION
GC : ill looking , labored breathing +
dehydration+
GCS: 15/15
VITALS-
SPO2- 80 % with FiO2 60% VM
PR- 130 BPM
BP- 150/80 MMHG
TEMP- 97 F
RR- 32/MIN
• CHEST : B/L equal air
entry ,B/L diffuse wheeze +
,crepts+
• CVS: S1S2M0
• P/A: soft, non tender
• CNS: Grossly intact
• THROAT : NAD
• In ER ; SPO2 was not maintained with VM 60%,
• case shifted to ICU ; kept in NIV
(Ps: 20 , PEEP: 10 ,FIO2; 100%)
• However no improvement ,GCS was dropping( E2 V3 M5 ;10/15 ),
gasping +
• Intubation done
( inj midazolam 2mg ,inj sux 70mg ,inj propofol 100mg)
kept in CMV mode ,VT: 380ml PEEP 16 FiO2: 90%,RR: 22,
• ABG: PH: 7.02 Po2: 96 PCO2: 76 HCO3: 19
PaO2/FiO2:: 96 (severe ARDS)
• CVP line, A-line , OG –tube inserted ,Foley’s insitu
INVESTIGATIONS
• TC: 17000; N 87 L 13
• Hb : 8.6 PLT: 258000
• RBS: 192
• UREA: 34 CREATININE:
0.5
• Na :146 K: 2.4
• URINE RE:
ALB;++ PUS: 6-8 RBC: 14-16
• CPK-MB :25
• TROPONIN-I : WEAK +VE
• ABG:
P H: 7.1 Po2: 76 PCO2: 38
HCO3: 14
PaO2/FiO2:: 84 (severe ARDS)
ISSUES:
• TC: 17000
• Respiratory system
B/l pneumonia (diffuse infiltrates in CXR)
Severe ARDS with hypoxemia (PF: <100)
• CVS
Troponin I : weak positive (? Septic cardiomyopathy )
Screening echo: decreased contractility ,no RWMA
Working diagnosis:
oB/L pneumonia with severe ARDS
oseptic cardiomyopathy
oHTN
• Patient kept in prone ventilation
MANAGEMENT
• INJ TEICOPLANIN 400MG IV BD 3DOSES THEN Q72HRLY
• INJ MEROPENEM 2GM IV STAT THEN 1GM IV BD
• INJ DOXYCYCLINE 100MG IV BD
• TAB TAMIFLU(OSELTAMIVIR) 75MG PO BD
• INJ HYDROCORT 50MG IV QID
• TAB THIAMINE 200MG PO BD
• TAB VIT C 1500MG PO QID
• INJ ENOXAPARIN 60MG SC STAT THEN 40MG OD
• TAB ECOSPIRIN 300MG PO STAT THEN 75MG PO OD
• TAB ATORVASTATIN 20MG PO HS
• INJ DOBUTAMINE 2.5ML/HR
• INJ ATRACURIUM 10MG/HR
• INJ MORPHINE 5MG /HR
• IVF 100CC/HR (RL)
• I/O CHARTING
• OG FEEDING
• SUCTIONING OF ET-TUBE, OROPHARYNX Q2HRLY
• Blood for tropical disease profile ,C/S
• Oropharyngeal swab sent for influenza serology
11/16 (D1):
Patient turned to supine position from prone ventilation (for
SEVERE ARDS with REFRACTORY HYPOXEMIA ) after 20hrs.
Patient under PCV mode ; FiO2:40% PEEP : 8
P H: 7.2 Po2: 83 PCO2: 36
HCO3: 14
(PF: 207)
TC: 15000; N 92 L 8
Hb : 10.3 PLT: 194,000
RBS:95
UREA: 75 CREATININE: 1.9
Na :143 K: 3.6
RENAL INVOLVEMENT
11/17(D2):
• Pt extubated @10:AM
• Persistent high BP
• TAB AMLOD 10MG PO BD
• TAB PRAZOSIN 5MG PO TDS
• TAB METOPROLOL XL 25MG PO OD
• INJ LABETALOL 10MG /HR
• PH: 7.27 Po2: 84
PCO2: 31 HCO3: 14 PF: 210
• TC: 16600; N 90 L 10
• Hb : 10 PLT: 181,000
• RBS:112
• UREA: 125 CREATININE: 3.8
• Na :144 K: 4.8
• CPK-MB :175
• TROPONIN-I : POSITIVE
Imp: B/L pneumonia with ARDS with septic cardiomyopathy with AKI
with HTN
• INFLUENZA A& B : NEGATIVE
• Scrub typhus (IgM Ab) : NEGATIVE
• BRUCELLA (ABORTUS/MELITENSIS) Ab: NEGATIVE
• LEPTOSPIRA IgM: NEGATIVE IgG: NEGATIVE
• URINE C/S : NO GROWTH SUCTION TIP C/S : NO GROWTH
• BLOOD C/S: NO GROWTH
• SPUTUM C/S: NO GROWTH AFB I & II : NEGATIVE
• ECHO : NORMAL STUDY
• USG A/P : MILDLY ECHOGENIC KIDNEY WITH MAINTAINED
CMD,SUBCUTANEOUS OEDEMA IN ANTERIOR ABDOMINAL WALL,
RT SIDED PLEURAL EFFUSION.
