Extensive thrombosis of the inferior vena cava and portal vein following electrical injury.

Full text

Page 1

UNCORRECTED PROOF
DTD 5
Case report
Extensive thrombosis of the inferior vena cava
and portal vein following electrical injury
Fujioka Masakia,*, Tasaki Isaoa, Yakabe Ayaa,
Riko Nakayamaa, Yasu Tadaakib, Teshima Hideyosib
aDepartment of Plastic and Reconstructive Surgery, National Nagasaki Medical Center, Nagasaki, Japan
bDepartment of Pediatrics, National Nagasaki Medical Center, Nagasaki, Japan
Accepted 11 January 2005
1. Introduction
Thrombosis of the vena cava inferior can develop as a
major complication of central venous catheter, inducing
fatal conditions including sepsis and pulmonary emboli
[1,2]. Although many patients with central venous (CV)
thrombosis have been presented, the pediatric cases
involving CV thrombosis following burn are rare [2]. In
this paper, we present an interesting case of extensive and
asymptomatic CV thrombosis following electrical burn.
2. Case report
A 12-year-old boy sustained extensive and severe burns
by touching a high-voltage power line (22,000 V) with his
fishing rod. The entrance point of the current was
suspected to be the right hand and the right lumbar area,
but the exit point was not clear. He was brought to our
emergency unit immediately. On arrival, he was conscious
without any neurological deficits, and brain, chest, and
abdomen computerized tomographic (CT) scan did not
detect any disorder. He sustained full thickness burns to
the right forearm, right hand, and right lumbar areas
comprising 9.5% of the total body surface area (BSA),
deep-dermal burns to the right cheek, bilateral upper
arm, back, chest, right lower extremity, and left thigh
comprising 43.5% of the BSA, and superficial-dermal
burns to the neck, chest, and back comprising 7% of the
BSA (Fig. 1a–c). Total burn area comprised more than 60%
of the BSA as shown in Fig. 2. He underwent several
surgical procedures, involving excision of burn tissue and
free skin graft.
Six months after injury, he underwent a seventh surgery
for free skin graft. At this time, he had a central venous
catheter (CVC) inserted via the left femoral vein for central
venous monitoring. However, the catheter was not inserted
to the inferior vena cava, but to the superficial circumflex
iliac vein (Fig. 3). These episodes and the CVC insertion
periods are summarized and shown in Fig. 4.
Nine months after injury, he suddenly developed
abdominal pain with vomiting. At that time, he had a
CVC inserted via the left subclavian vein for central venous
monitoring, because he underwent skin grafting two weeks
before. His general condition after surgery had been good
and he could eat everything per orally on the air-fluid-bed
until this episode. Level of serous amylase rose remarkably
and CT scan demonstrated swelling and inflammation of
the pancreas. A clinical diagnosis of acute pancreatitis
was made and conservative treatment was given. These
symptoms quickly decreased and he recovered within one
week.
During this course, the CT scan findings incidentally
detected thrombosis measuring 75 mm ? 13 mm adhering
to the posterior wall of the inferior vena cava (Fig. 5). The
thrombosis was large but the vena cava was not clogged
completely. Therefore, there was no lower extremity edema,
which is an early indicator of central venous obstruction.
Five days later, follow-up CT findings detected another
thrombosis in the portal vein, which was not detected in
the first examination (Fig. 6). Thrombolytic therapy was
initiated using continuous intraveneous heparin injection
(9000 mg/day) for twoweeks. Ten days later, the thrombosis
www.elsevier.com/locate/burns
Burns xxx (2005) xxx–xxx
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
* Corresponding author. Tel.: +957 52 3121; fax: +957 54 0292.
E-mail address: mfujioka@nmc.hosp.go.jp (F. Masaki).
0305-4179/$30.00 # 2005 Elsevier Ltd and ISBI. All rights reserved.
doi:10.1016/j.burns.2005.01.010
JBUR 2037 1–5

