Điều Trị Bỏng Toàn Diện (Bản Expert Consult)

Surgical management of complications of burn injury
425
with the institution of the aforementioned interventions, the
occurrence of clinically significant ulcers has decreased from
15% to 3%, as has mortality.22 Gastric ulcers are characteristi­
cally multifocal, whereas duodenal ulcers are typically soli­
tary, with 15% of patients having a combination of both.
Patients typically present with hemorrhage or, less com­
monly, perforation, which is seen in approximately 12% of
patients.
Although the exact pathogenesis of Curling’s remains
unknown, the hypoperfusion, hypermetabolism, and
immune dysregulation described above are all implicated in
ulcer formation. Specifically, intravascular depletion leads to
mucosal ischemia and disruption of the protective mucosal
barrier. Compounded by the production of prosta­glandins,
increased acid production, bile reflux, and direct mucosal
injury due to the presence of intraluminal tubes, the end
result is gastroduodenal ulceration.23 Recent studies have
proposed an additional mechanism of stress ulcer formation
secondary to the systemic production of reactive oxygen
species (ROS) in response to stress. Studies have confirmed
that the activation of ROS-producing pathways, such as p38
MAPK, results in gastroduodenal ulcer formation.24 These
pathways may provide important therapeutic targets through
more generalized reductions in oxidative reactants and
inflammatory cytokines. Some have suggested using antioxi­
dants, such as melatonin, to minimize the oxidative damage
caused by the original burn, inhibit proinflammatory
cytokines, and aid in the recovery of immunomodulation.25
An effective approach in the prevention of stress gastritis
in burn patients is early enteral feeding. It has been proposed
that this may be because of dilutional alkalinization or
because enteral feeds provide the energy required for mucosal
cell resiliency despite ischemia. Studies have shown that
intraluminal glucose provides significant protection to
ischemic cells of the small intestine and gastric mucosa.22
Additionally, aggressive fluid resuscitation along with H2-
receptor antagonists or PPIs have proven effective against
formation of stress gastritis. However, once a stress ulcer is
established, many of the same treatments described above
are initiated. Aggressive medical therapy, typically involving
intravenous vasopressin, somatostatin, and a high-dose
continuous PPI infusion, must be instigated in patients
with massive burns who develop hemorrhage. The PPIs have
been demonstrated to reduce instances of rebleeding and the
need for subsequent surgery and/or endoscopic treatment
(Cochrane Database).
If necessary, endoscopic cautery can be attempted, but
should medical therapy fail, an exploratory laparotomy may
be warranted. Specific surgical indications include massive
bleeding (>2.5 L in adults, >50% blood volume in children),
ongoing uncontrolled blood loss, and evidence of a perfo­
rated viscus. Operative repair of ulcers is rarely necessary, but
recent evidence suggests that a distal vagotomy and partial,
distal gastrectomy with subsequent Roux-en-Y reconstruc­
tion is superior to a Billroth II procedure, given that there is
less evidence of erosive gastritis at the anastomotic site and
fewer symptoms related to reflux.26 Although Curling’s ulcers
are far less common than in the past, they remain a potential
hazard to all burn-injured patients. The current low inci­
dence of stress ulceration is due to successful aggressive burn
injury management and the use of preventive measures.
bedside, thereby avoiding the potential complications
associated with an endoscopic or open procedure. In addi­
tion, nasogastric feedings can also neutralize gastric acid.
However, significant facial fractures may be a contraindica­
tion to the passage of a nasal tube. If tubes are left in place
long term they can be associated with significant sinus infec­
tions and aspiration, in addition to aspiration risks associ­
ated with tubes inadvertently displaced in the esophagus.
Placing feeding tubes past the pylorus has become standard
practice to minimize the risk of aspiration and complica­
tions of enteral feeding in patients with impaired gastric
emptying. However, a meta-analysis found that there was no
significant difference in the incidence of pneumonia, caloric
goal achieved, or mortality between gastric and postpyloric
tube feeding.20 Therefore, the paradigm has shifted to focus
more on early feeding and less on placing a postpyloric tube.
If gastric decompression is needed, a sump nasogastric
tube can be used even as enteral feedings are initiated.
Fluoroscopic or endoscopic placement of nasoduodenal
or nasojejunal feeding tubes has been performed success­
fully without major complication. Similarly, a jejunostomy
feeding tube can eliminate the risk of gastroesophageal
reflux associated with gastric tube feedings, but it also carries
the risks of an operative procedure. Whichever route is
chosen, careful volume titration of the chosen formula is
essential to avoid abdominal distension, diarrhea, and
discomfort. An open gastrostomy tube can be maintained
for extended periods and requires minimal experience to
manage. However, a surgical site in the vicinity of a burn
itself may be prone to poor wound healing, dehiscence, and
gastric prolapse. Percutaneous endoscopic or laparoscopic
gastrostomy tube placement is frequently used to minimize
the morbidity associated with an open procedure. Though
minimally invasive approaches to gastrostomy have become
standard in pediatric patients, a potential difficulty of achiev­
ing adequate abdominal insufflation in patients with signifi­
cant third-degree burns to the abdominal torso region must
be carefully considered.
The patient’s physiologic needs should be considered in
selecting an enteral formula because an inappropriate choice
can lead to catabolism and protein wasting, malabsorption,
and diarrhea, which further complicates wound healing and
local wound care. The pathophysiology of diarrhea in tube-
fed burn patients has been extensively studied. High-protein
feeds with glutamine supplementation have shown moder­
ate benefit by reducing muscle protein breakdown and
infection rates while improving wound healing.21 To
ensure adequate delivery of calories, enteral feeding should
be initiated early after a burn injury.
Stress gastritis
The incidence of acute gastroduodenal ulceration in burn
patients, known as Curling’s ulcer, has decreased dramati­
cally with the introduction of aggressive fluid resuscitation,
antacids, early enteral feeding, and proton pump inhibitors
(PPI). Figure 37.2 illustrates the management algorithm
for upper GI bleeding from suspected Curling’s ulcer. The
presence of Curling’s ulcer is clinically recognized in most
cases only by the onset of upper GI bleeding, and was once
associated with mortality rates of up to 70%. Fortunately,

Total Burn Care
37
426
local ischemia of the gallbladder wall, inflammation, gan­
grene, and perforation. Lastly, those who undergo multiple
transfusions can have alterations in the composition of bile
produced, thereby leading to an increased risk of AAC.
AAC commonly presents with fever, right upper quadrant
tenderness, leukocytosis, and elevated liver enzymes.
However, these findings are common in severely burned
patients; therefore, a high index of suspicion is required for
prompt diagnosis. AAC is a surgical emergency, as patients
may rapidly develop complications, including perforation or
gangrenous cholecystitis. The incidence of gangrenous gall­
bladder and perforation are noted to be 33–100% and 12%,
respectively.30 Mortality following perforation or gangrenous
emphysema is reported to be as high as 65%, but early diag­
nosis and intervention may reduce the likelihood of severe
complications significantly, as reflected by the reduction in
mortality to 7%.31
Suspected AAC may be confirmed by ultrasonography,
demonstrating a thickened gallbladder wall, pericholecystic
fluid, and intraluminal sludge. One particular study reported
that ultrasonography had a sensitivity of 30% and specificity
Acalculous cholecystitis
Acute acalculous cholecystitis (AAC) is a rare complication
of a burn injury, found in an estimated 0.4–3.5% of burned
patients, but it may result in significant mortality if not
quickly recognized and appropriately treated.27 Patients par­
ticularly susceptible to the development of AAC include
those with extensive burns (>40% TBSA), multiple transfu­
sions, sepsis, dependence on total parenteral nutrition
(TPN), and a history of narcotics usage. Recent multivariance
analysis has shown that age, number of packed red blood
cell transfusions, and duration of ventilatory support are
independent predictive factors for the development of AAC
in severely burned patients.28 Proposed etiologies of AAC
include bile stasis, hypoperfusion with resultant gallbladder
ischemia, cystic duct obstruction, and sepsis.29 Patients with
heavy narcotic use for pain control or who are dependent
on TPN because they are unable to tolerate enteral feeds tend
to experience bile stasis. Hypoperfusion secondary to either
intravascular blood loss or systemic sepsis affects circulating
vasoactive mediators and local tissue perfusion, leading to
Figure 37.2  Management algorithm for acute
upper gastrointestinal bleeding.
Upper GI bleed from suspected Curling’s ulcer
(i.e., hypotension, bloody NG output, melena/hematochezia)
Initiate high-dose PPI
and consider somatostatin
Vasopressin injection
and thermal cautery
Resuscitate with IVFs and PRBCs
and correct coagulopathies
Clinically stable?
Upper endoscopy
Bleeding controlled?
Yes
No
Yes
No
Actively bleeding ulcer
Ulcer with a clot or
visible vessel at base
Continue medical
management
Surgery
Repeat endoscopic
therapy or angiography

