Acute respiratory distress syndrome with many complication

1
Acute respiratory distress syndrome with many
complication

• SC???,???
• SupervisorCR???

2
Patients Profile

• Name?XX
• Age 40 y/o
• Gender Female
• Admission date 2005/12/08
• Chief complain
• Sudden onset of headache and conscious loss on
  the morning of 12/08

3
Brief History

• Present Illness
• This 40 y/o female patient has suffered from
  migrane for many years. Severe headache and
  concious when she is shopping in the market about
  10 a.m this morning. She was brought to
  ????hospital for help. SAH was suspected and
  referred to our ER. Angiography showed a aneurysm
  over right distal ICA. After angiography
  performed, short of breath, desaturation 70, SBP
  drop to 80mmHg were noted.Strider and wheezing
  also noted. Contrast medium allergy was
  suspected.Intubation was performed and steroid
  was administered.

4
Brief history

• Past history
• 1. Hyperthyroidism post operation
• 2. Drug and food allergy contrast
• Physical examination
• Consciousness E3V4M6 at ER
• T/P/R 38.1/110/12
• BP 150/90 mmHg

5
Progress Note

• 12/9 (200 am)
• Desaturation to 80, PH7.26, PO245.9
  HCO345.3, BE-10, CVP 13
• CXR Lung edema
• r/o fluid overload or anaphylaxis of
• contrast medium
• BP 88/60 mmHg
• Adjust PEEP 14 FiO2100 ? PH 7.38
• PO2 48.7, PCO2 32.6, HCO3 19.3, BE 4.4

6
Progress note

• 12/10
• T/P/R 36.9/120/19
• BP 99/71 mmHg
• SpO2 96
• FiO2 90 PEEP 14

• 12/11
• T/P/R 37/140/12
• BP 135/95 mmHg
• PaO2 60 mmHg
• FiO260 PEEP12
• CVP15

7
Progress note

• 12/12
• T/P/R 37.1/138/23
• BP 111/99mmHg
• SpO2 92
• FiO2 80 PEEP14
• Neurogenic lung edema

8
Progress note

• 12/12
• On CVP (800 am)
• Rt IJV failure?
• Lt IJV
• Desaturation to 72 (8.50 pm)
• Rt lung breathig sound decreased
• Pneumothorax

9

• Chest tube
• 100cc bloody fluid drainged
• SaO2 100

10
Progress note

• 12/13
• T/P/R37.7/122/16
• BP101/71 mmHg
• SpO2 96
• PEEP14 FiO2 100

11
Progress note

• 12/14 (130 am)
• On ECMO
• on Rt IJV and Rt FV
• due to severe hypoxia
• despite maximum MV support

12
Progress note

• 12/14 (745 pm)
• Facial and bilateral upper extremities swelling
• R/o SVC syndrome
• Change Venous catheter from
• Rt IJV ?Lt femoral V

13
Progress note

• 12/19
• Hypotension
• Asymmetric chest wall movement
• Needle aspiration a few blood
• Explored previous chest tube wound by finger
  blood 300500 ml
• Reon chest tube

14
Progression note

• 12/20 (0740)
• Hypotension
• Low tidal volume and compliance
• Chest tube 1100 ml blood drained
• Consult CS

15
Progress note (12/20)

• Massive transfusion in 12hours (pre-op)
• PRBC 10U
• FFP 24U
• PLT 36U
• Cryoprecipitate 12U

16
Discussion
17
Hemothorax

• Etiology
• Traumatic
• Blunt trauma
• Penetrating trauma (including iatrogenic)
• Nontraumatic or spontaneous
• Neoplasia (primary or metastatic)
• Complications of anticoagulation
• Pulmonary embolism with infarction infections
• Miscellaneous

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Pathophysiology

• Large hemothoraces are usually related to injury
  of vascular structures.
• Hemodynamic manifestations associated with
  massive hemothorax are those of hemorrhagic
  shock.
• Related respiratory manifestations include
  tachypnea and, in some cases, hypoxemia.

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Treatment

• Chest tube
• Surgical
• 1. Greater than 1000 mL of blood is evacuated
  immediately after tube thoracostomy.
• 2. Bleeding from the chest continues, defined as
  150-200 mL/h for 2-4 hours.
• 3. Persistent blood transfusion is required to
  maintain hemodynamic stability.

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ECMO
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Complication of ECMO

• Mechanical complication
• Clots in the circuit are the most common
  mechanical complication (19).
• Cannula placement can cause damage to the
  internal jugular vein
• Air in the circuit can range from a few bubbles
  to a complete venous air lock
• Oxygenator failure,pump, Heat exchanger

22
Complication of ECMO

• Neurologic
• Hemorhagic
• Cardiac
• Pulmonay

• Renal
• GI
• Infection
• Metabolic

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Acute respiratory distress syndrome

• The Acute respiratory distress syndrome
• NEJM, May.4 2000,
• SC???,??? SupervisorCR???

