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Interesting case Chief Complaint Interesting case Chief Complaint

Interesting case Chief Complaint - PowerPoint Presentation

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Interesting case Chief Complaint - PPT Presentation

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

fat survey embolism pulmonary survey fat pulmonary embolism primary fes vte sat secondary adjunct patients chest venous treatment left

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Presentation Transcript

Slide1

Interesting case

Slide2

Chief Complaint

หายใจเหนื่อย 4 ชั่วโมง

PTA

Slide3

Primary survey

Slide4

Primary survey

-Airway

- Can talk, No stridor

Slide5

Primary survey

-Breathing and Ventilation

- RR 24/min, O2 Sat 88% at Room air

- Equal breath sound both lungs, CCT Negative

Slide6

Primary 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

Slide7

Primary survey

-Disability

- E4V5M6

- Pupil 2 mm RTLBE

Slide8

Adjunct to Primary survey

Slide9

Adjunct to Primary survey

Retained Foley cath.

ได้

urine

สีเหลืองเข้ม 300

ml

Slide10

Adjunct 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 :

Slide11

Slide12

Adjunct to Primary survey

Monitor O2 Saturation

Slide13

Secondary survey

Slide14

Secondary survey

No food or drug allergy

No underlying medication disease

Current medication

Cefazolin 1 gm iv q 6 hr.

Gentamycin 240 mg iv OD

Slide15

Secondary 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%

Slide16

Physical 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

Slide17

Adjunct to Secondary survey

Slide18

EKG 12 L at

รพช.

Slide19

EKG 12 L at ER

Slide20

ABG (on Mask with bag)

pH 7.40

PO2 160 mmHg

PCO2 33.7 mmHg

HCO3 20.4

Slide21

CTA 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

Slide22

Adjunct to Secondary survey

Slide23

Adjunct to Secondary survey

Slide24

General approach to Dyspnea

Dyspnea

is a subjective feeling of difficult, labored, or uncomfortable

breathing .

Frequently associated with other respiratory symptoms or signs.

Slide25

Management

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

Slide26

Pulmonary Embolism

Slide27

Venous 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

Slide28

Pathophysiology

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)

Slide29

Pathophysiology

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.

Slide30

Pathophysiology

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

Slide31

Pathophysiology

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

Slide32

Pathophysiology

Slide33

Risk Factors

Slide34

Clinical 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.

Slide35

Clinical 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

Slide36

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.

Slide37

Diagnosis

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

Slide38

Chest radiograph showed increased radiolucency in right lung due to decreased vascularization (

Westermark

sign).

Slide39

Slide40

D-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.

Slide41

Slide42

Slide43

Chest 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%

Slide44

Treatment

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

Slide45

Slide46

Fat embolism syndrome

Slide47

Definition

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.

Slide48

Epidermiology

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.

Slide49

Epidermiology

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

Slide50

Pathyphysiology

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

Slide51

Clinical 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

Slide52

Slide53

Clinical 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

Slide54

Imaging

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.

Slide55

Diagnosis

FES should be suspected in those at risk who present with symptoms of respiratory failure

Slide56

Diagnosis

Chest CT angiography

exclude

pulmonary thromboembolism

Slide57

Criteria for Diagnosis

None of these criteria have been validated or have been universally accepted.

Slide58

Treatment

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

Slide59

References

Tintinalli’s

Emergincy

medicine

https://www.uptodate.com/contents/fat-embolism-syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665122/