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Eastern Journal of Medicine 18 (2013) 26-31

Case Report

Fat embolism: A report of three cases

Elif Tanrıverdio, Aysegul Karalezli, Aysegul Senturk, Berna Botan Yildirim

, Hatice Canan

Hasanoglu

Department of Pulmonology, Ataturk Training and Research Hospital, Ankara, Turkey

Abstract. Fat embolism syndrome (FES) is a rare complication which usually follows long bone fracture. Clinical

manifestations present immediately or 24 to 72 hours after injury. Symptoms are dyspnea, tachypnea, tachycardia,

fever, mental status changes and petechial rashes. We reported three cases of FES. The first case had admitted to

the pulmonology department with confusion and respiratory distress within 24 hours after tibia fracture. He had

petechial rashes on the axillar area and subconjunctival hemorrhages. He was diagnosed as FES and treated. The

second case who had right femur fracture had stupor after 48 hours. He had axillary petechial rashes and

respiratory distress. He was diagnosed as FES and treated. The third case had admitted to the pulmonology

department with the complaints of axillary petechial rashes, subconjunctival hemorrhages after a pelvic fracture.

Both first and second patients who had respiratory failure intubated. The third patient died despite treatment. The

signs of this syndrome must be carefully examined and considered in the diagnosis of the patients which attend the

emergency service with confusion and petechial rashes after long-bone fractures.

Key words: Fat embolism, diagnosis, therapy

1. Introduction

Fat embolism syndrome (FES) is a rare

complication that usually seen in long-bone

fractures. The incidence and mortality rates are

unknown because of comorbid injury and other

problems (1). Clinical findings can be seen

immediately after the fracture causing embolism

or may also occur between 24 and 72 hours after

the accident (2). It is a multisystemic disease

which pulmonary, neurological, hematological,

and dermatological system involvements are

observed. Dyspnea, tachypnea, tachycardia, fever,

axillary petechial rash, and mental changes are

the common symptoms of the disease and early

diagnosis and treatment is important (2).

We presented 3 cases of fat embolism as a rare

complication of long-bone fractures and we

believe that it will contribute for early diagnosis

and treatment.

Correspondence: Dr. Berna Botan Yildirim

Department of Pulmonology, Ataturk Training and Research

Hospital, Ankara, Turkey

E-mail: [email protected]

Tel: +903122912525/ 4304

Received: 18.05.2011

Accepted: 01.02.2012

2. Case report

2.1. Case

The 29 years old male patient with tibia

fracture had been admitted to the orthopedic

clinic and was referred to our clinic because of

respiratory distress and confusion. The patient

was also referred to neurology clinic because he

developed mental confusion in the last 24 hours

and this is followed by two generally tonic-clonic

seizures each lasted 5 minutes. Treatment was

started with intravenous mannitol, steroids, and

antiepileptic agents.

In physical examination there was no respond

to verbal stimuli. He had tachypnea, and

tachycardia. Arterial blood pressure was 100/80

mmHg, and fever was 37.2 °C. In the patient's

follow-up, the fever reached to 38°C,

subconjuctival hemorrhage, petechial rashes

occur in axillary and neck region was observed

(Figures 1a, b). Fundus examination was normal.

Arterial blood gases (ABG) analysis was pH:

7:48, PO

: 49.7 mmHg, pCO

: 30.4 mmHg, SaO

85.7%, HCO

: 22.9 mmol/L, respectively.

hemoglobin (Hb) level was 12.6 g/dL (N: 13.5-

18) and platelets (PLT) 344 K/uL at admission

and Hb level was 9.8 g/dL and PLT level was 144

E. Tanrıverdio et al / Fat embolism

Fig. 1(a, b). Subconjuctival hemorrhage, and petechial rashes are seen in the neck (case 1).

Fig. 2 (a, b). Axillary petechial rash, and subconjuctival hemorrhage are seen (case 2).

