หายใจเหนอย 4 ชวโมง PTA Primary survey Primary survey Airway Can talk No stridor Primary survey Breathing and Ventilation RR 24min O2 Sat 88 at Room air ID: 779656
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Slide1
Interesting case
Slide2Chief Complaint
หายใจเหนื่อย 4 ชั่วโมง
PTA
Slide3Primary survey
Slide4Primary survey
-Airway
- Can talk, No stridor
Slide5Primary survey
-Breathing and Ventilation
- RR 24/min, O2 Sat 88% at Room air
- Equal breath sound both lungs, CCT Negative
Slide6Primary survey
-Circulation
- BP 124/85 mmHg, HR 116 /min
- On Short arm slab both forearms
- On Vacuum drainage at Left femur with skin traction
- No active external bleeding
- No abdominal distension
Slide7Primary survey
-Disability
- E4V5M6
- Pupil 2 mm RTLBE
Slide8Adjunct to Primary survey
Slide9Adjunct to Primary survey
Retained Foley cath.
ได้
urine
สีเหลืองเข้ม 300
ml
Slide10Adjunct to Primary survey
On oxygen mask with bag
O2 sat 100%
ECHO bed side :
Good LV contraction
No RV dilatation
No pericardial effusion
No LV D shape
FAST : Negative
CXR :
Slide11Slide12Adjunct to Primary survey
Monitor O2 Saturation
Slide13Secondary survey
Slide14Secondary survey
No food or drug allergy
No underlying medication disease
Current medication
Cefazolin 1 gm iv q 6 hr.
Gentamycin 240 mg iv OD
Slide15Secondary survey
1 วัน
PTA
ตกจากที่สูง 2 ชั้น
admit
รพช.แม่สาย
Dx
Opened fracture Left Femoral shaft s/p DB c ORIF c broad DCP
Closed
Left Intertrochanteric
fracture
Opened fract
ure
Left Tibial plateau s/p DB
Closed
fra
cture
bilateral distal end radius
ระหว่าง
Admit
มีปัญหา
O2 Sat drop 88% RA
Oxygen canular O2 sat 93% Oxygen Mask with bag O2 sat 100%
Slide16Physical Examination
General appearance : A man good conscious
Vital signs : BP 124/85 mmHg HR 116/min RR 24/min O2 sat 100% (on Mask with bag)
HEENT : Contusion at face
Heart : Tachycardia
Lung : Clear, equal breath sound
Abdomen : Soft, not tender
Extremities : On skin traction left leg, on short arm slab both forearms
Neuro : E4V5M6, pupil 2mm RTLBE
Slide17Adjunct to Secondary survey
Slide18EKG 12 L at
รพช.
Slide19EKG 12 L at ER
Slide20ABG (on Mask with bag)
pH 7.40
PO2 160 mmHg
PCO2 33.7 mmHg
HCO3 20.4
Slide21CTA CHEST
CTA Chest : PE Protocol
Findings :
Intraluminal filling defect in segmental pulmonary arteries supplying RUL with wedge shape less enhancing lung lesion at posterior basal segment of RLL
Grossly patent remaining pulmonary arteries.
Minimal bilateral pleural effusion.
No cardiomegaly or pericardial effusion.
No significant mediastinal lymphadenopathy.
Normal included liver, spleen, pancreas, gallbladder, bilateral adrenal gland and kidneys.
Intact bones.
Impression :
Pulmonary embolism in segmental branches supplying RUL and RLL with pulmonary infarction at posterior basal segment of RLL
Slide22Adjunct to Secondary survey
Slide23Adjunct to Secondary survey
Slide24General approach to Dyspnea
Dyspnea
is a subjective feeling of difficult, labored, or uncomfortable
breathing .
Frequently associated with other respiratory symptoms or signs.