Page 2

UNCORRECTED PROOF
inthe portalveinhadresolved,whilethat inthe inferior vena
cava diminished to 70 mm ? 12 mm on CT scan (Fig. 7a
and b). Regarding the thrombolytic therapy as sufficiently
effective, the dose of heparin was decreased to 4500 mg/day
and continued for two more weeks. Further, warfarin
potassium (2.5 mg/day) and aspirin (100 mg/day) were
administeredorallyinsteadofintraveneousheparininjection
starting five weeks after onset. Three weeks later, he
received warfarin potassium (2.0 mg/day) only.
The size of intra venous thrombosis had decreased to
56 mm ? 8 mm on the 52nd day, 50 mm ? 6 mm on the
94th day and finally resolved in the nine months after onset
(Figs. 8–10). The changing thrombosis size and agents
administered are shown in Fig. 11. During the course, there
were no clinical symptoms of the central venous thrombosis
including leg edema, spike fever and respiratory difficulties
due to pulmonary emboli.
3. Discussion
Occurrence of CV thrombosis can be a life-threatening
complication following CVC placement, and it has become
more common because of the increasingly frequent use of
deep venous access [3,4]. Especially on the treatment of
extensive and severe burn due to electrical injury, CVC is
indispensable for monitoring general circulation, adminis-
tration of agents, and parenteral nutrition. Horattas et al.
reported that 28% of patients with subclavian CVC
developed asymptomatic thrombosis, and 12% of them
F. Masaki et al./Burns xxx (2005) xxx–xxx 2
DTD 5
JBUR20371–5
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
Fig.1. (a–c)Immediatelyaftertheelectricalinjury.Deepburnswerefoundovertherightforearm,hand,andrightlumbarareas.Deep-dermalburnswerefound
over his right cheek, arm, back, chest, leg, and left thigh.
Fig. 2. Burn area and depth. Total burn area comprised more than 60% of
the body surface area.
Fig. 3. Six months after injury. Abdominal X-ray after CVC insertion
showed that it was not inserted to the inferior vena cava, but to the
superficial circumflex iliac vein.

Page 3

UNCORRECTED PROOF
had pulmonary embolization [4]. Concerning burn patients,
Purdue and Hunt had evaluated 2106 patients and concluded
that 6 adults (0.4%) had sustained a pulmonary emboli [1].
Despite CV thrombosis development, most patients did
not complain any symptoms [5]. Therefore, CV thrombosis
is rarely diagnosed until some extremely dangerous disorder
develops, including septic thrombosis, pulmonary infarc-
tion, and severe edema of the extremities due to central
venous hypertension. Particularly, in cases of burn patients,
various clinical symptoms are developed including fever,
hypovolemic shock, septic shock, severegeneral edema, and
cardiopulmonary failure. These conditions tend to conceal
the symptoms of central venous thrombosis and make the
diagnosis more difficult, so the condition usually proves
fatal when the patients are diagnosed [1–3].
Variousgeneralsequelaehavebeenreportedsecondaryto
extensive electrical injury, but central thrombosis has rarely
been reported because most severe electrical injury patients
with thrombosis have died. A review of the literature found
some published cases involving burn patients. Germann and
Kania [6] presented two severely burned patients who
developed superior vena cava syndrome and sepsis, and
Wielosz et al. presented a severely burned child who
developedsepsisasaresultofcentral venousthrombosis[3].
In all of these patients, primary indicators were unusual
edema of the neck and extremities, and high fever due to
sepsis.
Ultrasonographic examination was recommended to
confirm the diagnosis and evaluate the extent of CV
thrombosis [1,3]. However, this method is sometimes
inadaptable for severely burned patients with burn wounds
on the chest and abdomen, as in our case. For this reason,
thrombosis in our patient was followed and evaluated using
CT scan.
At the time of electric injury, the direct electrolytic effect
of a current passing through tissue might damage the central
vessels, producing CV thrombosis. Other postulated
mechanisms have included: thermal injury of vessels, being
bedridden for a prolonged period, coagulopathy due to
disseminated intravascular coagulation or chronic inflam-
mation and CVC insertion. In our case, a current might have
passed through the central vessels and it might have
damaged the endothelium, but it is not likely to have been
the main cause of CV thrombosis because thrombosis did
F. Masaki et al./Burns xxx (2005) xxx–xxx3
DTD 5
JBUR20371–5
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
Fig. 4. Clinical course prior to CV thrombosis and the periods of CV catheter insertion.
Fig.
75 mm ? 13 mm adhering to the posterior wall of the inferior vena cava
(arrow).
5. InitialCT scanfindings detectedthrombosis measuring
Fig. 6. CT scan 5 days later showed another thrombosis in the portal vein
(arrow).