24
Whats in todays presentation

• Introduction
• Definitions
• Pathogenesis
• Clinical presentation
• Cause and predisposing conditions
• In our patient
• Treatment

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Epidemiology

• Common, devastating clinical syndrome.
• 75 per 100.000 population to 12.6-18 per 100.000
  population depending on definition.
• Mortality rate of 40 to 60 attributable to
  sepsis or MOD rather than primary cause
• Mortality of this disease may be decreasing.
• -- 53-68(1983) to 36(1993) (in Seattle)
• -- 66(1990-1993) to 34(1994-1997) (UK)
• Improvement in supportive care and mechanical
  ventilation.

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Latest Definition in 1994
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Clinical presentation

• Initially tachypnea, dyspnea, and normal
  auscultatory findings in the chest.
• Alter mental status may occur in elderly Pt.
• Tachycardia with mild cyanosis and coarse rales
  occur later.
• Disease progress is not correlated to the
  clinical finding
• --- Arterial blood gas is required.

28
Cause and predisposing conditions

• Massive transfusion
• (more than 50 percent of a patient's
• blood volume in 12 to 24 hours)

Chronic alcohol abuse, Chronic lung disease, Low
serum pH
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Etiology

• Sepsis
• Aspiration of gastric contents
• Infectious pneumonia (VAP)
• Severe trauma and surface burns
• Massive Blood transfusion
• Transfusion related acute lung injury (TRALI)
• Following relief of upper airway obstruction
• Lung and bone marrow transplantation
• Drugs Contrast allergy
• Others Neurogenic pulmonary edema

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Sepsis and Massive Transfusion

• Sepsis is the most common cause of ARDS.
• Unexplained ARDS with new fever, hypotension or a
  clinical predisposition to serious infections
  Sepsis should keep in mind.
• Alcoholism decrease glutathione, increase
  inappropriate leukocyte adhesion to endothelium.
• Transfusion of more than 15 units of blood is an
  important risk factor for ARDS.
• Massive transfusion induced SIRS mimic reaction
  in our bodies.

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Transfusion related acute lung injury (TRALI)
Introduction

• Also named pulmonary leukoagglutinin reactions
• TRALI is defined as noncardiogenic pulmonary
  edema related to transfusion therapy.
• TRALI can progress to ARDS.
• TRALI is a life-threatening adverse effect.
  (Third common transfusion related death)
• Mortality rate is 5 -8, lower than ARDS(30-50)

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Transfusion related acute lung injury Clinical
presentation Diagnosis

• Occured with plasma containing blood product --
  Whole blood, PRBCS, FFP, Platelets.
• Dyspnea, cough, fever (Very often)
• Systemic hypotension or hypertension
• Common occur after 1-2 h transfusion (lt 6h)
• Resolution lt4 days (81)
• Edema fluid/plasma protein gt0.75 more likely.
• TRALI is almost always combined with leukopenia

33
Transfusion related acute lung injury Double hit
hypothesis

• First hitUnderlying condition of the patient
• -- Adherence of neutrophils to lung
  endothelium
• -- Surgery, sepsis, trauma,massive
  trsansfusion
• Second hitTransfusion of injurious blood
• -- Activates these primed neutrophils
• -- Release reactive oxygen species
• -- Capillary leak and pulmonary edema

34
Transfusion related acute lung injury Prevention

• Excluding multiparous donor from donor pool.
• Multiparous donor are often motivated donor
• Avoid old blood component.

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Ventilator Associated PneumoniaIntroduction

• Hospital-acquired pneumonia (HAP)
• -- Any case of pneumonia starts gt48 hours
• after admission
• Ventilator associated pneumonia (VAP)
• -- HAP happen after gt48 hours intubation with
  no
• clinical evidence suggesting the presence
  or likely
• development of pneumonia at the time of
  initial
• intubation
• Second common nosocomial infections in medical
  ICUs

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Ventilator Associated PneumoniaRisk factor
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Ventilator Associated PneumoniaDiagnosis
Pathogen

• Often, a presumptive diagnosis of pneumonia is
  made when fever, leukocytosis, purulent
  secretions, a new infiltrate on chest radiography
• gt103 colony-forming units (CFU)/mL of bacteria
  grew from the protected specimen brush sample or
  gt 104 CFU/mL of bacteria grew from the
  bronchoalveolar lavage fluid.
• Pseudomonas aeruginosa, Enterobacter species,
  Klebsiella pneumoniae, Acinetobacter species,and
  MRSA

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Neurogenic Pulmonary EdemaIntroduction

• NPE usually developing after acute central
  nervous system injury.
• NPE is classified as ARDS, but the
  pathophysiology and prognosis are different
• NPE is a serious and common complication after
  SAH that contribute to pool survival and
  neurological deficits
• Post-mortem lung edema -- 46-52
• Survival after SAH lung edema -- 23 ,
• 6 threaten to life

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Neurogenic Pulmonary EdemaClinical presentation

• Dyspnea and mild hemoptysis present within
  minutes to hours of CNS insult.
• Tachypnea, tachycardia, basilar rales.
• Will resolve within hours to several days.

