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Transcript of Acute respiratory distress syndrome with many complication SC :張家豪,許崇善 Supervisor...
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?