網路內科繼續教育
有效期間:民國 89年12月01日 89年12月15日

    Case Discussion

A 19-year-old man suffered from progressive dyspnea and deteriorated consciousness in one day.

Brief History
The 19-years-old man experienced a traffic accident on the night of the 6th of October. He was sent to a local hospital where compound fracture of right femoral bone and multiple abrasion wounds over bilateral lower extremities were noticed without any evidence of chest or head trauma. ORIF (open reduction with internal fixation) was performed without blood transfusion on the next morning.

However, an episode of chills with spiking fever developed two days after the traffic accident. There was no obvious infection focus except mild local heat and swelling were found over the operating wound. An event of vomiting occurred on the morning of October 8 after narcotics injection for pain relief. Dyspnea with productive cough and consciousness disturbance developed gradually at that night. Chest radiograph revealed multiple patchy infiltrates over bilateral lung fields (Figure 1 ). Arterial blood gas showed severe hypoxemia. Under the impression of acute hypoxemic respiratory failure, he was transferred to MICU in a university hospital for further management on Oct. 9.

On arrival, his consciousness was clear with intact JOMAC. The blood pressure was 162/97 mmHg and pulse rate 102 per minute. Body temperature was 38.5℃. Respiratory distress was noted with a respiratory rate of 32 per minute, The oxygen saturation was kept around 90% under non-rebreathing mask. Conjunctiva was pale and sclera unicteric. Coarse crackles were auscultated over both lung fields. The surgical wound was clear with no evidence of local infection. No petechiae or skin rash could be detected over the trunk. The remaining physical and neurological examinations were unremarkable.

Laboratory Data

1. CBC/DC
 

WBC
(K/μL)

RBC
(M/μL)

HB
(g/dL)

MCV
(fL)

PLT
(K/μL)

Seg
(%)

Lym
(%)

Eos
(%)

10/9

5.16

3.48

10.3

87.6

105.0

84.1

7.2

1.9

10/11

3.86

3.21

10.0

90.3

28.0

71.6

12.7

6.9

10/13

7.90

3.92

11.5

89.9

167.0

69.7

16.1

4.1

 2. ABG
 

pH

 PaCO2
(mmHg)

PaO2
(mmHg)

HCO3-
(mEq/L)

B.E(mEq/L)

FiO2
(PEEP)

VentilatorMode

 10/9

7.42

33.9

58.8

21.5

-2.0

0.8

Non-rebreath

10/11

7.39

39.8

61.0

23.7

-0.6

0.5 (10)

CMV

10/16

7.44

39.9

76.7

26.5

2.7

0.35 (5)

SIMV

3. BCS
 

Albumin
(g/dL)

T-Bil
(mg/dL)

AST
(U/L)

ALT
(U/L)

BUN
(mg/dL)

Cre
(mg/dL)

CK
(U/L)

10/9

2.3

0.7

112

40

13

0.9

720

10/12  

0.8

88

36

14

0.8

210

10/15

2.9

1.3

57

47

17

0.9

41


 

Na
(mmole/L)

K
(mmole/L)

Cl
(mmole/L)

Mg
(mmole/L)

CRP
(mg/dL)

LDH
(U/L)

Lactic acid
(mmole/L)

10/9

140

4.5

109

0.7

>12

1213

1.1

10/12

142

3.7

106

1.0

     
10/15

137

4.0

107

1.2

     

 4. Coagulation profile
 

PT

PTT

Fibrinogen
(mg/dL)

3P

 FDP
(μg/mL)

D-Dimer
(μg/mL)

10/9

16.4/12.4

48.6/37.1

160

1+

20-40

2.47

10/12

14.4/12.1

40.5/38.7

       

 5. Urinalysis
 

pH

Protein
(mg/dL)

Ket

O.B

Uro.bil
(IU/dL)

RBC
(/HFL)

WBC
(/HFL)

Epi

Cast

Bact

10/9

7.5

100

-

+

1.0

10-15

1-3

0-2

-

+

 

Clinical Course & Treatment

After admission, endotracheal intubation with mechanical ventilation was performed. Chest computed tomography (CT) revealed multiple alveolar infiltrates and consolidations over bilateral lung fields (Figure 2). Since sepsis with lung involvement can not be excluded by clinical features, empirical antibiotics with ticarcillin/clavulaniate and gentamicin were prescribed. Component therapy was also given for his coagulation dysfunction. Under the impression of fat embolism syndrome with acute lung injury, ventilator setting was adjusted to high PEEP and low tidal volume. The patient experienced an episode of vomiting with elevated blood pressure and relative bradycardia on Oct. 10. Emergent cranial CT disclosed mild brain swelling. The condition was ameliorated after infusion with osmotic agent. All the microbiologic studies yielded negative results. Gas exchange was improving without any specific pulmonary pharmacotherapy. The bleeding tendency recovered. Ventilator weaning was performed smoothly and he was extubated on Oct. 17. The patient was discharged without any sequelae.