Surgical management of complications of burn injury
427
gastrointestinal series demonstrating duodenal dilation with
or without gastric dilation, retention of barium within the
duodenum, and extrinsic pressure on the third portion of
the duodenum with a characteristic sharp cutoff.37
Management of SMA syndrome is primarily medical,
with early enteral feeding not only limiting weight loss
to <5% of pre-burn weight, but also reducing the overall
occurrence. Once present, SMA syndrome is treated by maxi­
mizing caloric delivery either via a fluoroscopically or endo­
scopically placed nasojejunal feeding tube or parenteral
nutrition. Alternatively, a combination of enteral and
parenteral feeding may be necessary to meet nutritional
needs until the duodenal obstruction resolves. Surgical
procedures are rarely indicated, but when necessary, the
operative goal should be to bypass the point of obstruction
caused by the superior mesenteric vascular pedicle. The
operation of choice is duodenojejunostomy, in which a
lateral duodenotomy is made and the proximal jejunum is
then used to create a side-to-side anastomosis. A laparo­
scopic approach has been used to relieve the duodenal
obstruction in patients with SMA syndrome, with some
success.38 Gastrojejunostomy and the Strong procedure
(division of the ligament of Treitz with mobilization of the
duodenum) are alternative surgical options, but they have
proved inferior to duodenojejunostomy because of failure to
adequately relieve the obstruction, peptic ulceration, and
blind loop syndrome. The latter procedure has a success rate
of only 75% in the general population, as opposed to a
98.5% success rate with duodenojejunostomy and division
of the ligament of Treitz.39
of 93% in critically ill trauma patients.32 Thus, if ultrasound
examination proves equivocal, a cholecystoscintigraphy
(HIDA scan) can confirm the diagnosis. CT can also demon­
strate thickened gallbladder with pericholecystic fluid.
However, many patients are on narcotics, which can obscure
the results due to sphincter of Oddi constriction, and false
positives can be seen with TPN use and hyperbilirubinemia
from massive transfusion. In extremely ill patients for whom
surgical intervention is not an option, ultrasound-guided
percutaneous cholecystostomy should be considered, as
there is a clinical response rate between 56% and 100%.33 In
a recent review of 163 patients who underwent percutaneous
cholecystostomy, over 80% were able to undergo removal of
the cholecystostomy tube and did not require a cholecystec­
tomy.34 Caution must be employed when using this tech­
nique, as the incidence of gangrenous cholecystitis is marked
in thermally injured patients, and a lack of clinical response
after percutaneous cholecystostomy should prompt the
surgeon to proceed with an open cholecystectomy.
Pancreatitis
Acute pancreatitis is an under-recognized complication fol­
lowing thermal injury. Elevated levels of pancreatic enzymes
have frequently been associated with burns, but the non-
specific symptoms, such as epigastric pain radiating to the
back, are often overlooked. In 1995, a retrospective review
of adult burn patients identified elevations in amylase and
lipase in 40% of their patients with large burns, and this
correlated in most cases with symptoms related to pancrea­
titis.35 A recent study examined 2699 pediatric burn patients
and found an incidence of acute pancreatitis of 0.05%.36
Despite its rarity, it was associated with a significant increase
in mortality, as survival rates were reported to be only 69%
compared to 87% in burn patients unaffected by pancreati­
tis.36 Management for acute pancreatitis in the burn patient
is the same as in non-burn patients: supportive care,
bowel rest, fluid resuscitation, and IV nutrition. Ultrasound
examination of the biliary tract should be performed to
rule out gallstone disease. Occasionally, a more detailed
work-up with an abdominal CT scan is necessary to identify
complications such as pseudocyst formation, pancreatic
necrosis, or pancreatic abscess. Operative intervention is
rarely indicated unless these complications are noted, and
would consist of a cystogastrostomy, necrosectomy, and
drainage, respectively.
Superior mesenteric artery syndrome
Superior mesenteric artery (SMA) syndrome, or Wilkie’s syn­
drome, occurs when the third part of the duodenum is
extrinsically compressed by the superior mesenteric vascular
pedicle (Fig. 37.3A, B). SMA syndrome is usually precipi­
tated by rapid and substantial weight loss, leading to a loss
of retroperitoneal fat. In burned patients, weight loss through
malnutrition, loss of abdominal wall muscle, and a recum­
bent position contribute to the severity of the duodenal
compression. Patients typically present with non-specific
symptoms such as nausea, bilious vomiting, intolerance to
tube or oral feedings, and abdominal pain aggravated
by feeding and relieved by placing the patient in a knee-to-
chest position. The diagnosis is established by an upper
Figure 37.3  Superior mesenteric artery syndrome. (a, b) Schematic
illustrations of the mechanism of superior mesenteric artery syndrome,
where superior mesenteric vessels extrinsically compress the third portion of
the duodenum. SMA: superior mesenteric artery, MCA: middle colic artery,
IVC: inferior vena cava. (Adapted from Townsend CM, Jr., Naoum J. Vascular
Compression of the Duodenum, In: Fischer JE (ed.), Mastery of Surgery, 5th ed., Philadelphia;
Lippencott Williams & Wilkins; 2007: p.956).
SMA
Left renal vein
Aorta
MCA
SMA
IVC
MCA
Uncinate process of pancreas
Duodenum
Duodeno-jejunal flexure
Aorta
Ligament of Treitz
Stomach
L1
L2
L3
L4
A
B

Total Burn Care
37
428
or metronidazole should be initiated. If medical manage­
ment fails, a partial colectomy of the involved segment is
warranted. With increasing incidence of invasive fungal
infections in burn patients, a case of aspergillosis causing
invasive systemic infection and mycotic enterocolitis has
even been reported.47
Vascular complications
Suppurative thrombophlebitis
Suppurative thrombophlebitis is characterized by venous
thrombosis associated with inflammation and bacteremia.
Not all of these infections occur in association with venous
thrombosis, and specific risk factors for suppurative throm­
bophlebitis include both burn injury and prolonged intra­
venous catheterization. The diagnosis may be made based
on culture results together with radiographic evidence of
thrombosis. The classic physical examination findings of
edema, erythema, pain, and a palpable cord may not all be
Necrotizing enterocolitis
Splanchnic hypoperfusion occurs as a result of hypovolemia
and circulating vasoactive mediators. The degree of intestinal
insult ranges from mucosal atrophy to full-thickness necrosis
and perforation, and is a product of the severity and duration
of ischemia combined with reperfusion by resuscitative
efforts. Moreover, the presence of virulent bacteria and fungi
in the immunocompromised state contributes to intestinal
complications and can lead to sepsis. In a study of 2114
patients with burn injury, only 10 (0.5%) patients demon­
strated clinically apparent ischemic necrotic bowel disease,
and they tended to have more severe burns.40 Although only
2–5% of patients are clinically diagnosed with this condi­
tion, autopsy findings identify pathologic changes consistent
with ischemia in 50% of burn patients who die as a result
of their injuries.41 Unfortunately, the mortality rate of
patients experiencing ischemic enterocolitis is reported to be
extremely high, in the range of 60–69%.42
Patients with ischemic bowel demonstrate intolerance to
enteral tube feedings and high gastric residuals. Abdominal
radiographs often demonstrate massively dilated loops of
bowel and pneumatosis intestinalis (Fig. 37.4A). Because the
overall incidence is quite low, early recognition and interven­
tion requires a high index of suspicion. Burn patients with
sepsis or an inability to tolerate tube feeds should be started
on broad-spectrum antibiotics. Failure to respond to medical
treatment mandates surgical intervention, in which frankly
necrotic intestinal segments should be resected (Fig. 37.4B).
However, questionable areas of necrosis, particularly when
they involve extensive lengths, should be re-examined at a
second-look operation within 24–48 hours. Thus, the
primary goal is to eliminate obviously non-viable bowel
while preserving as much intestine as possible to avoid the
additional risk of short gut syndrome.
Intestinal ischemia may result in transmural mucosal
damage, which predisposes already immunocompromised
patients to bacterial translocation and systemic sepsis. Nearly
75% of burn patients with bowel ischemia at autopsy had
concomitant sepsis documented at the time of their death,
which emphasizes the high incidence of sepsis and mortality
associated with intestinal ischemic complications.43 Infec­
tions are the most common cause of death in autopsied burn
patients (61%), with sepsis secondary to the Gram-negative
pathogens Pseudomonas aeruginosa and Klebsiella pneumoniae
most frequently seen in the military subpopulation.44 Mas­
sively burned patients are at high risk for pseudomembra­
nous colitis as they are frequently treated with multiple
antibiotics for documented systemic infections and for
prophylaxis during burn wound excision and grafting.
Clostridium difficile overgrowth can result in pseudomembra­
nous colitis, with the potential to progress to fulminant toxic
megacolon and bowel perforation. In a report of 180 ther­
mally injured patients, the overall incidence of Clostridium
difficile colitis was ~8% with mean TBSA of 42%.45 The use
of antibiotics and topical silver sulfadiazine has been shown
to cause toxic megacolon and places patients at higher risk
for colonic perforation.46 Thus, symptoms of colitis, such as
leukocytosis, abdominal pain, distension, and grossly bloody
diarrhea, must be promptly recognized. Stool samples are
tested for C. difficile antigen. All unnecessary systemic anti­
biotic therapy should be discontinued, and oral vancomycin
Figure 37.4  Necrotizing enterocolitis. (a) Representative radiograph
demonstrating abdominal catastrophe. Multiple dilated persistently ‘fixed’
bowel loops are an ominous sign for full-thickness necrosis of involved
segments of bowel. (b) At operation, multiple necrotic bowel loops were
found.
A
B