Slide25Management
Oxygen Mask with bag 10
lpm
keep O2 sat ≥ 94%
NSS 1000ml IV 100 ml/
hr
MO 6 mg IV q 6
hr
prn for pain
Med Note : PE from Fat embolism (multiple
Fx
)
เนื่องจากเพิ่ง
Sx
และ
risk bleeding
สูง จึงยังไม่ให้
Enoxaparin
ถ้า
stable +
ไม่
bleed
ให้ฉีด
Enoxaparin ได้
Slide26Pulmonary Embolism
Slide27Venous Thromboembolism
Pulmonary embolism occurs when clotted blood
enters the pulmonary artery circulation
Most PE result from DVT in the legs, arms, or pelvis and jugular vein or IVC
The term
venous thromboembolism
(VTE) includes PE and DVT
Slide28Pathophysiology
Blood clots occur when coagulation exceeds the removal by fibrinolysis
Thrombophilias
are conditions that tip the balance of coagulation fibrinolysis toward excessive clotting
Most guidelines categorize VTE as provoke (secondary) or
unprovoked (idiopathic)
Slide29Pathophysiology
Provoked
VTEs are
acquired
and often time-limited conditions, generally often
following
recent surgery, trauma, or any condition associated with limb or body immobility
Unprovoked
VTE patients have
no known
risk factors, suggesting an increased tendency to clot.
Slide30Pathophysiology
Most VTEs diagnosed in the ED are
unprovoked
.
Patients with
unprovoked
VTE have a
15%
chance of recurrence in the next year compared with 5% for those with a provoked episode
Unprovoked VTE usually receive longer treatment than patients
with provoked VTE
Slide31Pathophysiology
Blood clots that form in the
large veins of the legs
leading to
scarring and poor function of the venous valves
pooling of
venous blood in the legs
varicose veins, pain, swelling, skin
hyperpigmentation, and ulcers
postthrombotic
syndrome
With larger clot burden
↑
pulmonary arterial pressure
RV
dilation and myocardial damage
release of troponin and B-type natriuretic peptide
Right heart failure
increased risk of circulatory shock and death
Slide32Pathophysiology
Slide33Risk Factors
Slide34Clinical features of PE
PE symptoms range from none to sudden death.
The hallmark of PE is
dyspnea
.
Chest pain with pleuritic features is the
second most common
symptom.
The classic PE pain is in the thorax between the clavicles and the costal margin that increases with cough or breathing; it is not purely substernal and not manifested from the skin or muscle.
Slide35Clinical features of PE
3% to 4% of ED patients with PE have syncope
1% to 2% present with new-onset seizure (or convulsion-like
activity) or confusion
Paradoxical embolism syndrome
PE that increases right-sided pressures can lead to
right to left
transit of thrombotic material in the atria and showers into the brain circulation, producing
stroke-like
symptoms
20% of people have a
patent foramen
ovale
Physical Examination
PE does
not predictably
alter any vital sign
The amount of clot burden
does not predict
vital sign changes reliably, with no clear correlation between measured clot
and initial heart rate or oximetry
Most patients with PE have clear lungs on auscultation. Wheezes or
bilateral rales make an alternative diagnosis of bronchospasm or
pneumonia possible but do not exclude PE.
May hear a right ventricular S3 or a split S2 with a loud
second sound.
Slide37Diagnosis
Routine cardiopulmonary testing in the ED generally demonstrates
nonspecific findings
in patients with PE
The EKG 12L is usually
nonspecific
, with sinus tachycardia or
nonspecific ST- and T-wave changes
CXR : one or more abnormalities, including cardiomegaly, basilar atelectasis, infiltrate,
orpleural
effusion; all are nonspecific for PE
Westermark
sign
Hampton hump
Slide38Chest radiograph showed increased radiolucency in right lung due to decreased vascularization (
Westermark
sign).
Slide39Slide40D-dimer testing
The d-dimer assay is the best blood test to
exclude VTE
d-Dimer increases with age
adjusted for age
age × 10 nanograms/mL (e.g., an 80-year-old patient would have an adjusted threshold for abnormal at 800 nanograms/mL)
the conventional d-dimer cutoff 500 nanograms/mL when used
in conjunction with a Wells’ score ≤4 or a simplified revised Geneva
score <5.