K/uL at diagnosis. Other biochemical parameters

and urinary findings were normal. D-dimer was

2607 ng/mL (N: 000-500), and fibrinogen was

587 mg/dL (N: 150-400). Chest radiography was

normal. In Thoracic CT, suspicious filling defects

suggesting of pulmonary embolism were reported

in the middle segmental and subsegmental

branches of the left pulmonary artery. Bilateral

lower extremity venous doppler ultrasound was

normal. The current clinical findings suggested

FES and the patient underwent supporting

treatment, intravenous steroids, and subcutaneous

low-molecular-weight heparin. He regained

consciousness in the fifth day. The patient

clinically recovered and was discharged after

being operated.

2. 2. Case

23-year-old male patient was admitted to

orthopedics service with right femoral shaft

fracture and was consulted to our clinic because

of confusion and respiratory distress, 48 hours

after the accident. Considering that confusion

may be due to trauma, brain CT was taken within

12 hours interval and no pathology was detected.

He did not respond to verbal stimuli in physical

examination. Arterial blood pressure was 100/55

mmHg, and pulse rate was 106/min. Respiratory

system examination was normal. There was

petechial rash on right axillary (Figure 2a). The

patient had subconjuctival hemorrhage (Figure

2b) Ocular fundus evaluated by ophthalmology

service, and clinical examination was normal.

Fever rose up to 39.5 °C during follow-up. ABG

analysis results were as follows: pH: 7:51, pO2:

61.4 mmHg, pCO2: 26 mmHg, SO2: 90.4% and

HCO3: 20.7 mmol/L, respectively. Hematology

results were as follows: Leucocyte: 15.7 K/uL,

neutrophils 84.6%, lymphocytes 8.7%, Hb: 13.5

g/dL, Htc: 38.2%, and PLT: 299 K/uL. He had

higher levels of WBC but it returned to normal

after one day. Urine output, urea and creatinine

Eastern Journal of Medicine 18 (2013) 26-31

Case Report

levels were normal. There were no fat globules in

urine and serum lipase level was normal. Thorax

CT revealed pleuritis on both hemithorax and

alveolar consolidation areas (areas of ground

glass density) consistent with pleural contusion in

bilateral lower lobes (Figures 3a, 3b). The patient

was diagnosed as FES due to existing clinical

findings. Low molecular weight heparin and

steroid treatment was started. The patient

regained consciousness and oxygen saturation

improved. The patient was discharged from the

hospital after being operated.

Fig. 3 (a, b). Ground-glass density areas, and bilateral pleural effusion are seen on Thorax CT (case 2).

Fig. 4 (a, b). Case 3, subconjuctival hemorrhage, and axillary petechial rashes are seen (case 3).

2. 3. Case

The patient was 38-year-old male. The patient

was brought to hospital because of a traffic

accident and was diagnosed with pelvic fracture,

subtrochanteric fracture in right femur and shaft

fracture on left femur. The patient was referred to

our clinic due to the development of drowsiness

and respiratory failure within 48 hours. He was

tachypneic and blackout of consciousness.

Arterial blood pressure was 110/60 mmHg, heart

rate was 120/min, and fever was 37.5 °C.

Respiratory system examination was normal.

Petechial rash and subconjuctival hemorrhage

were detected on patient's axillary region of

anterior chest wall (Figures 4a, 4b). Fundus

examination was normal.

The results of ABG analysis without oxygen

were as follows: pH: 7:45, PO

: 48.2 mmHg,

pCO

: 31.2 mmHg, SaO

: 85.7%, HCO

: 21.7

mmol/L. Other assays were detected as fallows:

AST 90 U/L (N: 5-37), ALT 59 U/L (N: 10-49),

CK 3722 U/L (N: 21-215), CK-MB: 28.5 U/L (N:

0-15), LDH 400 U/L (N: 100-190), Hb: 8.2 g/dL

(N: 12-16), Htc: 23.7% (N: 36-45), D-dimer:

4154 ng/mL (0-500), and fibrinogen: 920 mg/dL

(N: 150-400). Kidney function tests, erythrocyte

sedimentation rate, platelet count and other

laboratory parameters were normal. Brain CT was

taken with 12 hours interval and no pathology

was detected. The patient was diagnosed with

FES with the current clinical findings. The

patient was transferred to intensive care unit

because of general poor health and intubated

because did not respond to continuous oxygen

therapy and non-invasive mechanical ventilation.