Surgical management of complications of burn injury
429
observation or a small-caliber (8 Fr) pigtail tube thoracos­
tomy. However, if unrecognized, especially in patients receiv­
ing positive-pressure ventilatory support, it can rapidly
progress to a tension pneumothorax with hemodynamic
compromise. In order to reduce the risk of puncturing the
lung parenchyma during central venous line placement, it is
crucial to be familiar with the central venous anatomy. For
example, because of venous anatomical differences in small
children, percutaneous access to the subclavian vein may
require a more acute and cephalad angle of approach under
the clavicle. Recently, the use of ultrasound guidance has
become more widely accepted in central venous catheter
placement to reduce some of the obvious risks associated
with ‘blind’ percutaneous central venous access.
Bleeding complications associated with central venous
access vary in location and can be local, mediastinal,
intrathoracic, or pericardial. Local hemorrhage typically
occurs in patients with a coagulopathy and can be controlled
with local pressure. Hemorrhage into the thoracic space can
occur at the time of catheter insertion, but it can also be seen
when the catheter erodes through the vein wall. The most
common situation leading to venous wall perforation occurs
during the insertion of the percutaneous introducer sheath
over a guidewire. As the sheath is introduced, it can fail to
negotiate the path of the vein and traumatize the vein wall.
Consequently, blood may accumulate into the mediastinum,
pleural space, or pericardium.
If the injury is small, it should resolve on its own with
thrombosis formation. However, in cases of a larger venous
tear rapid bleeding into the thoracic cavity can occur, and
emergency thoracostomy may be necessary. Bleeding or infu­
sion of fluid into the pericardial space can rapidly compro­
mise cardiac function and result in hemodynamic collapse.
Pericardial tamponade typically presents with hypotension,
muffled heart sounds, and distended neck veins (Beck’s
triad). However, all components of the classic triad of symp­
toms are rarely present, and a physician must have a high
index of suspicion in order to recognize this condition early.
Echocardiography can confirm the clinical suspicion, and
pericardiocentesis or pericardial window is therapeutic.
Distal limb ischemia
Arterial monitoring is frequently required in patients with
major burns. Although radial and pedal arterial catheters are
routinely placed without significant complications, they can
be associated with problems such as hematoma, thrombosis,
and pain. Occasionally the common femoral artery is con­
sidered for access, given its larger caliber. Because the femoral
artery is the major blood supply to the lower extremity, this
site should be approached with caution for fear that throm­
bosis can lead to distal limb ischemia. Especially in pediatric
burn patients, the femoral artery is quite small and the cath­
eter within the vessel can result in near complete occlusion
of blood flow to the distal limb. However, our review of
femoral artery catheterization in pediatric burn patients
showed that the complication rate was quite minimal, while
providing a more accurate measure of hemodynamics (Table
37.3).51 During the 7-year study period 234 pediatric burn
patients underwent 745 femoral arterial catheter placements;
a total of 12 (1.9%) suffered complications ranging from
transient distal limb ischemia to amputation.51 Eight patients
present. Burned patients frequently have positive blood cul­
tures and clinical sepsis without an obvious source, and in
the setting of suppurative thrombophlebitis, the most com­
monly cultured organisms from infected veins reflect those
cultured from the burn wound.
The incidence of suppurative thrombophlebotic complica­
tions in burn patients has been estimated to be as high as
7%, with significant risk in patients with >20% TBSA burns,
and is associated with significant mortality.48 The principles
of treatment include removing the source of infection,
administration of intravenous antibiotics, and/or anticoagu­
lation. Two weeks of parenteral antibiotics usually suffices,
but longer therapy may be necessary when central veins are
involved. Surgical treatment consists of surgical cutdown
and evacuation of vein contents. If pus or clot is found, the
vein segment should be excised to a normal-appearing vein
(usually up to the first uninvolved tributary). If exploration
is negative at one site, then sequential exploration of other
sites is necessary until the source of infection is identified.
Prompt surgical intervention is necessary to prevent hema­
togenous dissemination and septic emboli that can result in
endocarditis and osteomyelitis. The wound should be loosely
packed and allowed to heal either by secondary intention or
by delayed closure upon resolution of the infection.
In order to minimize the incidence of catheter-related
complications, the current standard of practice for central
venous access at most institutions involves aseptic care at the
catheter insertion site along with regularly scheduled cath­
eter site dressing changes. Some advocate that central venous
catheters should be changed over a guidewire every 3 days
and a completely new central venous catheter placed at a
new site every 6 days. This results in a more acceptable, but
by no means ideal, infection rate of 3.2%.49 Even so, this
practice is not widely instituted.
Central venous access
Adequate venous access is imperative in the acute post-burn
period for aggressive fluid resuscitation. Although large-bore
peripheral intravenous catheters are the preferred route for
resuscitating trauma patients, placement can be extremely
difficult in those with major burns involving the extremities.
Therefore, central venous catheters have become standard
practice in major burns. Particular attention should be given
to the use of various available cannulation sites, depending
on the size of the patient, as well as taking into consideration
the clinical condition of the burn wounds. The rate of
catheter-related bloodstream infections in burn patients is
estimated to be 20 per 1000 catheter days.50 Therefore, com­
pulsory site care is required. As it is more difficult to resite
lines in severely burned than in non-burned patients,
guidewire exchange is acceptable unless there is clinical evi­
dence of infection, such as erythema, drainage from the site,
or bacteremia.
Central venous line placement is associated with poten­
tially serious complications. In order to reduce the risk of
bleeding complications, many burn centers rely on fluoro­
scopic or ultrasound guidance during the insertion of central
venous lines. Although the overall incidence is quite small
(1–4%), thoracic complications, resulting from line place­
ment can potentially lead to life-threatening conditions.
For example, small pneumo­thoraces can be treated with

Total Burn Care
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430
Chest radiographs may demonstrate pleural effusion along
with areas of pulmonary consolidation, if detected at an
early serous fluid stage. A lateral decubitus chest radiograph
can be helpful to show layering of pleural fluid, but this is
often difficult to obtain in burn patients. When this condi­
tion progresses to form organized fibrous collections, a
bedside ultrasound examination can be extremely helpful to
discern loculations in the chest. The diagnosis can also be
confirmed with a chest CT scan, on which a parapneumonic
effusion may be apparent. CT can also be helpful to differ­
entiate dense consolidation of lung parenchyma from para­
pneumonic effusion. When detected early, tube thoracostomy
is sufficient to drain serous pleural effusions. However, for
advanced-stage empyema, which characteristically has thick,
fibrous loculations, video-assisted thoracoscopic surgery
(VATS) may be necessary to evacuate parapneumonic collec­
tions and wash out the chest cavity.
Summary
When presented with patients with multiple organ injuries,
the protocols for ATLS should be initiated first, followed by
a systematic approach to the management of any and all
other injuries. Complications requiring operative manage­
ment in the setting of a burn injury can compound an
already overwhelming physiological response. When there is
an exaggerated systemic inflammatory response non-thermal
injuries are often masked, thereby delaying diagnosis and
resulting in worsened outcomes. Surgical issues and com­
plications in this patient population are inevitable, and
clinicians must be thorough and astute in the evaluation
of patients with a significant burn injury.
responded to femoral arterial catheter removal along with
systemic heparinization, with complete resolution of distal
limb ischemia. Three patients underwent surgical explora­
tion with thrombectomy. One patient required amputation.
Considering the frequency of invasive arterial monitoring
required for large burn patients, the overall complication
rate was low.
If distal blood flow is compromised the catheter should
be removed immediately, and a Doppler flow study is
obtained to assess for the presence of an intimal flap.
Recently, magnetic resonance arteriography has been used as
a diagnostic tool with excellent results. Conservative treat­
ment coupled with systemic heparinization is usually ade­
quate to restore blood flow; therefore, surgical intervention
is rarely necessary. Should conservative management fail,
exploration of the femoral artery with thrombectomy, fasci­
otomy, and completion arteriography is recommended.
Although rare, amputation may be required if flow is not
re-established and tissue salvage is not possible.
Thoracic complications
Apart from central line placement, other concomitant tho­
racic complications can also occur. When thoracostomy
placement is needed, site care must be meticulous. If the
chest tube is placed under unsterile conditions, it should be
changed out as soon as possible to reduce the risk of
empyema. Burn patients are particularly susceptible to the
development of empyema owing to high bacterial coloniza­
tion of wounds and impaired local defenses due to loss of
skin integrity. Patients with empyema can present with
fevers, leukocytosis, and increased ventilatory requirements.
Table 37.3  Complications of femoral arterial catheterization2
Age
(yr)
Weight
(kg)
% TBSA
burn/3rd
Catheter
size (Fr.)
Cather
site burn
Burns
to limb
Operator
*Onset of
ischemia (Hr)*
Surgical
exploration†
  1
2.2
17.7
36.5/36.5
3
No
Yes
Anesthesiologist
6
Yes
  2
0.9
12.5
95/95
3
No
Yes
Surgeon
12
Yes
  3
2.0
12.7
51/51
3
No
No
Surgeon
4
Yes
  4
0.5
6.5
18/1
2.5
No
No
Surgeon
24
No
  5
2.1
15.8
70/70
3
No
Yes
Surgeon
4
No
  6
12.4
36.3
48/20
3
No
No
Surgeon
12
No
  7
2.2
13.5
62/58
3
Yes
Yes
Surgeon
4
No
  8
1.7
13.1
64/59
3
No
Yes
Surgeon
6
No
  9
2.7
13.7
69/18
3
No
Yes
Surgeon
4
No
10
3.8
15.1
57/5
3
No
Yes
Surgeon
6
No
11
6.3
22.0
87/87
3
Yes
Yes
Anesthesiologist
6
No
12
1.9
13.3
47/47
3
No
No
Anesthesiologist
4
Yes
*Hours after catheter placement.
†All patients received IV heparin therapy.