• TFT:; T3: 2.1 T4: 10.6 TSH: 0.22
• ANA: negative ds DNA : 5 (N <30)
• HBsAg: NR HCV; NR HIV 1&2: NR
INVX 11/18 (D 3) 11/19(D4) 11/20(D 5) 11/21 (D 6) 11/22(D 7)
TC/DC 12200;
90;10
12600;
90;10
13300;
85;13
11500
78;20
11200
73;23
Hb 9.9 10.2 12.3 10.8 10.8
PLT 165000 191000 183000 190000 200000
RBS 105 151 100 101 82
UREA 145 140 125 104 83
CREATININE 4.1 3.3 2.5 2.4 1.7
Na - 138 148 143 142
K - 3.2 3 3.1 4.3
URINE RE Alb :++
PUS: 4-6
RBC: 15-20
Yeast cells: 12-15
Alb : nil
Pus: 4-6
RBC: 3-5
Alb : nil
Pus: 4-6
RBC: 0-2
TROPONIN-I
CPK-MB
92
NEGATIVE
ABG P H: 7.34
Po2: 65
PCO2: 23
HCO3: 12
P H: 7.35
Po2: 81
PCO2: 26
HCO3: 14
DAY OF ADMISSION 7TH DAY
• Antibiotics and Tamiflu stopped after completion of 7th day
• BP maintained with Tab amlod ,metoprolol,prazopress
• SPO2 maintained in RA
• RFT improving ,I/O status;N
• CXR: N URME :N , ABG : N
• Patient feeding well
• No fresh complains
• Shifted to Medical ward 8th day (2075/11/23)
PRONE VENTILATION
ACUTE RESPIRATORY DISTRESS SYNDROME
ARDS is an acute life threatening inflammatory lung injury manifested
by hypoxia and stiff lungs due to increased pulmonary vascular
permeability and almost always requiring mechanical ventilation
support.
• American-European Consensus Conference (AECC) ,1994
VS Berlin Definition ,2012
• better prediction for mortality with increased percentage of
mortality associated with increasing stages of ARDS .
ARDS Berlin defination ,2012
(1) Timing: Respiratory symptoms must have begun within one week of a
known clinical insult, or the patient must have new or worsening symptoms
during the past week.
(2) Chest imaging: Bilateral opacities consistent with pulmonary
edema must be present on a chest radiograph or computed tomographic scan,
which is not fully explained by pleural effusions, lobar collapse, lung collapse, or
pulmonary nodules.
(3) Origin of edema: The patient’s respiratory failure must not be fully
explained by cardiac failure or fluid overload. An objective assessment
(e.g., echocardiography) to exclude hydrostatic pulmonary edema is required if
no risk factors for ARDS are present.
(4) Oxygenation: A moderate to severe impairment of oxygenation must
be present, as defined by the PaO2/ FiO2 ratio.
The severity of the hypoxemia defines the severity of the ARDS:
(A) Mild ARDS:
PaO2/FiO2 :200 -300 mmHg,
on a ventilator with a positive end-expiratory pressure (PEEP) or
continuous positive airway pressure ≥ 5 cm H2O.
(B) Moderate ARDS:
PaO2/ FiO2 : 100 - 200 mmHg,
on a ventilator with a PEEP ≥ 5 cm H2O.
(C) Severe ARDS :
PaO2/ FiO2 : ≤ 100 mmHg
on a ventilator with a PEEP ≥ 5 cm H2O.