Low molecular weight heparin and steroid

treatment was started. Chest X-ray on admission

E. Tanrıverdio et al / Fat embolism

was normal (Figure 5a). CT scan of thorax taken

because of the formation of bilateral basal

reticular pattern on the tenth day of the follow-up

(Figure 5b) and revealed minimal pleural effusion

in both lungs and consolidations compatible with

atelectasis in lower lobes. There was fat density

in the atelectatic field on the right. The current

symptom was reported to be due to fat embolism

(Figures 6a, 6b). Despite the supporting treatment

patient died on the 13

day of admission.

Fig. 5 (a,b). Chest X-ray on admission( Fig. 5a) and on the tenth day (Fig. 5b).

Fig. 6 (a, b). Torax BT, on cross-section of mediastinum, minimal bilateral pleural effusion, areas of atelectasis

and fat density areas (arrow) in atelectasis are observed (case 3).

3. Discussion

Fat embolism syndrome was first identified by

Von Bergman, in 1873, in a patient with fracture

of the femur (3). FES usually occurs as a

complication of the lower extremity long bone

and pelvic fractures. The other etiological factors

include total knee and hip replacement, renal

transplantation, sickle cell anemia, osteomyelitis,

burns, severe infections, blood transfusions,

diabetes mellitus, alcohol-related hepatic failure,

high-dose corticosteroid therapy, chronic

pancreatitis, parenteral lipid infusion, and

liposuction (2-4). Incidence and mortality rates

are unknown because of the comorbid injury and

other problems (1). FES has a wide range of

incidence between 0% - 35% reported in patients

with bone fractures. Incidence depends on bone

involvement [isolated or multiple], age and

gender. Rarely occurs as a result of medical

conditions. Classical triad includes symptoms in

pulmonary (dyspnea), skin (petechiae) and central

nervous system (mental confusion) (5). History

and clinical symptoms are important for the

diagnosis. The presence of major and minor

clinical symptoms, characterized by Gurd and

Wilson (Table 1), should be investigated (1-6).

Diagnosis is made by the presence of at least two

major, or one major and four minor criteria (1).

Eastern Journal of Medicine 18 (2013) 26-31

Case Report

All of the major criteria and the minor criteria in

part were defined in all three cases we presented.

Two theories have been suggested for

pathogenesis of the disease. The mechanical

theory explains particularly fat embolisms

occurred after long bone fractures; fat droplets

released from the bone marrow after fracture

cause blockage of the pulmonary and systemic

vessels. Biochemical theory explains rather

pathogenesis of non-traumatic fat embolisms.

Hormonal changes after the trauma or sepsis

induce systemic release of free fatty acids. Fatty

acids are toxic on the capillary endothelium and

pneumocytes. As a result, vasculitis in lung, brain

and skin vessels, hemorrhage, edema and tissue

damage occurs (1-3-7). The second effect may be

more important because it may cause leakage

from cerebral, pulmonary and other vascular

veins and diffuse vasculitis (7).