Surgical management of complications of burn injury
431
Mourot JM, Oliveira HM, Woodson LC, et al. Complications of
femoral artery catheterization in pediatric burn patients. J Burn
Care Res. 2009 May-Jun;30(3):432-436.
Oliveira HM, Sallam HS, Espana-Tenorio J, et al. Gastric and small
bowel ileus after severe burn in rats: the effect of cyclooxygenase-2
inhibitors. Burns. 2009 Dec;35(8):1180-1184.
Williams FN, Jeschke MG, Chinkes DL, et al. Modulation of the
hypermetabolic response to trauma: temperature, nutrition, and
drugs. J Am Coll Surg. 2009 Apr;208(4):489-502.
Further reading
Gan HT, Pasricha PJ, Chen JD. Blockade of p38 mitogen-activated
protein kinase pathway ameliorates delayed intestinal transit in
burned rats. Am J Surg. 2007 Apr;193(4):530-537.
Jeschke MG, Kraft R, Emdad F, et al. Glucose control in severely
thermally injured pediatric patients: what glucose range should
be the target? Ann Surg. 2010 Sep;252(3):521-527; discussion
7-8.
 
Access the complete reference list online at

Surgical management of complications of burn injury
431.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
References
1. Dougherty W, Waxman K. The complexities of managing severe
burns with associated trauma. Surg Clin North Am. 1996
Aug;76(4):923-958.
2. Santaniello JM, Luchette FA, Esposito TJ, et al. Ten year experience
of burn, trauma, and combined burn/trauma injuries comparing
outcomes. J Trauma. 2004 Oct;57(4):696-700; dicussion 700-701.
3. Brandt CP, Yowler CJ, Fratianne RB. Burns with multiple trauma.
Am Surg. 2002 Mar;68(3):240-243; discussion 243-244.
4. Soto JA, Munera F, Morales C, et al. Focal arterial injuries of the
proximal extremities: helical ct arteriography as the initial method
of diagnosis. Radiology. 2001 Jan;218(1):188-194.
5. Hettiaratchy S, Dziewulski P. Abc of burns: pathophysiology and
types of burns. BMJ. 2004 Jun 12;328(7453):1427-1429.
6. Banks RO, Gallavan Jr Rh, Zinner MH, et al. Vasoactive agents in
control of the mesenteric circulation. Fed Proc. 1985 Sep;44(12):
2743-2749.
7. Jones 2nd WG, Minei JP, Barber AE, et al. Splanchnic
vasoconstriction and bacterial translocation after thermal injury.
Am J Physiol. 1991 Oct;261(4 pt 2):h1190-h1196.
8. Tokyay R, Zeigler ST, Traber DL, et al. Postburn gastrointestinal
vasoconstriction increases bacterial and endotoxin translocation.
J Appl Physiol. 1993 Apr;74(4):1521-1527.
9. Hart DW, Wolf SE, Mlcak R, et al. Persistence of muscle
catabolism after severe burn. Surgery. 2000 Aug;128(2):312-319.
10. Williams FN, Jeschke MG, Chinkes DL, et al. Modulation of the
hypermetabolic response to trauma: temperature, nutrition, and
drugs. J Am Coll Surg. 2009 Apr;208(4):489-502.
11. Sologub VK, Zaets TL, Tarasov AV, et al. Enteral hyperalimentation
of burned patients: the possibility of correcting metabolic
disorders by the early administration of prolonged high calorie
evenly distributed tube feeds. Burns. 1992 Jun;18(3):245-249.
12. Kupper TS, Deitch EA, Baker CC, et al. The human burn wound
as a primary source of interleukin-1 activity. Surgery. 1986
Aug;100(2):409-415.
13. Jeschke MG, Kraft R, Emdad F, et al. Glucose control in severely
thermally injured pediatric patients: what glucose range should
be the target? Ann Surg. 2010 Sep;252(3):521-527; discussion
527-528.
14. Hemmila MR, Taddonio MA, Arbabi S, et al. Intensive insulin
therapy is associated with reduced infectious complications in
burn patients. Surgery. 2008 Oct;144(4):629-635; discussion
635-637.
15. Ramzy PI, Wolf SE, Irtun O, et al. Gut epithelial apoptosis after
severe burn: effects of gut hypoperfusion. J Am Coll Surg. 2000
Mar;190(3):281-287.
16. Samonte VA, Goto M, Ravindranath TM, et al. Exacerbation of
intestinal permeability in rats after a two-hit injury: burn and
enterococcus faecalis infection. Crit Care Med. 2004
Nov;32(11):2267-2273.
17. Gan HT, Pasricha PJ, Chen JD. Blockade of p38 mitogen-activated
protein kinase pathway ameliorates delayed intestinal transit in
burned rats. Am J Surg. 2007 Apr;193(4):530-537.
18. Kadesky K, Purdue GF, Hunt JL. Acute pseudo-obstruction in
critically ill patients with burns. J Burn Care Rehabil. 1995
Mar-Apr;16(2 pt 1):132-135.
19. Oliveira HM, Sallam HS, Espana-Tenorio J, et al. Gastric and
small bowel ileus after severe burn in rats: the effect of
cyclooxygenase-2 inhibitors. Burns. 2009 Dec;35(8):1180-1184.
20. Marik PE, Zaloga GP. Gastric versus post-pyloric feeding: a
systematic review. Crit Care. 2003 Jun;7(3):r46-51.
21. Prelack K, Dylewski M, Sheridan RL. Practical guidelines for
nutritional management of burn injury and recovery. Burns. 2007
Feb;33(1):14-24.
22. Raff T, Germann G, Hartmann B. The value of early enteral
nutrition in the prophylaxis of stress ulceration in the severely
burned patient. Burns. 1997 Jun;23(4):313-318.
23. Battal MN, Hata Y, Matsuka K, et al. Effect of a prostaglandin i2
analogue, beraprost sodium, on burn-induced gastric mucosal
injury in rats. Burns. 1997 May;23(3):232-237.
24. Jia YT, Wei W, Ma B, et al. Activation of p38 mapk by reactive
oxygen species is essential in a rat model of stress-induced gastric
mucosal injury. J Immunol. 2007 Dec 1;179(11):7808-7819.
25. Maldonado MD, Murillo-Cabezas F, Calvo JR, et al. Melatonin as
pharmacologic support in burn patients: a proposed solution to
thermal injury-related lymphocytopenia and oxidative damage.
Crit Care Med. 2007 Apr;35(4):1177-1185.
26. Csendes A, Burgos AM, Smok G, et al. Latest results (12–21 years)
of a prospective randomized study comparing billroth ii and
roux-en-y anastomosis after a partial gastrectomy plus vagotomy
in patients with duodenal ulcers. Ann Surg. 2009 Feb;249(2):
189-194.
27. Mcclain T, Gilmore BT, Peetz M. Laparoscopic cholecystectomy in
the treatment of acalculus cholecystitis in patients after thermal
injury. J Burn Care Rehabil. 1997 Mar-Apr;18(2):141-146.
28. Theodorou P, Maurer CA, Spanholtz TA, et al. Acalculous
cholecystitis in severely burned patients: incidence and
predisposing factors. Burns. 2009 May;35(3):405-411.
29. Barie PS, Fischer E. Acute acalculous cholecystitis. J Am Coll Surg.
1995 Feb;180(2):232-244.
30. Hsu JC, Yang TL, Wang TC. Acute acalculous cholecystitis.
Zhonghua Yi Xue Za Zhi (TaiPei). 1993 Apr;51(4):266-270.
31. Flancbaum L, Choban PS. Use of morphine cholescintigraphy in
the diagnosis of acute cholecystitis in critically ill patients.
Intensive Care Med. 1995 Feb;21(2):120-124.
32. Puc MM, Tran HS, Wry PW, et al. Ultrasound is not a useful
screening tool for acute acalculous cholecystitis in critically ill
trauma patients. Am Surg. 2002 Jan;68(1):65-69.
33. Sosna J, Copel L, Kane RA, et al. Ultrasound-guided percutaneous
cholecystostomy: update on technique and clinical applications.
Surg Technol Int. 2003;11:135-139.
34. Wise JN, Gervais DA, Akman A, et al. Percutaneous
cholecystostomy catheter removal and incidence of clinically
significant bile leaks: a clinical approach to catheter management.
Ajr Am J Roentgenol. 2005 May;184(5):1647-1651.
35. Ryan CM, Sheridan RL, Schoenfeld DA, et al. Postburn
pancreatitis. Ann Surg. 1995 Aug;222(2):163-170.
36. Rivero HG, Lee JO, Herndon DN, et al. The role of acute
pancreatitis in pediatric burn patients. Burns 2011;37:82-85.
37. Jain R. Superior mesenteric artery syndrome. Curr Treat Options
Gastroenterol. 2007 Feb;10(1):24-27.
38. Kingham TP, Shen R, Ren C. Laparoscopic treatment of superior
mesenteric artery syndrome. JSLS. 2004 Oct-Dec;8(4):376-379.
39. Munene G, Knab M, Parag B. Laparoscopic duodenojejunostomy
for superior mesenteric artery syndrome. Am Surg. 2010
Mar;76(3):321-324.
40. Kowal-Vern A, Mcgill V, Gamelli RL. Ischemic necrotic
bowel disease in thermal injury. Arch Surg. 1997 Apr;132(4):
440-443.
41. Groger A, Bozkurt A, Franke E, et al. Ischaemic necrosis of small
and large intestine in a 2-year-old child with 20% partial
thickness burns: a case report. Burns. 2005 Nov;31(7):930-932.
42. Wilson MD, Dziewulski P. Severe gastrointestinal haemorrhage
and ischaemic necrosis of the small bowel in a child with 70%
full-thickness burns: a case report. Burns. 2001 Nov;27(7):
763-766.
43. Desai MH, Herndon DN, Rutan RL, et al. Ischemic intestinal
complications in patients with burns. Surg Gynecol Obstet. 1991
Apr;172(4):257-261.
44. Gomez R, Murray CK, Hospenthal DR, et al. Causes of mortality
by autopsy findings of combat casualties and civilian patients
admitted to a burn unit. J Am Coll Surg. 2009 Mar;208(3):
348-354.
45. Crabtree SJ, Robertson JL, Chung KK, et al. Clostridium difficile
infections in patients with severe burns. Burns. 2010 Nov 1.