Slide41Slide42Slide43Chest CT angiography
Chest CT angiography
is the most common imaging modality for PE
The diagnostic sensitivity and specificity
of a technically adequate MDCT scan are
about 90%
Slide44Treatment
Treatment of VTE requires
systemic anticoagulation
to prevent further
clot formation and allow endogenous fibrinolysis to proceed
The two most common options are unfractionated heparin or a low molecular-weight heparin
Current data favor the use of
low-molecular-weight heparins
over
unfractionated heparin for treatment of both PE and DVT
Slide45Slide46Fat embolism syndrome
Slide47Definition
Fat embolism is defined by the presence of
fat globules
in the pulmonary circulation.
Fat embolism syndrome (FES) refers to the clinical syndrome that follows an identifiable insult which releases fat into the circulation, resulting in pulmonary and systemic symptoms.
Slide48Epidermiology
Fat embolization occurs frequently following
orthopedic trauma
Almost all cases of FES are due to
long bone and pelvic fractures
(bone marrow contains a high content of fat).
The rate of FES is also higher in those with
multiple fractures
.
It is more frequent in
closed fractures
than open fractures.
Slide49Epidermiology
Nonorthopedic
trauma
: soft tissue injury, particularly injury to adipose tissue, burns, liposuction,
lipoinjection
, fat grafting, panniculitis, CPR,
nonorthopedic
surgery (
eg
, cardiopulmonary bypass, caesarean section)
Nontrauma
-related
: pancreatitis, sickle or thalassemia-related hemoglobinopathies (especially during a crisis), osteonecrosis, bone marrow necrosis, lipid-based infusions or contrast agents, intramuscular injections of oil for cosmetic purposes, fatty liver disease
Slide50Pathyphysiology
The pathogenesis of fat embolism is
unknown
.
The mechanical theory
: ↑intramedullary
pressure
release
of fat through open venous sinusoids. But the theory does not explain embolisms within the systemic capillaries beds. Patients have been shown to have systemic fat embolization without a patent foramen
ovale
The biochemical theory
: the inflammatory
response
release
of free fatty acids from the bone marrow into the venous system
↑
free fatty acids
damage to capillary beds, hypoxemia, induce inflammation within the lungs
Slide51Clinical presentation
FES typically manifests
24 to 72 hours
after the initial insult
Classic triad: hypoxemia, neurologic abnormalities, petechial rash
Hypoxemia, dyspnea, and tachypnea are the most frequent early findings
Neurologic abnormalities are typically manifest after hypoxemia
Red-brown petechial rash may be the last component of the triad
nondependent regions including the head, neck, anterior thorax, axillae, and sub-conjunctiva
Slide52Slide53Clinical presentation
FES is a
multiorgan
disease. Fat has been reported to embolize to the lungs, brain, skin, retina, kidneys, liver, and even the heart.
A number of other less common and nonspecific manifestations of FES may also be present. These include
Anemia and thrombocytopenia
Retinal scotomata
Lipiduria
Fever
Coagulopathy, rarely DIC
Myocardial depression
Right ventricle dysfunction
Hypotension
Slide54Imaging
CXR are normal
CT of the lung may also be normal but bilateral well-demarcated ground glass opacities or ill-defined centrilobular nodules may be present
The CT brain can be normal in most
cases
may
be evidence of diffuse edema with scattered low-attenuating areas and hemorrhage in some situations.
Slide55Diagnosis
FES should be suspected in those at risk who present with symptoms of respiratory failure
Slide56Diagnosis
Chest CT angiography
exclude
pulmonary thromboembolism
Slide57Criteria for Diagnosis
None of these criteria have been validated or have been universally accepted.
Slide58Treatment
Treatment of the cause : early correction of fractures may prevent FES
Supportive care : is the
mainstay
of therapy
fluid resuscitation, oxygenation
The administration of systemic corticosteroids is controversial
Hydrocortisone 100 mg IV q 8hr
Methylprednisolone 1 to 1.5 mg/kg/day
Slide59References
Tintinalli’s
Emergincy
medicine
https://www.uptodate.com/contents/fat-embolism-syndrome
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665122/