ARDS PREDICTED
MORTALITY
mild 27%,
moderate 32%
severe 45%
PRONE VENTILATION
PRONE VENTILATION
• Bryan et al ,1974
from studies on the effects of sedation and paralysis on the diaphragm.
• Piehl et al, 1976
reported dramatic effects on oxygenation improvement by prone position in
five patients with ARDS
• Douglas et al ,1977
confirming that prone positioning could effectively improve oxygenation in 6
pts with ARDS
• Earlier trials could not demonstrate a mortality benefit of prone-
position over supine position ventilation
• Proning Severe ARDS Patients (PROSEVA) trial , 2013
demonstrated a significant mortality benefit with prone ventilation.
• Subsequent meta-analyses, support the role of prone positioning as
an effective therapy to reduce mortality in severe ARDS
Physiological aims of prone positioning are:
1) to improve oxygenation
2) to improve respiratory mechanics
3) to homogenise the pleural pressure gradient, the alveolar inflation and the ventilation
distribution
4) to increase lung volume and reduce the amount of atelectatic regions
5) to facilitate the drainage of secretions
6) to reduce ventilator-associated lung injury
1. Gravity
2. Shape of
chest wall
3. Heart and
diaphragm
SUPINE PRONE
Conclusion
• PP improves oxyygenation , prevent VALI, decrease
complications , mortality and ICU stay .
• Patients with ARDS and severe hypoxemia can benefit
from prone treatment
when it is used early
relatively long sessions(min 16hrs/day).
Low tidal volume
REFERENCES
• Acute Respiratory Distress Syndrome: An Update and Review ,Gautam
Rawal,*,1 Sankalp Yadav,2 and Raj Kumar3
• ARDS Definition Task Force. Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND,
Caldwell E. et al. ARDS Definition Task Force. Acute respiratory distress syndrome: The Berlin
Definition. JAMA. 2012;307:2526–33.
• Prone Positioning in Severe Acute Respiratory Distress Syndrome: NEJM
Claude Guérin, M.D., Ph.D., Jean Reignier, M.D., Ph.D., Jean-Christophe Richard, Ph.D., Pascal Beuret, M.D.,Arnaud
Gacouin, M.D., Thierry Boulain, M.D., Emmanuelle Mercier, M.D., Michel Badet, M.D.
• Treatment of ARDS With Prone Positioning
Eric L. Scholten, MD,a,∗ Jeremy R. Beitler, MD, MPH,a G. Kim Prisk, PhD, DSc,b and Atul Malhotra, MDa
• The efficacy and safety of prone positioning in adults patients
with acute respiratory distress syndrome: a meta-analysis of
randomized controlled trials
So Young Park1, Hyun Jung Kim2, Kwan Ha Yoo3, Yong Bum Park1, Seo Woo Kim4, Seok Jeong Lee4, Eun
Kyung Kim5, Jung Hyun Kim5, Yee Hyung Kim6, Ji-yong Moon7, Kyung Hoon Min8, Sung Soo Park9,
Jinwoo Lee9, Chang-Hoon Lee9, Jinkyeong Park10, Min Kwang Byun11, Sei Won Lee12, ChinKook Rlee13,
Ji Ye Jung11, Yun Su Sim14
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Prone ventilation

  • 1. PRONE VENTILATION Dr Raman Ghimire Department of anesthesiology & Intensive Care
  • 2. OBJECTIVES • Case presentation • Discussion on Prone Ventilation