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46. Jennings LJ, Hanumadass M. Silver sulfadiazine induced
clostridium difficile toxic megacolon in a burn patient: case
report. Burns. 1998 Nov;24(7):676-679.
47. Andres LA, Ford RD, Wilcox RM. Necrotizing colitis caused by
systemic aspergillosis in a burn patient. J Burn Care Res. 2007
Nov-Dec;28(6):918-921.
48. Gillespie P, Siddiqui H, Clarke J. Cannula related suppurative
thrombophlebitis in the burned patient. Burns. 2000
Mar;26(2):200-204.
49. Sheridan RL, Weber JM, Peterson HF, et al. Central venous
catheter sepsis with weekly catheter change in paediatric burn
patients: an analysis of 221 catheters. Burns. 1995 Mar;21(2):
127-129.
50. O’mara MS, Reed NL, Palmieri TL, et al. Central venous catheter
infections in burn patients with scheduled catheter exchange and
replacement. J Surg Res. 2007 Oct;142(2):341-350.
51. Mourot JM, Oliveira HM, Woodson LC, et al. Complications of
femoral artery catheterization in pediatric burn patients. J Burn
Care Res. 2009 May-Jun;30(3):432-436.

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Electrical injuries
Brett D. Arnoldo, John L. Hunt, Jose P. Sterling, Gary F. Purdue*
Electrical burns
Introduction
Electricity is an indispensable part of civilization, invisible
and often taken for granted. Electrical burns typically com­
prise only a small percentage of total admissions to major
burn centers – reportedly about 5–7%.1–3 They are, however,
the most devastating of all thermal injuries on a size-for-size
basis, usually involving both the skin and deeper tissues.
They primarily affect young, working men, often have legal
involvement, and are the most frequent cause of amputations
on the Burn Service. In addition to power company linemen,
electricians, construction workers, laborers, and crane opera­
tors are at special risk.4 These devastating injuries account for
nearly 6% of all occupational fatalities annually.5
Electrical burns have multiple acute and chronic manifesta­
tions not seen with other types of thermal injury. These inju­
ries therefore require the specialized care and expertise
available at a burn center. Even in the best-case scenario,
morbidity, length of hospital stay, and number of operations
are much higher than expected based on burn size alone.
Pathophysiology
Electrical burn severity is determined by voltage, current
(amperage), type of current (alternating or direct), path of
current flow, duration of contact, resistance at the point of
contact and individual susceptibility. Electrical burns are
arbitrarily classified as low-voltage (<1000 V) and high-
voltage injuries (1000 V and higher). Whereas low-voltage
burns are generally localized to the area immediately sur­
rounding the injury, the high-voltage burn is associated with
deep extension and underlying tissue damage, very closely
resembling a crush injury.6 Domestic wiring in the United
States operates on alternating current (AC) at 120 V. There­
fore, nearly all burns occurring indoors, except in specialized
industrial settings, are of the low-voltage type. Although the
victim or witness(es) often knows the voltage involved, the
amount of current is unknown, with current flow related to
voltage by Ohm’s Law where:
Current I
Voltage (E
Resistance R
( )
)/
( )
=
Animal experiments have demonstrated that resistance
varies continuously with time, initially dropping slowly,
then much more rapidly until arcing occurs at the contact
sites. Resistance then rises to infinity and current flow ceases.7
Temperature measurements taken simultaneously showed
that the rate of temperature rise parallels changes in amper­
age. Interestingly, tissue temperature, the critical factor in the
magnitude of tissue damage, does not increase distal to the
contact points.
In North America, more than 99% of all electrical burns
are caused by 60 cycle-per-second commercial alternating
current, which reverses its polarity 120 times per second.
Only an occasional low- or high-frequency industrial injury
is encountered. With half of the time spent positive with
respect to ground and one half spent negative, the terms
‘entrance’ and ‘exit’ wounds are archaic, as one does not
know whether a given point on the body contacted the wire
or the ground. These terms have now been replaced by
‘contact points.’ One or more contact points may be clearly
visible or at times pinpoint, subtle, or hidden, for example
beneath the hairline (Fig. 38.1). A descriptive term such as
blow-out type injury describes concentration of current and
not its causation.
The path of current makes a significant difference in pre­
hospital fatalities, but in patients reaching the hospital alive,
current path determinations are often less than precise and
meaningful. The patient may have no, one or many visible
contact points and an untold number of invisible contacts.
An example of this is surgical electrocautery, where the large
grounding pad contact site is not visible (hopefully). Despite
some misconceptions, the term ‘electrocution’ does not
apply to these living patients, as electrocution is defined as
‘to kill by electric shock.’8
Alternating current causes tetanic muscle contractions,
which may either throw victims away from the contact
or draw them into continued contact with the electrical
source – the ‘no-let-go’ phenomenon, creating the potential
for continually increasing severity. This phenomenon occurs
because both flexors and extensors of the forearm are stimu­
lated by current flow. However, the muscles of flexion are
stronger, making the person unable to let go voluntarily.
Altered levels of consciousness, reported in about half of
high-voltage victims, also contribute to prolonged periods
of contact.9 More than 99% of the body’s resistance to elec­
tric current flow is at the skin. Resistance is measured in
ohms (Ω). Resistance at the point of contact varies from very
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00038-2
CHAPTER 38 
Access the complete reference list online at

*We gratefully acknowledge the work of our deceased colleague, Gary F. Purdue.