Table 1. Criteria for Fat Embolism Syndrome by Gurd and Wilson

Major Criteria Minor Criteria

1. Hypoxemia with PaO

< 60 mmHg, FIO

≤0.4 1. Pyrexia (temperature > 38.5°C)

2. Petechiae in a vest distribution 2. Tachycardia (heart rate > 110 beats per minute)

3. Pulmonary edema

4. Central nervous system depression

disproportionate to hypoxemia

3. Emboli visible in retina

4. Fat in sputum

5. Fat urine

6. Unexplained drop in hematocrit or platelet

count

7. Increasing erytrocite sedimentation rate (>71

mm/h)

There are no specific laboratory and imaging

methods for fat embolism syndrome (6). Hypoxia

and hypocapnia observed with the measurement

of arterial blood gases. Laboratory findings

include decrease in platelet and hematocrit levels,

increased sedimentation rate, increase in the level

of lipase, presence of fat globules in urine,

sputum, and bronchoalveolar lavage (3-8). Some

authors suggest bronchoalveolar lavage for rapid

and specific diagnosis of FES, but being an

invasive method restricts the availability of it (9).

Radiological findings are nonspecific in FES.

Radiographic examinations of the patients may be

normal. Although most patients had normal

radiographs initially after the trauma, symptoms

may occur within approximately 72 hours.

Resolution is expected usually in the second

week of the hospitalization (10). Frequently

observed CT findings include focal or diffuse

areas of consolidation, and/or ground-glass

opacities, nodules smaller than 10 mm and rarely

filling defects of fat density which were

determined with a Hounsfield unit in pulmonary

arteries. Filling defects consistent with

subsegmental pulmonary embolism were

observed in the chest CT of the first patient.

There were bilateral ground-glass density and

bilateral minimal pleural effusion in the second

patient.

In the third patient there were patchy infiltrates

bilaterally in the lower zones on chest radiograph

and areas with fat density in the atalectasis areas

in the lower lobes were observed on the thorax

CT. Although, often one of the first signs of FES

is respiratory failure, cerebral symptoms may be

prominent. In the acute phase cranial diffusion

MR has high sensitivity to detect cerebral fat

embolisms and may be preferred for diagnosis of

suspected patients (9).

Clinical approach to patients with FES

includes, general patient assessment involving the

traumatic situation, coordination of patient care,

active nutritional support, symptomatic treatment,

and adequate physical intervention (11).

Accepted treatment dosage and duration of

treatment with steroids is not known for FES

(12). However, heroically known beneficial

effects of steroids includes stabilizing pulmonary

capillary membrane, suppression of inflammatory

response, reduction of interstitial edema,

preventing activation of the complement system

and has such as preventing platelet activation

(12). The use of albumin in patients with fat

embolism syndrome, causes a decrease in free

fatty acid concentrations (11,12). Different

treatment methods with medications such as

heparin, ethanol, dextran, nonsteroidal anti-

inflammatory and heparin-glucose infusion had

been tried, but no contribution to a decrease in

morbidity and mortality had been reported.

Therefore, none of these are considered in routine

practice (11,12). On the other hand, Wang et al.

E. Tanrıverdio et al / Fat embolism

(13) reported that they achieved 92.3% success

with administering hydrocortisone, dextran 40

glucose and Dan Shen Root injection as a

treatment along supporting impaired respiratory

functions and restoring hypoxemia in patients

with fat embolism syndrome at 12 May 2008

Wenchuan earthquake.

A meta-analysis of studies showing the effects

of prophylactic steroid therapy in patients with

lower extremity fractures, revealed a reduction in

the incidence of hypoxemia and FES. Suggested

prophylactic treatment is to administer a total of

5 doses of 1 mg/kg intravenous

methylprednisolone in every 8 hours after

admission to hospital (14). Our first and second

cases were supported by oxygen inhalation

therapy; in the third case ventilator support was

needed. All three of our cases were not given

prophylactic steroid treatment. We preferred to

start steroid and low molecular weight heparin

therapy with strict monitoring of bleeding, after

the differential diagnosis.

As a result, in patients with confusion and

axillary petechial rash after bone fractures, fat

embolism should be considered in the diagnosis

and signs should be sought. Early diagnosis and

prompt supporting treatment is important in terms

of clinical course.

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