  • 3. HISTORY • SAMBHA SHAH (W/O H/C BIRENDRA SHAH ) • 36yrs/F ; Bara ( currently Kathmandu),housewife • Presented to NPH ER in (2075/11/15)@ 7;30 am C/O : Cough X 5days ;dry SOB X 3 days ; increased 1 day : MMRC GR IV Fever X 3 days ;not documented ,chills-,rigors-, sorethroat+ No H/O chest pain, hemoptysis ,swelling of limbs ,LOC ,pain abdomen , burning micturation No H/O similar illness in family members No H/O recent visit to terai Taking medication for cough from local medical shop ;4days H/O visit to Kathmandu model hospital before arrival, managed for RD in ER nebulization ,inj solumedrol, inj durataz,inj hydrocort ,inj lasix
  • 4. MH: regular LMP: 2075/11/08 OH: G4 P3+1 L3 P1=12yrs/F ;home delivery P2=10yrs /F ;NVD @ Hospital A1=Medical termination after sex determination P3= 6months /M ;Elective LSCS for GHTN @39WOG PMH: H/O Gestational HTN ;Tab amlodipine 10mg BD was started; took for 3months then left
  • 5. EXAMINATION GC : ill looking , labored breathing + dehydration+ GCS: 15/15 VITALS- SPO2- 80 % with FiO2 60% VM PR- 130 BPM BP- 150/80 MMHG TEMP- 97 F RR- 32/MIN • CHEST : B/L equal air entry ,B/L diffuse wheeze + ,crepts+ • CVS: S1S2M0 • P/A: soft, non tender • CNS: Grossly intact • THROAT : NAD
  • 6. • In ER ; SPO2 was not maintained with VM 60%, • case shifted to ICU ; kept in NIV (Ps: 20 , PEEP: 10 ,FIO2; 100%) • However no improvement ,GCS was dropping( E2 V3 M5 ;10/15 ), gasping + • Intubation done ( inj midazolam 2mg ,inj sux 70mg ,inj propofol 100mg) kept in CMV mode ,VT: 380ml PEEP 16 FiO2: 90%,RR: 22, • ABG: PH: 7.02 Po2: 96 PCO2: 76 HCO3: 19 PaO2/FiO2:: 96 (severe ARDS) • CVP line, A-line , OG –tube inserted ,Foley’s insitu
  • 7. INVESTIGATIONS • TC: 17000; N 87 L 13 • Hb : 8.6 PLT: 258000 • RBS: 192 • UREA: 34 CREATININE: 0.5 • Na :146 K: 2.4 • URINE RE: ALB;++ PUS: 6-8 RBC: 14-16 • CPK-MB :25 • TROPONIN-I : WEAK +VE • ABG: P H: 7.1 Po2: 76 PCO2: 38 HCO3: 14 PaO2/FiO2:: 84 (severe ARDS)
  • 8. ISSUES: • TC: 17000 • Respiratory system B/l pneumonia (diffuse infiltrates in CXR) Severe ARDS with hypoxemia (PF: <100) • CVS Troponin I : weak positive (? Septic cardiomyopathy ) Screening echo: decreased contractility ,no RWMA
  • 9. Working diagnosis: oB/L pneumonia with severe ARDS oseptic cardiomyopathy oHTN
  • 10. • Patient kept in prone ventilation
  • 11. MANAGEMENT • INJ TEICOPLANIN 400MG IV BD 3DOSES THEN Q72HRLY • INJ MEROPENEM 2GM IV STAT THEN 1GM IV BD • INJ DOXYCYCLINE 100MG IV BD • TAB TAMIFLU(OSELTAMIVIR) 75MG PO BD • INJ HYDROCORT 50MG IV QID • TAB THIAMINE 200MG PO BD • TAB VIT C 1500MG PO QID • INJ ENOXAPARIN 60MG SC STAT THEN 40MG OD • TAB ECOSPIRIN 300MG PO STAT THEN 75MG PO OD • TAB ATORVASTATIN 20MG PO HS • INJ DOBUTAMINE 2.5ML/HR • INJ ATRACURIUM 10MG/HR • INJ MORPHINE 5MG /HR
  • 12. • IVF 100CC/HR (RL) • I/O CHARTING • OG FEEDING • SUCTIONING OF ET-TUBE, OROPHARYNX Q2HRLY • Blood for tropical disease profile ,C/S • Oropharyngeal swab sent for influenza serology
  • 13. 11/16 (D1): Patient turned to supine position from prone ventilation (for SEVERE ARDS with REFRACTORY HYPOXEMIA ) after 20hrs. Patient under PCV mode ; FiO2:40% PEEP : 8 P H: 7.2 Po2: 83 PCO2: 36 HCO3: 14 (PF: 207) TC: 15000; N 92 L 8 Hb : 10.3 PLT: 194,000 RBS:95 UREA: 75 CREATININE: 1.9 Na :143 K: 3.6 RENAL INVOLVEMENT