Total Burn Care
38
434
heat so that the periosseous tissues, especially between two
bones (i.e. tibia–fibula, radius–ulna) often sustain a more
severe injury than superficial tissue. The associated macro-
and microscopic vascular injury appears to occur nearly
immediately and is not reversible.11 A recent study employ­
ing a rabbit animal model and optical microscopy demon­
strated severe injury to blood vessels. Necrosis of vascular
walls and thrombosis with destruction of arterial endothe­
lium, pyknosis of vascular smooth muscle and fibrinous
exudates accompanying the thrombotic changes was noted.
This study also showed progressive muscle necrosis over the
first 72 hours after injury that the investigators surmised may
have been related to the vascular injury.12 Of note, there was
also pathologic evidence of injury to organs remote from the
contact points (heart, lung, liver and kidney).
Direct and indirect electrical destruction of cells also plays
a role in tissue injury. The major mechanisms of injury
include Joule heating, electroporation, and electroconforma­
tional denaturation of transmembrane proteins.13,14 In all of
these mechanisms damage is caused by disruption or modu­
lation of cell membranes. Joule heating can be thought of
as the frying of tissue. This is the transfer of energy from
charged particles bumping up against tissue molecules and
losing energy to the tissue in the form of heat. Temperature
causes denaturation of macromolecules, which is usually
irreversible. Electroporation is the formation of aqueous
pores in lipid bilayers exposed to a supraphysiologic electri­
cal field. The formation of these pores allows calcium influx
into the cytoplasm and triggers a subsequent cascade leading
to apoptosis. Electroconformational denaturation of trans­
membrane proteins refers to the changes in polarity of
amino acids in response to exposure to electrical fields.
Experimentally, voltage-gated channel proteins were found
to change their conductance and ion specificity after expo­
sure to a powerful pulsed field.15
Acute care
The electrically burn-injured patient presents some unique
challenges in the acute setting. There are essentially three
acute management concerns differentiating these patients
from the thermally injured without flow of electric current.
In addition to the application of the basic principles of ATLS,
the three issues that need to be addressed in the ‘golden
hour’ are: (1) which patients require electrocardiographic
monitoring and for how long, (2) which patients are at risk
for compartment syndrome and may need emergency surgi­
cal intervention (often directly from the emergency depart­
ment), and (3) how should fluid resuscitation proceed in
light of the preponderance of deep tissue injury that may not
be appreciated on physical examination, in particular in the
presence of pigmented urine?
Electrocardiographic monitoring
All studies reviewed in a recent American Burn Association
Guidelines paper confirmed that cardiac abnormalities,
including dysrhythmias and myocardial damage, occur after
both low-voltage and high-voltage injuries, thus reinforcing
the need for ECG evaluation as part of the initial evaluation
low values for sweat-soaked hands or skin in the summer to
more than 100 000 Ω for heavily calloused hands or feet
during very dry winter weather. Individual susceptibility is a
non-quantifiable term to explain why two or more individu­
als exposed to the same situation have extremely varied
injuries.
The burn injury has the potential for three different com­
ponents: the true electrical injury caused by current flow, an
arc injury resulting from the electrical arc generated as the
current passes from the source to an object, and a flame
injury caused by ignition of clothing and/or surroundings.
Electricity arcs at temperatures of up to 4000°C create a flash
type injury,10 most often seen in electricians working with
metal objects in close proximity to an electrical source. The
victim may be thrown by the force, and suffer ruptured ear­
drums and contused internal organs. When electrical injuries
occur without actual current flow through the victim,
they are treated and classified in the same manner as any
flash burn.
The exact mechanism of electrical injury continues to be
the subject of much research, very often appearing clinically
to be a multifactorial combination of both thermal and non-
thermal causes. Electricity flowing through tissue generates
heat, much as it does flowing through the wire of a toaster,
with Joule’s law defining the amount of power (heat) deliv­
ered to an object:
Power J-Joule
I Current
R Resistance
(
)
(
)
(
)
=
×
2
Tissue resistance is from lowest to highest in nerves, blood
vessels, muscle, skin, tendon, fat and bone, respectively.
Theoretically, current flow would be distributed in propor­
tion to resistance, with tissues having the highest resistance
generating the most heat. However, in animal models the
body acts as a single uniform resistance rather than a collec­
tion of different resistances, i.e., it behaves as a volume con­
ductor.7 Severity of injury is inversely proportional to the
cross-sectional area of the body part involved. Thus the most
severe injuries are often seen at the wrist and ankle, with
severity decreasing proximally. Deep tissues appear to retain
Figure 38.1  Contact point on scalp.

Electrical injuries
435
as administration of mannitol for osmotic diuresis. These
adjuncts are not supported by level I evidence, but many
burn centers have successfully adopted their use in various
forms. The required urinary output is generally very high
for several hours following injury, followed by a significant
reduction in urine requirements, as venous return from
the injured part to the central circulation is thrombosed.
Failure to clear pigment from the urine is generally an
indication of significant muscle necrosis and/or ongoing
ischemia. This should prompt a thorough evaluation of the
likely current path and underlying muscle damage, as
this failure of therapy can often be taken as an indication
for operative intervention for decompression versus
debridement/amputation.
In the absence of gross myo/hemoglobinuria, the goal of
resuscitation is to maintain normal vital signs and a urine
output of 30–50 mL/h with Ringer’s lactate, whose rate is
adjusted on an hourly basis to achieve these goals.
Traumatic injuries
Approximately 15% of electrical burn victims sustain trau­
matic injuries in addition to their burn, a rate nearly double
that of other burn patients. Most of these injuries are caused
by a fall from a height or being thrown against an object,
but some resulting from the tetanic muscle contractions
associated with the electrical shock itself, forces strong
enough to cause compression fractures.28 A careful history
and physical examination should select those patients who
require a full trauma evaluation.
Compartment syndrome
Patients with high-voltage electrical injuries of the extremi­
ties are at risk for the development of compartment syn­
dromes during the first 48 hours post injury. Damaged
muscle, and swelling in the investing fascia of the extremity,
may increase pressures to the point where muscle blood flow
is compromised. Loss of pulses is one of the last signs of a
compartment syndrome, unlike the early loss of pulses occur­
ring in a circumferentially burned extremity requiring escha­
rotomy. A high index of suspicion is paramount for an
early diagnosis, usually by serial examinations. Compart­
ment pressure measurement is generally not necessary and
may even be misleading (Figs 38.2 and 38.3). Whereas a very
aggressive approach to fasciotomy has been advocated in the
past, significant morbidity attends a fasciotomy and its
closure. Amputation rates were generally reported to be in the
35–40% range in most of these early series.29–33 Mann et al.
have made a convincing argument for a conservative course
regarding the indications for fasciotomy, that is, for the usual
clinical signs of compartment syndrome, progressive nerve
dysfunction or failure of resuscitation, with other patients
undergoing exploration and aggressive debridement on the
third to fifth post burn days.34 Elevated CK levels have been
correlated to the extent of muscle damage, with the authors
advocating early decompression and aggressive surgical man­
agements in patients with strongly elevated CK levels.35 In the
author’s experience making the decision to operate is gener­
ally not difficult. These are rarely subtle injuries. There is
often an obvious indication for operative intervention on the
in all patients.16 Non-specific ST-T changes are the most
common ECG abnormality and atrial fibrillation is the most
common dysrhythmia.17,18 This has also been the authors’
experience, and all dysrhythmias have responded to appro­
priate medical management as per ACLS protocols.
Direct myocardial injury may also result. This injury
behaves more like a traumatic myocardial contusion than a
true myocardial infarction, not having the hemodynamic or
recurrence consequences of atherosclerotic myocardial inf­
arctions. Housinger et al. have shown that creatine kinase
(CK) and MB-creatine kinase (MB-CK) levels are poor indi­
cators of myocardial injury in the absence of ECG findings
of myocardial damage, especially in the presence of signifi­
cant skeletal muscle injury.19–21 Myocardial damage and dys­
rhythmias are manifested very soon after injury.22 Although
cardiac troponins are the preferred biomarkers for detecting
myocardial injury in most clinical settings, this has not been
adequately studied in the setting of electrical injuries. A
recent study using serum troponin levels and serial echocar­
diography in 20 patients surviving high-voltage injury con­
cluded that this was not a useful diagnostic test for predicting
impaired left ventricular contractility.23 The interpretation of
cardiac biomarkers is problematic and needs to be correlated
with other clinical findings. All patients should be moni­
tored during transport and in the emergency room. Rather
than a policy of more prolonged cardiac monitoring for all
patients, a selective policy makes most efficient use of expen­
sive medical resources, without patient risk.4,22
Indications for cardiac monitoring include (1) loss of
consciousness, (2) ECG abnormality and/or evidence of
ischemia, (3) documented dysrhythmia either before or
after admission to the emergency room, and (4) CPR in
the field.
No published studies have directly studied the appropri­
ate duration of telemetry monitoring, but most series indi­
cate 24–48 hours.24–27 Our institutional bias is to monitor
for approximately 24 hours post injury in those patients
with an indication. Low-voltage injuries not meeting the
criteria for cardiac monitoring and no other indication for
admission can be safely discharged from the emergency
room. This is not applicable to high-voltage injuries,
although there is retrospective evidence that dysrhythmias
will occur early if at all in these patients.22
Myoglobinuria
The presence of pigmented (darker than light pink) urine
in a patient with an electrical burn indicates significant
muscle damage with potentially ongoing ischemia.
Myoglobin and hemoglobin pigments present a risk of acute
renal failure and must be cleared promptly. Whereas low
levels are of little clinical concern, grossly visible urinary
pigmentation requires a rapid response to minimize tubular
obstruction. Urine with a color darker than light pink is
promptly treated by titrating resuscitation fluid (Ringer’s
lactate) to maintain a urine output double the goal rate, or
approximately 100 mL/h in an adult. Therapy continues
until the urine appears clear clinically. In addition, other
methods have been adopted to enhance renal clearance of
myoglobin. These include alkalinization of the urine with
a sodium bicarbonate bolus or continuous infusion, as well