Page 4

UNCORRECTED PROOF
not appear immediately after injury, and was thought to have
developed several months later.
On the other hand, some investigators indicated that
portal vein thrombosis was a rare complication of pancreatic
inflammatory disease [7–9]. Berney et al. retrospectively
reviewed 45 patients who were diagnosed as portal and
superior mesenteric vein thrombosis, and concluded that
22% of them were caused by pancreatitis [10]. The
thrombosis occurred in portal vein, which could not be
recognized at the first CT examination, and melted away
within 10 days. This episode suggested that thrombosis of
portalveinandCVweregeneratedbydifferent etiology.The
former might be caused by a complication of pancreatitis
because it seemed to be fresh and immature, and the latter
would be caused by other complex factors, that were
narrated before, because it was already large at the first
examination and needed long period to melt away.
Once CV thrombosis is verified, immediate thrombolytic
therapy is important [6]. Generally, urokinase and heparin
are chosen as thrombolytic agents. We were concerned that
radical thrombolytic therapy might induce scattering of
thrombotic fragments, resulting the acute pulmonary
emboli. Furthermore, this patient had never shown any
clinical symptoms of thrombosis. Therefore, moderate
thrombolytic therapy with continuous heparin injection
without urokinase was initiated. This treatment was
sufficiently effective and thrombosis in the portal vein
was soon resolved, while that in the inferior vena cava
F. Masaki et al./Burns xxx (2005) xxx–xxx4
DTD 5
JBUR20371–5
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160
161
162
163
164
165
166
167
168
Fig. 7. (a and b) CT scan 10 days later demonstrated that the thrombosis in the portal vein was resolved and that in the inferior vena cava was diminished
(arrows).
Fig. 8. The CT on the 52nd day showed the size of CV thrombosis to
56 mm ? 8 mm (arrows).
Fig. 9. CTon the 94th day demonstrated that the size of CV thrombosis to
56 mm ? 8 mm (arrow).
Fig. 10. CT scan on nine months later demonstrated that CV thrombosis
was resolved (arrow).

Page 5

UNCORRECTED PROOF
diminished within 10 days. Then, the dose of heparin was
decreased and later changed to oral administration of
warfarin potassium and aspirin. We continuously monitored
the patient for sudden development of pulmonary emboli
that would require emergency surgical thrombectomy and
thecirculatoryteam duringthrombolytictherapy.Duringthe
course, the patient did not show any clinical symptoms of
central venous thrombosis including leg edema, spike fever
and respiratory difficulties due to pulmonary infarction.
In silent CV thrombosis (asymptomatic) cases, moderate
thrombolytic therapy would be recommended to decrease
the risk of wound bleeding and pulmonary emboli even
though the clinical period prolonged.
4. Conclusion
We report a rare case of extensive silent thrombosis of
the inferior vena cava and portal vein following electrical
injuries. The clinical course was demonstrated by serial CT
scans.
Moderate thrombolytic therapy using heparin injection
was effectivein this case and isrecommendedforsuch silent
CV thromboses.
References
[1] Purdue GF, Hunt JL. Pulmonary emboli in burn patients. J Trauma
1988;28:218–20.
[2] JarrettF,MakiDG,ChanCK.Management ofsepticthrombosisofthe
inferior vena cava caused by Candida. Arch Surg 1978;113:637–9.
[3] Wielosz M, Dybiec E, Brodzisz A, et al. Ultrasound images of
thrombosis of caval vein inferior—three selected cases. Ann Univ
Mariae Curie Sklodowska 2001;56:457–63.
[4] Horattas MC, Wright DJ, Fenton AH, et al. Changing concept in deep
venous thrombosis of upper extremity. Surgery 1988;104:561–7.
[5] Williams EC. Catheter related thrombosis. Clin Cardiol 1990;13:134–
6.
[6] Germann G, Kania NM. Extensive thrombosis of the caval venous
system after central venous catheters in severely burned patients.
Burns 1995;21(5):389–91.
[7] Aytekin C, Boyvat F, Kurt A, Yologlu Z, Coskun M. Catheter-directed
thrombolysis with transjugular access in portal vein thrombosis sec-
ondary to pancreatitis. Eur J Radiol 2001;39(2):80–2.
[8] Janssen HL. Changing perspectives in portal vein thrombosis. Scand J
Gastroenterol Suppl 2000;232:69–73.
[9] Lambert L, Vermaut D, Verbrugghe J, Brugman E, Friberg J, Fiey J, et
al. Portal vein thrombosis after acute pancreatitis: diagnostic con-
firmation with computed tomography during arterial portography. J
Belge Radiol 1992;75(6):476–8.
[10] Berney T, Morales M, Broquet PE, Mentha G, Morel P. Risk factors
influencing the outcome of portal and mesenteric vein thrombosis.
Hepatogastroenterology 1998;45:2275–81.
F. Masaki et al./Burns xxx (2005) xxx–xxx5
DTD 5
JBUR20371–5
169
170
171
172
173
174
175
176
177
178
179
180
181
182
183
184
185
186
187
188
189
190
191
192
193
194
195
196
197
198
199
200
201
202
203
204
205
206
207
208
209
210
211
212
213
214
215
216
217
Fig. 11. Changing thrombosis size and agents.