Acute respiratory distress syndrome with many complication

SC ：張家豪，許崇善 Supervisor ： CR 康庭瑞

Patient’s Profile Name：翁 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

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 永和耕莘 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.

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

Progress Note12/9 (2:00 am) Desaturation to 80%, PH:7.26, PO2:45.9

HCO3:45.3, BE:-10, CVP: 13 CXR: Lung edema

r/o fluid overload or anaphylaxis of contrast medium

BP : 88/60 mmHg Adjust PEEP :14 FiO2:100% PH 7.38

PO2 48.7, PCO2 32.6, HCO3 19.3, BE – 4.4

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 FiO2:60% PEEP:12 CVP:15

Progress note

12/12 T/P/R: 37.1/138/23 BP: 111/99mmHg SpO2: 92% FiO2: 80% PEEP:14 Neurogenic lung edem

a

Progress note12/12 On CVP (8:00 am)

R’t IJV failureL’t IJV

Desaturation to 72% (8.50 pm)

R’t lung breathig sound decreased

Pneumothorax

Chest tube 100cc bloody fluid dra

inged SaO2: 100%

Progress note

12/13 T/P/R:37.7/122/16 BP:101/71 mmHg SpO2: 96% PEEP:14 FiO2: 100%

Progress note

12/14 (1:30 am)

On ECMO on R’t IJV and R’t FV due to severe hypoxia

despite maximum MV support

Progress note

12/14 (7:45 pm) Facial and bilateral upper extremities

swelling R/o SVC syndrome Change Venous catheter from

R’t IJV L’t femoral V

Progress note12/19 Hypotension Asymmetric chest wall mo

vement Needle aspiration: a few b

lood Explored previous chest tu

be wound by finger: blood 300~500 ml

Reon chest tube

Progression note 12/20 (07:40) Hypotension Low tidal volume and

compliance Chest tube: 1100 ml

blood drained Consult CS

Progress note (12/20) Massive transfusion in 12hours (pre-op)

PRBC 10U

FFP 24U

PLT 36U

Cryoprecipitate 12U

Discussion

HemothoraxEtiology Traumatic

Blunt trauma Penetrating trauma (including iatrogenic)

Nontraumatic or spontaneous Neoplasia (primary or metastatic) Complications of anticoagulation Pulmonary embolism with infarction infectionsMiscellaneous

Pathophysiology Large hemothoraces are usually related to in

jury of vascular structures. Hemodynamic manifestations associated wi

th massive hemothorax are those of hemorrhagic shock.

Related respiratory manifestations include tachypnea and, in some cases, hypoxemia.

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.

ECMO

Complication of ECMO

Mechanical complication Clots in the circuit are the most common m

echanical complication (19%). Cannula placement can cause damage to th

e internal jugular vein Air in the circuit can range from a few bubbl

es to a complete venous air lock Oxygenator failure,pump, Heat exchanger

Complication of ECMO Neurologic Hemorhagic Cardiac Pulmonay

Renal GI Infection Metabolic

Acute respiratory distress syndrome

The Acute respiratory distress syndrome

NEJM, May.4 2000,

SC ：張家豪，許崇善 Supervisor ： CR 康庭瑞

What’s in today’s presentation

IntroductionDefinitionsPathogenesisClinical presentationCause and predisposing conditionsIn our patientTreatment

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.

Latest Definition in 1994

Clinical presentation

Initially tachypnea, dyspnea, and normal auscultatory findings in the chest.

Alter mental status may occur in elderly P’t. Tachycardia with mild cyanosis and coarse ral

es occur later. Disease progress is not correlated to the clinic

al finding

--- Arterial blood gas is required.

Cause and predisposing conditions

Most common 40%

Chronic alcohol abuse, Chronic lung disease, Low serum pH

Massive transfusion

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

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

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.

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. (Thir

d common transfusion related death) Mortality rate is 5 -8%, lower than ARDS(30-50

%)

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 (< 6h) Resolution <4 days (81%) Edema fluid/plasma protein >0.75 more likely. TRALI is almost always combined with leukop

enia

Transfusion related acute lung injury Double hit hypothesis

First hit： Underlying condition of the patient

-- Adherence of neutrophils to lung endothelium

-- Surgery, sepsis, trauma,massive trsansfusion Second hit： Transfusion of injurious blood

-- Activates these primed neutrophils

-- Release reactive oxygen species

-- Capillary leak and pulmonary edema

Transfusion related acute lung injury Prevention

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

Ventilator Associated PneumoniaIntroduction

Hospital-acquired pneumonia (HAP)

-- Any case of pneumonia starts >48 hours

after admission Ventilator associated pneumonia (VAP)

-- HAP happen after >48 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

Ventilator Associated PneumoniaRisk factor

Ventilator Associated PneumoniaDiagnosis & Pathogen

Often, a presumptive diagnosis of pneumonia is made when fever, leukocytosis, purulent secretions, a new infiltrate on chest radiography

>103 colony-forming units (CFU)/mL of bacteria grew from the protected specimen brush sample or > 104 CFU/mL of bacteria grew from the bronchoalveolar lavage fluid.

Pseudomonas aeruginosa, Enterobacter species, Klebsiella pneumoniae, Acinetobacter species,and MRSA

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

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.

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

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

In our patient, ARDS

12/9 – Desaturation to 80%, hypotension (88/60mmHg).

CXR– Bilateral lung edema. Fi02—100% PaO2=45.9, pH=7.26 CVP=13cmH20 Acute lung edema or ARDS? -- Fluid overload? -- Previous pneumonia? -- Contrast anaphylatic shock induce? -- Other cause?

In our patient, ARDS Etiology

Sepsis, Infection

-- No fever (36.8), Leukocytosis (15.51K/μL), Seg(95.2)

-- CRP=0.12

-- 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

In our patient, ARDS Etiology

Infectious pneumonia (VAP)

-- After 48 hours using ventilator

-- No fever (36.9), Leukocytosis (22.53K/μL), Seg(93.3)

-- CRP=3.38, VAP is highly suspected

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 = 50x70=3500ml -- Must be a risk factor of ARDS

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 can’t 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

In our patient, ARDS Etiology

Neurogenic lung edema combine and massive transfusion .

Contrast media allergy and TRALI can not be rule out.

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

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)

Mechanical ventilation

Fi02 titrated to 0.6 if the SaO2>90%

Higher PEEP (>12mm Hg) will decrease cardiac output – monitor CO, SaO2 is needed

Low tidal volume (<6ml/Kg) is rocommanded. Permissive hypercapnia (PaCO2 =50-77 mmHg, pH=7.

2-7.3) can be will tolerated Limiting airway pressure take priority over FiO2 ECMO alone has shown no advantage, but combine w

ith other strategy will have a role. (Fetal bleeding) Combine strategies better than single strategy

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?