Total Burn Care
38
436
or electrocautery, with care taken to assure complete release
of all affected muscle groups. Coverage of the ensuing wound
may include dressings soaked q 4–6 hours with 5% mefa­
nide acetate (Sulfamylon) solution or a biologic dressing
such as porcine heterograft, and the extremity is kept ele­
vated to hasten resolution of edema.33 The initial operation
is followed by a second look in 24–48 hours, with debride­
ment or amputation. However, a conservative tissue-sparing
approach is generally prudent. Fasciotomy wound closure is
often not possible in these injuries, and skin grafting may be
required for wound coverage. The Vacuum Assisted Closure
device (VAC) has made the management of burn wounds
considerably easier. Primary amputations are not generally
performed, except to remove mummified, contracted extrem­
ities where there is no question about viability.
Wound care
Local burn care is performed using 11.1% mafenide acetate
cream (Sulfamylon) on the thick eschar of the contact points,
because of its excellent penetration. Silver sulfadiazine is
used for microbial control on the deep flash/flame compo­
nents and a biologic dressing on more superficial areas.
Surgical excision is begun 2–3 days post burn, either as a
second-look operation following fasciotomy or as the first
procedure in patients not requiring fasciotomies. All obvi­
ously necrotic tissue is removed, but tissues of questionable
viability are retained and re-evaluated every 2–3 days until
all non-viable tissue is ultimately removed. A very conserva­
tive course of tissue removal and wound closure with a
combination of skin grafts and/or flaps for soft tissue cover­
age gives the best functional results. An ongoing program
of physical therapy and functional splinting is begun the
day of admission if practical, and continued throughout
the hospital stay. Serial neuromuscular examinations are
performed to document neurologic status. Regional
anesthesia is avoided to minimize medical legal complica­
tions should late neurologic dysfunction arise.
Pain management
Pain management in electrically injured patients has not
been well studied. Standard regimens in the acute phase of
care are similar to those for other thermally injured patients
and include opioids, NSAIDs, and benzodiazepines for pain
and associated anxiety. Pain concerns and management regi­
mens change over the treatment course as the patient enters
rehabilitation and the more chronic stage of care. In a recent
study the most common medications in the acute setting
were opioids and acetaminophen, and in the rehabilitation
phase antidepressants and NSAIDs.37 Non-pharmacologic
treatments were also used, such as massage therapy and
cognitive behavioral therapy. This reflects the changing
requirements and concerns in these complex patients as well
as the need for a multidisciplinary team approach.
Diagnosis
Multiple diagnostic modalities have been investigated in
attempting to speed up the process of identifying the extent
of deep tissue necrosis. These include xenon-133 and tech­
netium pyrophosphate scans as well as gadolinium-enhanced
initial evaluation, or else there are minimal findings. However,
vigilance in the first 24–48 hours is required.
Four compartment fasciotomies of the lower leg and ante­
rior (including the ‘mobile wad’) as well as posterior fasci­
otomies of the upper extremity are performed in the
operating room under general anesthesia.36 Upper extremity
decompression will generally always include a carpal tunnel
release, as this is usually the location of the most severe
injury. This is relatively easy to perform if one takes care to
locate the incision on the ulnar side of the palmaris longus
tendon. In addition, the accumulation of edema fluid at the
injury site works in the surgeon’s favor, as it creates a plane
between knife (or scissors) and the median nerve below. In
the event of contact points on the palmar surface near the
wrist (which is usually the case) the incision can begin near
the wrist and cross onto the palm following the thenar
crease. The incision can then be extended proximally up the
arm if required. Rarely, medial and lateral fasciotomies of
the thigh and upper arm are required to completely release
all damaged areas. Incisions can be made with either a knife
Figure 38.3  Forearm fasciotomy, Carpal tunnel release.
Figure 38.2  Forearm fasciotomy for high voltage injury.

Electrical injuries
437
minimal cutaneous burn to significant burns equal in depth
to commercial high-voltage electricity. Major cutaneous
injury is rare unless a nearby object is turned incandescent,
causing a flash/flame type injury, as when a bag of golf clubs
on the victim’s back is struck. The pathognomonic sign of a
lightning strike is a dendritic, arborescent or fern-like branch­
ing erythematous pattern on the skin. Lichtenberg figures
(also known as keraunographic markings), consist of extrava­
sation of blood in the subcutaneous tissue which appears
within an hour of injury and fades rapidly, much like
a wheal and flare reaction.56,57 Full-thickness isolated
burns on the tips of the toes have also been reported as
characteristic. Both findings are useful in determining the
cause of injury in the patient found down under uncertain
circumstances.58
Lightning may cause both respiratory and cardiac stand­
still, for which CPR is especially effective when promptly
initiated.59 Patients may respond to resuscitation even when
they appear dead, and even when the interval between injury
and resuscitation is prolonged. It is important to realize that
dilated or non-reactive pupils are not necessarily a reliable
sign of brain death in the early post-injury period, nor is
GCS a predictor of outcome.60–62 The ears should be carefully
examined as injuries are frequent, ranging from ruptured
tympanic membranes (most common) to middle and inner
ear destruction.63
Neurologic complications are relatively common and
include unconsciousness, seizures, paresthesias and paraly­
sis, which may develop over several days after injury. The
term keraunoparalysis (Charcot’s paralysis) has been used to
describe the latter symptom complex and is associated with
vasomotor disorders. Fortunately these are usually transient.
Surgically treatable lesions, including epidural, subdural and
intracerebral hematomas, may occur, mandating a high
index of suspicion for altered levels of consciousness.55
The prognosis of many lightning-caused neurologic injuries
is generally better than for other types of traumatic
cause, although subtle neurologic changes may persist,
suggesting a very conservative, watchful waiting and sup­
portive approach with serial neurologic examinations after
an initial CT scan to rule out correctable causes. A study by
Muehlberger et al. with follow-up to 12.3 years after injury
showed that none of their 10 patients had long-term neuro­
logic or psychological deficits.64 However, post-traumatic
stress disorder is common, occurring in about 30% of
patients after lightning injury.65
Low-voltage burns
Low voltage alternating current injury is usually localized to
the points of contact, although with prolonged contact,
tissue damage may extend into deep tissues with little lateral
extension, as seen in high-voltage wounds. These wounds are
treated by excision to viable tissue and appropriate coverage
based on wound depth and location.
Burns of the oral cavity are the most common type of
serious electrical burn in young children.66 Most of these
injuries are the result of an unattended small child (com­
monly < 4 years of age) chewing on an electric cord. Injuries
involving only the oral commissure are almost never excised,
as the extent of injury is difficult to predict (Fig. 38.4).
Simple wound care is performed as an outpatient
magnetic resonance imaging.38–42 Albeit very sensitive
and specific, diagnostic scans add little to direct clinical
evaluation, and for all practical purposes are expensive and
unnecessary.
Problem areas
Contact points on the scalp, chest and abdomen provide
additional specific management problems. Scalp burns
which spare the galea are managed by excision and skin
grafting directly onto the galea, whereas wounds that pene­
trate or expose the outer table of the skull or deeper require
a different approach. Exposure of non-viable calvarium has
historically been approached by providing a viable wound
bed after removing the dead bone with an osteotome or a
dental burr. Drilling multiple holes in a close-set pattern,
deep enough to cause bleeding from viable cancellous bone,
is another method to develop granulation tissue which even­
tually covers the entire area. The latter method is still useful
in situations where a patient’s advanced age or large burn
size precludes more aggressive approaches to wound closure.
All of the above methods require weeks to months of care
before the wound is ready for autograft coverage. The best
and most expedient approach to these deep skull burns is a
rotation scalp flap(s) over the burned area. Split-thickness
skin grafts cover the resulting adjacent defect. This provides
rapid closure and is associated with minimal morbidity.43
Skin expansion of the hair-bearing area can be performed
12–18 months later to obliterate the areas of alopecia. Scalp-
tissue expansion for coverage of open wounds is, however,
described only in case reports.44,45 Larger scalp defects are
closed with free flaps anastomosed to appropriate vessels
lying outside the zone of injury. A recent study evaluated the
outcomes of early free tissue transfers in 13 cases at various
anatomic locations.46 Operations occurred between 24 hours
to 3 weeks post burn. All but one flap survived. Once again
this reinforces the concept of multidisciplinary care and the
early involvement of a qualified plastic surgeon in appropri­
ate cases.
Chest wall injuries present special closure problems (adja­
cent or remote soft tissue flaps) for coverage of exposed
bone and cartilage. Costal chondritis is the most frequent
complication of deep chest wall burns, often becoming
a source of long-term morbidity, requiring multiple
debridements.
Abdominal wounds provide the potential for internal inju­
ries, both directly under contact points and remotely as the
result of late ischemic necrosis.47,48 Patients must be fre­
quently evaluated for changes in their abdominal examina­
tion and/or feeding tolerance. Deterioration mandates
laparotomy.
Lightning injury
Lightning is the second leading cause of weather-related
death in much of the world, but under-reporting likely influ­
ences the data.49–52 Approximately 100 000 thunderstorms
occur in the US each year, with lightning killing more people
than any other weather phenomenon – about 80 fatalities
per year – with Florida and Texas having the most deaths.53–55
Although lightning strikes involve millions of volts of elec­
tricity, the spectrum of burn injury is extremely varied, from

