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Objectives
Present a case ARDS
Define ARDS and describe the pathological
process Know causes of ARDS, and differential diagnosis Understand specific challenges in mechanical ventilation of patients with ARDS Understand treatment strategies and evidence behind them
General Data
25 M
Day of Admission
3 days PTA
Review of System
No weight loss
No jaundice
No edema No orthopnea and PND No cough
Physical Examinations
At the emergency room conscious, coherent and not in respiratory distress BP - 70/50mmHg HR - 115 bpm T36.8C RR - 24 cpm Sunken eyeball, anicteric sclerae JVP was 2-3 cm, no neck vein engorgement Symmetrical chest expansion,clear breath sounds Adynamic precordium, tachycardic with loud S1 at apex and base, soft pulses Hyperactive bowel sounds
Physical Examinations
At the ward
Awake, conscious, coherent, in respiratory distress BP 60/20 mmHg HR 110 bpm RR 28 32 cpm O2 sat 92 95% Sunken eyeball, icteric sclerae, conjunctival suffusion JVP at 4 cm, no neck vein engorgement Supraclavicular and intercostals muscle contractions,
T - 38.5 C
symmetrical chest expansion, crackles all over his lung fields Adynamic precordium, tachycardic, S1 was louder at both apex and base Soft abdomen, non-tender, normoactive bowel sounds, liver Span - 9 10 cm at right midclavicular line, tymphanitic traubes space Calf tenderness
Diagnosis
Consider Acute Respiratory Distress
1994 Consensus Definition Acute onset (<2 weeks) Bilateral infiltrates on chest xray PCWP 18mmHg or lack of evidence of left atrial hypertension Acute lung injury if PaO2/FiO2 300 ARDS if PaO2/FiO2 200
Differentials
Community Acquired Pneumonia
Management
Initially managed as AGE with severe dehydration
Diagnostics Complete blood count Stool examination, stool culture and sensitivity Serum electrolytes Na, K Creatinine, BUN Long lead II Chest radiograph
Management - therapeutics
Hydrated with normal saline at 90 ml /kg
Initial laboratory results CBC Hgb 79 Hct 0.23 BP - 60/20 mm Hg RBC 3.02 HR 110 bpm Additional diagnostics WBC 16.80 T 38.5C N 0.93 oMAT for leptospires RR 28 32 cpm L 0.04 oBlood culture and Platelet 64 Oxygen saturation 92 95%
sensitivity Conjunctival suffusion, icteric Creatinine 711.9 umol/L oABG sclerae Sodium 140 JVP at 4 cm,Crackles ALF Potassium 3.1 oStarted on inotropics dopamine at 10 Calf tenderness ug/kg/hr No urine output o(ideally norepinephrine) Respiratory to oTarget MAP of Failure 65 mmsecondary Hg Acute drip Respiratory Distress oFurosemide once SBP is at least 100 Syndrome probably secondary to mm Hg Weils Syndrome to oAntibiotic coverage forsecondary leptospirosis Leptospirosis oStarted on mechanical ventilation
FIO2 100%
PEEP 12 cm H20 BUR 20 22 cpm TV 8ml/kg BW for the first
oLow tidal volumes 6-8mL/kg PBW omale = 50 + 0.91(centimeters of height 152.4) = 494.64 ml ofemale = 45.5 + 0.91(centimeters of height 152.4) oPlateau (end-inspiratory) pressures <30cm H20 not done oPEEP allowable combinations
BP stabilize, still with fever and tachycardia Still with inadequate urine output Noted frothy secretion per ETT
Failures.....