  • 14. 11/17(D2): • Pt extubated @10:AM • Persistent high BP • TAB AMLOD 10MG PO BD • TAB PRAZOSIN 5MG PO TDS • TAB METOPROLOL XL 25MG PO OD • INJ LABETALOL 10MG /HR • PH: 7.27 Po2: 84 PCO2: 31 HCO3: 14 PF: 210 • TC: 16600; N 90 L 10 • Hb : 10 PLT: 181,000 • RBS:112 • UREA: 125 CREATININE: 3.8 • Na :144 K: 4.8 • CPK-MB :175 • TROPONIN-I : POSITIVE Imp: B/L pneumonia with ARDS with septic cardiomyopathy with AKI with HTN
  • 15. • INFLUENZA A& B : NEGATIVE • Scrub typhus (IgM Ab) : NEGATIVE • BRUCELLA (ABORTUS/MELITENSIS) Ab: NEGATIVE • LEPTOSPIRA IgM: NEGATIVE IgG: NEGATIVE • URINE C/S : NO GROWTH SUCTION TIP C/S : NO GROWTH • BLOOD C/S: NO GROWTH • SPUTUM C/S: NO GROWTH AFB I & II : NEGATIVE • ECHO : NORMAL STUDY • USG A/P : MILDLY ECHOGENIC KIDNEY WITH MAINTAINED CMD,SUBCUTANEOUS OEDEMA IN ANTERIOR ABDOMINAL WALL, RT SIDED PLEURAL EFFUSION. • TFT:; T3: 2.1 T4: 10.6 TSH: 0.22 • ANA: negative ds DNA : 5 (N <30) • HBsAg: NR HCV; NR HIV 1&2: NR
  • 16. INVX 11/18 (D 3) 11/19(D4) 11/20(D 5) 11/21 (D 6) 11/22(D 7) TC/DC 12200; 90;10 12600; 90;10 13300; 85;13 11500 78;20 11200 73;23 Hb 9.9 10.2 12.3 10.8 10.8 PLT 165000 191000 183000 190000 200000 RBS 105 151 100 101 82 UREA 145 140 125 104 83 CREATININE 4.1 3.3 2.5 2.4 1.7 Na - 138 148 143 142 K - 3.2 3 3.1 4.3 URINE RE Alb :++ PUS: 4-6 RBC: 15-20 Yeast cells: 12-15 Alb : nil Pus: 4-6 RBC: 3-5 Alb : nil Pus: 4-6 RBC: 0-2 TROPONIN-I CPK-MB 92 NEGATIVE ABG P H: 7.34 Po2: 65 PCO2: 23 HCO3: 12 P H: 7.35 Po2: 81 PCO2: 26 HCO3: 14
  • 17. DAY OF ADMISSION 7TH DAY
  • 18. • Antibiotics and Tamiflu stopped after completion of 7th day • BP maintained with Tab amlod ,metoprolol,prazopress • SPO2 maintained in RA • RFT improving ,I/O status;N • CXR: N URME :N , ABG : N • Patient feeding well • No fresh complains • Shifted to Medical ward 8th day (2075/11/23)
  • 20. ACUTE RESPIRATORY DISTRESS SYNDROME ARDS is an acute life threatening inflammatory lung injury manifested by hypoxia and stiff lungs due to increased pulmonary vascular permeability and almost always requiring mechanical ventilation support. • American-European Consensus Conference (AECC) ,1994 VS Berlin Definition ,2012 • better prediction for mortality with increased percentage of mortality associated with increasing stages of ARDS .
  • 21. ARDS Berlin defination ,2012 (1) Timing: Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week. (2) Chest imaging: Bilateral opacities consistent with pulmonary edema must be present on a chest radiograph or computed tomographic scan, which is not fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules. (3) Origin of edema: The patient’s respiratory failure must not be fully explained by cardiac failure or fluid overload. An objective assessment (e.g., echocardiography) to exclude hydrostatic pulmonary edema is required if no risk factors for ARDS are present. (4) Oxygenation: A moderate to severe impairment of oxygenation must be present, as defined by the PaO2/ FiO2 ratio.
  • 22. The severity of the hypoxemia defines the severity of the ARDS: (A) Mild ARDS: PaO2/FiO2 :200 -300 mmHg, on a ventilator with a positive end-expiratory pressure (PEEP) or continuous positive airway pressure ≥ 5 cm H2O. (B) Moderate ARDS: PaO2/ FiO2 : 100 - 200 mmHg, on a ventilator with a PEEP ≥ 5 cm H2O. (C) Severe ARDS : PaO2/ FiO2 : ≤ 100 mmHg on a ventilator with a PEEP ≥ 5 cm H2O.
  • 24.