40
Neurogenic Pulmonary EdemaEtiology Pathogenesis

• Epileptic seizure
• Head injury (After CNS surgery)
• Cerebral hemorrhage (SAH)
• Increase of capillary hydrostatic pressure.
  (Initially)
• -- Sympathetic activation
• -- Pulmonary vasoconstriction
• -- Increase starling force (Hydrostatic
  pressure )
• Increase pulmonary capillary permeability. (Late)
• -- Massive epinephrine, Norepinephrine induce

41
Contrast media induce lung edema

• The pulmonary adverse effects after contrast
  media injection including bronchospasm, pulmonary
  edema and increase in the pulmonary arterial
  blood pressure
• Induced pulmonary edema can be secondary to
  endothelial injury causing an increase in the
  permeability of the microcirculation
• Mechanism is not well-established

42
In our patient, ARDS

• 12/9 Desaturation to 80, hypotension
  (88/60mmHg).
• CXR Bilateral lung edema.
• Fi02100 PaO245.9, pH7.26
• CVP13cmH20
• Acute lung edema or ARDS?
• -- Fluid overload?
• -- Previous pneumonia?
• -- Contrast anaphylatic shock induce?
• -- Other cause?

43
In our patient, ARDS Etiology

• Sepsis, Infection
• -- No fever (36.8), Leukocytosis
  (15.51K/µL), Seg(95.2)
• -- CRP0.12
• -- Sepsis is not likely
• Aspiration of gastric contents
• -- No history and no witness of aspiration
  but coma, NG?
• -- Temporary rule out
• Severe trauma and surface burns
• -- No history
• -- Not likely

44
In our patient, ARDS Etiology

• Infectious pneumonia (VAP)
• -- After 48 hours using ventilator
• -- No fever (36.9), Leukocytosis
  (22.53K/µL), Seg(93.3)
• -- CRP3.38, VAP is highly suspected

45
In our patient, ARDS Etiology

• Transfusion related acute lung injury (TRALI)
• -- During OP 4U PRBCs, 6U FFP
• -- Noncardiogenic pulmonary edema onset
  before 6 hours
• -- Leukocytosis (15.51K/µL)
• -- No resolution, TRALI can not be ruled out
• Massive Blood transfusion
• -- During OP 4U PRBCs, 6U FFP
• -- 12/19-12/20 PRBC10U, FFP 24U, PLT 36U,
  Cryo 12U
• -- Blood volume 50x703500ml
• -- Must be a risk factor of ARDS

46
In our patient, ARDS Etiology

• Contrast allergy
• -- After angiogram, short of breath,
  desaturation 70
• SBP drop to 80 mmHg, Strider and
  wheezing.
• -- No case report of contrast induce ARDS
  was found
• -- Cause of pulmonary edema cant be ruled
  out
• Neurogenic lung edema
• -- SAH S/P CNS surgery
• -- Mild resolution from hours or several
  days
• -- Our patient no resolution may due to
  complex
• disease (Hemothorax, Massive
  transfusion, Contrast)
• -- Highly suspected

47
In our patient, ARDS Etiology

• Neurogenic lung edema combine and massive
  transfusion .
• Contrast media allergy and TRALI can not be rule
  out.

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Treatment of ARDS

• Remove of underlying cause of risk factor
• Prone position
• Mechanical ventilation
• Fluid and hemodynamic management
• Surfactant therapy
• Inhaled nitric oxide and other vasodilators
• Glucocorticoid and other antiinflammatory agents

49
Ventilator induce lung injury (VILI)

• High volume and pressures can increase
  permeability pulmonary edema in uninjured lung
  and enhanced edema in the injured lung.
• Alveolar over distension and cyclic opening and
  closing of atelectatic alveoli
• -- Initiated proinflammatory cytokines
  cascade
• Traditional mechanical ventilation (10-15ml/kg)
• may promote further lung injury,(
  resolution)

50
Mechanical ventilation

• Fi02 titrated to 0.6 if the SaO2gt90
• Higher PEEP (gt12mm Hg) will decrease cardiac
  output monitor CO, SaO2 is needed
• Low tidal volume (lt6ml/Kg) is rocommanded.
• Permissive hypercapnia (PaCO2 50-77 mmHg,
  pH7.2-7.3) can be will tolerated
• Limiting airway pressure take priority over FiO2
• ECMO alone has shown no advantage, but combine
  with other strategy will have a role. (Fetal
  bleeding)
• Combine strategies better than single strategy

51
Fluid and hemodynamic management

• Persistence of positive fluid balance is
  associated with poor prognosis.
• Maintain the intravascular volume at the lowest
  level that is consistent with adequate systemic
  perfusion.
• Fluid? Or Vasopressor?