To start broad spectrum antibiotics to cover other
possible causes of sepsis AGE Inavailability of Norepinephrine NO ABG To follow ARDS network guidelines on mechanical ventilation
ABG
PH 7.2 HCO3 12.2 PCO2 31.9 PaO2 - 107.7 SaO2 96.9% PaO2/ FIO2 = 107.7 Metabolic acidosis, partially compensated
Referred to Nephrologist Suggested to correct HCO3 deficit Suggested to do emergency renal replacement therapy refused
At 40 hours of admission
oHypotensive even with maximal dose of dopamine, tachycardic, desaturation at 80-90%, T 38.5 C oEdema with crepital sounds at anterior neck and trunk oCrackles all lung field o1 ml/kg/24 hr urine output
Rounds with Pulmonologist Adjusted TV to 6 ml/kg PBW Decrease PEEP to 8cm H2O Suggested to start broad spectrum antibiotics to cover for sepsis
Patient expired....
ARDS
First described 1967 by Ashbaugh and colleagues Severe lung injury characterized by non-cardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemia 1994 Consensus Definition
Acute onset (<2 weeks) Bilateral infiltrates on chest xray PCWP 18mmHg or lack of evidence of left atrial
Epidemiology
Incidence of acute lung injury (ALI): 17.9-78.9
cases per 100,000 person-years Incidence of acute respiratory distress syndrome (ARDS): 13.5-58.7 cases per 100,000 personyears Approx 9% of ICU beds in US
Sepsis (27%)
Aspiration (15%) Trauma (11%)
Pulmonary contusion Multiple fractures
Causes of ARDS
NEJM 2000;342,18:1334-1349
Differential diagnosis
Pulmonary edema from left BOOP or COP Hypersensitivity
heart failure Diffuse alveolar hemorrhage Acute eosinophilic pneumonia Lupus pneumonitis Acute interstitial pneumonia Pulmonary alveolar proteinosis
pneumonitis Leukemic infiltrate Drug-induced pulmonary edema and pneumonitis Acute major pulmonary embolus Sarcoidosis Interstitial pulmonary fibrosis
patients with AIP tended to have more honeycombing and a more symmetrical and lower zone distribution of abnormalities than patients with ARDS
Edema
Hypercapne a
Microvascular occlusion Reductions in pulmonary arterial blood dead space and pulmonary hypertension
enough air
Hypoxemia refractory to oxygen
disorders
cardiogenic pulmonary edema Alveolar and interstitial opacities involving at least three-quarters of the lung fields Bilateral infiltrates worse in dependent lung zone Infiltrates may be
rarely shows
Cardiomegaly Pleural effusions Pulmonary vascular redistribution
NEJM 2000;342,18:1334-1349
Pathology findings
Diffuse alveolar damage
Neutrophils, macrophages, erythrocytes Hyaline membranes Protein-rich edema in alveolar spaces
Alveolar Filling
Hyaline Membranes
Persistent hypoxemia
Pulmonary hypertension
ventilation
May still present with dyspnea, tachypnea and
hypoxemia
Not present in every patient with ARDS, but does
Fibroproliferative - Radiograph
Linear opacities
Fibroproliferative - Radiograph
CT Scan
diffuse interstitial
Proliferative - Histology
First signs of lung repair
Organization of alveolar exudates Neutrophilic to lymphocytic infiltrates
Fibrosing alveolitis
Recovery phase
Usually on the 3rd to 4th week
Gradual resolution of hypoxemia
Hypoxemia improves as edema resolves via active
transport Na/Cl, aquaporins Protein removal via endocytosis Re-epithelialization of denuded alveolar space with type II pneumocytes that differentiate into type I cells
Improved lung compliance
Emphysema-like changes
Management of ARDS
Recent reductions in ARDS/ALI mortality
(1) Recognition and treatment of the underlying
medical and surgical disorders (e.g., sepsis, aspiration, trauma) (2) Minimizing procedures and their complications (3) Prophylaxis against venous thromboembolism, gastrointestinal bleeding, and central venous catheter infections (4) Prompt recognition of nosocomial infections; (5) Provision of adequate nutrition
Keys to management
Treat underlying illness Supportive care
Low tidal volume ventilation Nutrition Prevent ICU complications Stress ulcers DVT Nosocomial infections Pneumothorax No routine use of PA catheter Diuresis/avoidance of volume overload
ARDS Network
NIH-funded consortium of 10 centers, 24
hospitals, 75 intensive care units Goal to design large RCTs to determine effective treatments Key ARDSnet studies:
body weight and plateau pressure 50cmH2O vs Vt 6-8 mg/kg IBW and plateau pressure 30cm H2O KEYS
Low tidal volumes 6-8mL/kg ideal body weight Maintain plateau (end-inspiratory) pressures <30cm
Low Attempt to Tidal Overdistention inflate the of normal lung affected lung volum e
Harrisons Principle of Internal Medicine, 17 th
NEJM 2000;342:1301-8.