  案例分析

本案例是一個典型脂肪栓塞症候群的病程,通常於外傷後24-48小時發生,病人常有皮膚紫斑、呼吸急促及意識障礙的情形。若病人進行到急性呼吸窘迫症候群的程度,通常需要給予氣管插管及機械通氣的協助,此時肺部所呈現的病徵必須與 (1)敗血症引起的急性肺損傷 (2)胃酸吸入引起的肺炎 (3)神經性肺水腫 (4)輸血反應等作鑑別診斷。本案例雖有呼吸急促、發燒、但病程中並無休克、白血球增加及明顯感染源情形,之所以會給予經驗性抗生素治療是因為無法從臨床表徵中絕對區分是嚴重感染症或是脂肪栓塞症候群,因為兩者皆會出現血小板減少及有瀰漫性血管內凝血症之情形。脂肪栓塞症候群好發於外傷長腿骨折的病人,也可發生於非外傷病人,其治療一般建議是 (1)給予外傷長骨骨折病人儘早外科固定 (2)維持適當水分電解質平衡 (3)適當的機械通氣及氧氣治療,類固醇的使用目前仍然沒有定論,肺部通常在經過7-12 天後可以得到完全的恢復。

繼續教育考題
1.
(D)
案例中病人於車禍2天後所發生的症狀為何?
(1)視力模糊(2)低血容性休克(3)意識障礙(4)呼吸急促
A(1),(4)
B(2),(4)
C(2),(3)
D(3),(4)
2.
(C)
承上題,病人有上述症狀,是因為何種病因引起的?
A肺部挫傷(Lung contusion)
B頭部外傷(Head injury)
C脂肪栓塞症候群(Fat embolism syndrome)
D下肢間隔症候群(Compartment syndrome of lower extremity)
3.
(D)
承上題,病人是因為何種原因而造成低血氧症?
A輸血反應(transfusion reaction)
B敗血性休克(septic shock)
C心因性肺水腫(cardiogenic pulmonary edema)
D非心因性肺水腫(non-cardiogenic pulmonary edema)
4.
(B)
承上題,病人肺部斷層掃描所呈現的影像是屬於何種型態(pattern)?
AInterstitial pattern
BAlveolar pattern
CMass lesions
DCavitary lesions
5.
(C)
承上題,病人經過何種針對肺部之藥物治療(pulmonary pharmacotherapy)使得急性呼吸衰竭得以痊癒?
A類固醇
B吸入性一氧化氮(Inhaled nitric oxide)
C無給予特別之治療
D以上皆非
6.
(B)
典型的脂肪栓塞症候群(Fat embolism syndrome),包括有哪些臨床的特徵?
(1)紫斑(petechiae) (2)急性腎衰竭 (3)呼吸急促 (4)心臟衰竭 (5)意識障礙
A(2),(3),(4)
B(1),(3),(5)
C(2),(3),(5)
D(1),(2),(3)
7.
(A)
脂肪栓塞症候群(Fat embolism syndrome),包括有哪些實驗室檢查數據的特徵?
(1)血小板減少 (2)血液凝固值(PT,PTT)延長 (3)血紅素下降(4)低血氧 (5)肝功能異常
A(1),(2),(4)
B(2),(4),(5)
C(1),(4),(5)
D(2),(3),(4)
8.
(B)
目前對於脂肪栓塞症候群引起急性呼吸窘迫症候群(ARDS)的機轉為
A急性肺栓塞
B肺部血管因脂肪微粒水解引起微血管通透性增加及肺泡損傷
C病人因意識障礙引起吸入性肺炎
D骨骼肌因外傷而受損、溶解,釋放有毒物質,造成肺部微血管損傷
9.
(C)
下列敘述何者為非?
A脂肪栓塞症候群可發生於非外傷的病人
B脂肪栓塞症候群易發生於長腿骨骨折的病人(Long bone fracture)
C脂肪栓塞症候群發生瀰漫性血管內凝血症(DIC)是因為敗血症引起的
D脂肪栓塞症候群通常發生臨床症狀為在外傷之後24-48小時
10.
(D)
對於脂肪栓塞症候群的診斷及治療,下列何者為非?
A發生呼吸衰竭的病人必須與吸入性肺炎、敗血症合併肺損傷及神經性肺水腫(neurogenic pulmonary edema)作鑑別診斷
B於合併有呼吸衰竭的情況下,類固醇的使用,仍然沒有定論
C有些病人可能於肺泡沖洗液中發現巨噬細胞有吞噬脂肪微粒的情形
D脂肪栓塞症候群主要的臨床表現為紫斑(Petechiae)、急性腎衰竭、呼吸急促

答案解說

答案解說:

1、

 2、

 3、脂肪栓塞症候群引起低血氧症是因為肺微血管通透性增加,而引起非心因性肺水腫

4、脂肪栓塞症候群,胸部斷層掃描呈現為Multiple focal alveolar densities or diffuse alveolar infiltrates,肋膜積水不是常見表現,如本案例圖二所示

5、本案例病人沒有接受針對肺部給予特殊的藥物治療

6、脂肪栓塞症候群典型的表現於外傷24-48小時後發生(1)意識障礙(2)呼吸急促(3)皮膚紫斑

7、脂肪栓塞症候群比較特殊的表現會發生瀰漫性血管內凝血症,而使得血小板減少、血液凝固值延長

 8、脂肪栓塞症候群引起急性呼吸窘迫症候群,其機轉為脂肪微粒水解成自由脂肪酸造成肺微血管內皮細胞損傷,引起血管通透性增加及肺泡發炎反應形成

9、脂肪栓塞症候群可發生於非外傷病人,如糖尿病、慢性胰臟炎、酗酒者、嚴重感染症、燒傷病人及潛水夫病等

10、有些人嘗試由肺泡沖洗溶液中巨噬細胞吞噬脂肪微粒之比率,來作為診斷參考,通常佔有40%以上,建議可能是此疾病,但專一性不高


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