  • 26. PRONE VENTILATION • Bryan et al ,1974 from studies on the effects of sedation and paralysis on the diaphragm. • Piehl et al, 1976 reported dramatic effects on oxygenation improvement by prone position in five patients with ARDS • Douglas et al ,1977 confirming that prone positioning could effectively improve oxygenation in 6 pts with ARDS
  • 27. • Earlier trials could not demonstrate a mortality benefit of prone- position over supine position ventilation • Proning Severe ARDS Patients (PROSEVA) trial , 2013 demonstrated a significant mortality benefit with prone ventilation. • Subsequent meta-analyses, support the role of prone positioning as an effective therapy to reduce mortality in severe ARDS
  • 28. Physiological aims of prone positioning are: 1) to improve oxygenation 2) to improve respiratory mechanics 3) to homogenise the pleural pressure gradient, the alveolar inflation and the ventilation distribution 4) to increase lung volume and reduce the amount of atelectatic regions 5) to facilitate the drainage of secretions 6) to reduce ventilator-associated lung injury
  • 29. 1. Gravity 2. Shape of chest wall 3. Heart and diaphragm
  • 31.
  • 32.
  • 33.
  • 34.
  • 35. Conclusion • PP improves oxyygenation , prevent VALI, decrease complications , mortality and ICU stay . • Patients with ARDS and severe hypoxemia can benefit from prone treatment when it is used early relatively long sessions(min 16hrs/day). Low tidal volume
  • 36. REFERENCES • Acute Respiratory Distress Syndrome: An Update and Review ,Gautam Rawal,*,1 Sankalp Yadav,2 and Raj Kumar3 • ARDS Definition Task Force. Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E. et al. ARDS Definition Task Force. Acute respiratory distress syndrome: The Berlin Definition. JAMA. 2012;307:2526–33. • Prone Positioning in Severe Acute Respiratory Distress Syndrome: NEJM Claude Guérin, M.D., Ph.D., Jean Reignier, M.D., Ph.D., Jean-Christophe Richard, Ph.D., Pascal Beuret, M.D.,Arnaud Gacouin, M.D., Thierry Boulain, M.D., Emmanuelle Mercier, M.D., Michel Badet, M.D. • Treatment of ARDS With Prone Positioning Eric L. Scholten, MD,a,∗ Jeremy R. Beitler, MD, MPH,a G. Kim Prisk, PhD, DSc,b and Atul Malhotra, MDa • The efficacy and safety of prone positioning in adults patients with acute respiratory distress syndrome: a meta-analysis of randomized controlled trials So Young Park1, Hyun Jung Kim2, Kwan Ha Yoo3, Yong Bum Park1, Seo Woo Kim4, Seok Jeong Lee4, Eun Kyung Kim5, Jung Hyun Kim5, Yee Hyung Kim6, Ji-yong Moon7, Kyung Hoon Min8, Sung Soo Park9, Jinwoo Lee9, Chang-Hoon Lee9, Jinkyeong Park10, Min Kwang Byun11, Sei Won Lee12, ChinKook Rlee13, Ji Ye Jung11, Yun Su Sim14

Hinweis der Redaktion

  1. LCB: 6m
  2. IN VIEW of severe ARDS with hypoxemia
  3. Teico: gm+ve : + MRSA …… mero: gm + /_ ,,,antiviral for influenza a/b MARIK COCKTAIL IN SEPSIS
  4. Recommended duration is at least for 16 hrs
  5. AECC: pwcp <18mmhg… ALI PF<300 ARDS< 200 (No PEEP )
  6. Carrico index and the PF ratio…
  7. After 40 yrs…proseva
  8.  the alveolar density is more posteriorly. [12] In supine position, these posterior alveoli get compressed due to various reasons such as: (1) Action of gravity, (2) shape of the chest wall: The anterior lung parenchyma is more conical than the posterior lung parenchyma. The anterior alveoli thus have a greater volume of intra-thoracic cavity available to expand and are thus more distended than the posterior alveoli and (3) the heart and diaphragm further act under gravity to compress posterior alveoli. he total recruitment of alveoli is more in prone-position than in supine position because the posterior lung parenchyma comes in non-dependent position and hence their compression due to gravity is prevented and also because the heart and diaphragm no longer act under gravity to compress alveoli.
  9. Proseva landmark trial However, meta-analyses have suggested that survival is significantly improved with prone positioning PROSEVA has shown significant decrease in mortality (about 50%)
  10. A reduction of 50% in mortality is absolutely unheard of in the ARDS literature.  While the results seem “too good to be true”, it’s difficult to ignore.