Permissive Hypercapnea
Allowing increased CO2 retention
(usually 8-12 mL/kg) to 4-6 mL/kg Decrease barotrauma by decreasing ventilatory peak airway pressures Leads to improved respiratory recovery respiratory acidosis Hypoxemia is a major life threatening condition and hypercapnia is not, one might choose to accept the latter.
Irwin and Rippe's Intensive Care Medicine (Fifth
end-expiratory alveolar collapse (and therefore rightto-left shunt) Can also decrease venous return, cause hemodynamic compromise, worsen pulmonary edema
ARDSnet PEEP trial of 549 patients show no
NEJM 2004:351(4):327-336
Mechanism of PEEP
Positive endexpiratory pressure
Presence of alveolar and interstitial edema and Loss of surfactant
Alveolar collapse
Mechanism of PEEP
Static pressure-volume curve Lower inflection of the curve alveolar opening Inverse ratio ventilation Inspiratory time > expiratory time Dynamic hyperinflation
tidal volume
Further damaging epithelium Increased fluid leak, indistinguishable from ARDS damage
Barotrauma Rupture alveolar membranes Pneuomothorax, pneumomediastinum Sheer stress Opening/closing alveoli Inflammatory reaction, cytokine release
Oxygen toxicity
Free radical formation
Oxygen toxicity
Damage the pulmonary epithelium and inactivate the surfactant Intra-alveloar edema and interstitial thickening Fibrosis and pulmonary atelectasis
o100% oxygen - tolerated for about 24 - 48 hours without any serious tissue damage oLonger exposures produce definite tissue injury.
pulmonary edema SUPPORT trial (retrospective study) first raised doubts about utility Two multicenter RCTs confirmed lack of mortality benefit of PA catheters in ARDS (ARDSnet FACTT) Monitoring CVP equally effective, so PAC not recommended in routine management
Drug therapy
Agents studied:
Corticosteroids Ketoconazole Inhaled nitric oxide Surfactant
No benefit demonstrated
Steroids in ARDS
Earlier studies showed no benefit to early use steroids,
but small study in 1990s showed improved oxygenation and possible mortality benefit in late stage ARDSnet trial (Late Steroid Rescue Study LaSRS lazarus) of steroids 7+ days out from onset of ARDS
80 patients enrolled, RCT methylprednisolone vs placebo Overall, no mortality benefit Steroids increased mortality in those with sx >14 days
Steroids in ARDS
surfactant had no effect on 30-day survival, ICU LOS, duration of mechanical ventilation or physiologic function
Inhaled Nitric oxide
177 patients RCT, improved oxygenation, but no effect on
Fluid Management
Dry lungs are happy lungs
ARDSnet RCT of 1000 patients (FACTT),
Conservative vs liberal fluid strategy using CVP or PAOP monitoring to guide, primary outcome: death. Conservative fluids
Improved oxygenation More ventilator-free days More days outside ICU No increase in shock or dialysis No mortality effects
According to Harrisons...
Normal or low left atrial filling pressure Minimizes pulmonary edema and prevents further decrements in arterial oxygenation and lung compliance Improves pulmonary mechanics Shortens ICU stay and the duration of mechanical ventilation Associated with a lower mortality
NEJM 2006;354:2564-75.
studies in range 30-40% Nonetheless survivors report decreased functional status and perceived health 79% of patients remember adverse events in ICU
29.5% with evidence of PTSD
through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI. Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.