Total Burn Care
38
438
of peripheral neuropathy, with 50% resolving. They reported
no late-onset central neuropathies. Singerman et al. reported
neurological and psychological complication rate of 81.6%
and 71%, respectively.76 The most common neurological
symptoms were numbness (42%), weakness (32%), memory
problems (32%), paresthesias (24%), and chronic pain
(24%). The most common psychological symptoms were
anxiety (50%), nightmares (45%), insomnia (37%), and
flashbacks to the event (37%). Interestingly, the low-voltage
injuries resulted in more long-term sequelae than high-
voltage injuries. Further studies from the same center dem­
onstrated only a 30% return to work after low-voltage
electrical injuries.77 In a study by Chudsamama et al. the
high-voltage injuries had more complex and longer hospital
stays and more frequent complications than low-voltage
injured patients.78 In spite of this the low-voltage group
experienced similar rates of neuropsychiatric sequelae,
limited return to work, and delays in return to work. Ko et al.
reported on 13 patients with delayed onset of spinal cord
injuries, postulating on a vascular cause of the deficit.79 The
most common peripheral defect is a peripheral neuropathy,
with weakness being the most commonly found clinical
finding.80 In general, resolution of early-onset lesions is
much better than for late onset, spasticity is more frequent
than flaccidity, and function is affected more than sensation.
Sympathetic overactivity with changes in bowel habits,
urinary and sexual function is the primary autonomic
complex complication. Although the exact mechanism of
nerve injury has not been explained, both direct injury by
electrical current and/or a vascular cause receive the most
attention. To date, imaging studies, including angiography
and MRI, have not been helpful in either predicting or evalu­
ating the extent of deficit. Very often, neuropsychological
status is abnormal. In a study comparing electrical burn
patients with non-burned electricians, Pliskin et al. showed
significantly higher cognitive, physical and emotional
complaints not related to injury or litigation status.81 A full
neurologic examination must be performed on admission,
documenting the initial presentation. Early involvement of
an experienced, interested physiatrist is important in assess­
ing long-term needs and participating in the creation of a
therapy plan.
Heterotopic ossification occurring at the cut ends of ampu­
tation sites is unique to the electrically burned patient. This
occurs in about 80% of patients with long bone amputa­
tions, but not in patients with disarticulations or small bone
amputations. Ossification was severe enough to require sur­
gical revision of the bone end in 28%.82 This is easily accom­
plished by opening the stump incision and using a bone
rongeur to remove the soft heterotopic bone and reclosing
the stump.
Although electrical burns comprise only about 3% of all
burn injuries, they consume enormous amounts of
resources, requiring a carefully planned team approach for
optimal care.
Further reading
Arnoldo B, Klein M, Gibran NS. Practice guidelines for the
management of electrical injuries. J Burn Care res. 2006
Jul-Aug;27(4):439-447.
procedure.67,68 The most serious complication is bleeding
from the labial artery, occurring 10–14 days after injury.
Families are instructed to compress the labial artery digitally
if bleeding occurs and to return to the ER. Following healing,
treatment varies according to the severity of injury. Gentle
stretching and the use of oral splints gives good cosmetic
and functional results in most patients, with reconstructive
surgery being reserved for the remainder. Severe microstomia
is corrected by mucosal advancement flaps. Burns of the
mid-portion of the mouth heal poorly and may require a
more aggressive surgical approach.69,70
Complications
The primary early complications of electrical injury include
renal, septic, cardiac, neurologic and ocular manifestations.
Neurologic deficits may be present on admission or develop
days to weeks after injury.
Cataract formation is the most frequent ocular complica­
tion of electrical injury, although ocular manifestations may
affect all portions of the eye.71,72 The exact pathophysiology
is unknown, but ocular changes may affect as many as
5–20% of patients with true electrical burns. Saffle et al.
reported on seven patients with 13 cataracts, noting a high
rate of bilaterality and little association with voltage or loca­
tion of contact points, although often thought of as being
more frequently associated with contact points of the head,
neck and upper trunk.73 Of this series, 77% eventually pro­
gressed to the point where surgical therapy was necessary,
the results of which were uniformly good. Lag time before
appearance may be as short as 3 weeks and as long as 11
years after injury.74
Neurologic complications are protean in their diversity
and may present either early or late (occurring up to 2 years
after injury). Neuromuscular defects including paresis, paral­
ysis, Guillain–Barré syndrome, transverse myelitis or amyo­
trophic lateral sclerosis can be caused by electrical injury.75
Several studies put the incidence of post electrical injury
sequelae into perspective. Grube et al. reported on 64
patients with high-voltage burns, 67% of whom developed
immediate central or peripheral neurologic symptoms.9
One-third had peripheral neuropathies and one-third of
those were persistent. Furthermore, 12% had delayed onset
Figure 38.4  Low-voltage burn to the mouth.

Electrical injuries
439
always necessary? J Trauma. 1996 Apr;40(4):584-587; discussion
587-589.
Rai J, Jeschke MG, Barrow RE, et al. Electrical injuries: a 30-year
review. J Trauma. 1999 May;46(5):933-936.
Ritenour AE, Morton MJ, McManus JG, et al. Lightning injury: a
review. Burns. 2008 Aug;34(5):585-594.
Arnoldo B, Purdue G, Kowalske K, et al. Electrical injuries: A 20 year
review. J Burn Care Rehabil. 2004;25:479-484.
Grube B, Heimbach D, Engrav L, et al. Neurologic consequences of
electrical burns. J Trauma. 1990;30:254-258.
Mann R, Gibran N, Engrav L, et al. Is immediate decompression
of high voltage electrical injuries to the upper extremity
 
Access the complete reference list online at

Electrical injuries
439.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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Electrical injury: reconstructive
problems
Peter M. Vogt, Andreas D. Niederbichler, Andreas Jokuszies
Introduction
’Severe cases [of electrical injury] coming for
reconstruction present a formidable problem of flexion
contracture and loss of many tendons and nerves,
new pedicled skin and grafted-in tendons and nerves
usually being necessary. One encounters inside the
limb the same type of destruction and cicatrix as is
found after any severe infection.’
Sterling Bunnell, 1948
This chapter will focus on the multitude of surgical and
reconstructive problems that result from electrical injury. The
injury severity is complex due to various factors determining
manifestation and the distribution of the resulting tissue
damage. In common with other types of trauma, especially
burn injuries, the consequences of electrical injury may affect
a wide range of physiological functions. Its distinct features
warrant a differentiated approach to this unique kind of
trauma. The resulting tissue loss and the damage to essential
structures of the involved body areas often require extensive
plastic-reconstructive procedures.
Although the incidence of low-voltage burns has declined
steadily over recent decades, most probably due to progress
made in the field of home and occupational safety education
and equipment, electrical injuries still account for 3–5% of
all admissions to major burn centers.1,2 Electrical fatalities
are relatively uncommon and most of them occur acciden­
tally. Earlier reported limb amputation rates of up to 71%
decreased over recent decades with the increasing ability to
reconstruct anatomic parts and restore function, but limb
salvage remains a surgical challenge.3,4
Physiological basis of tissue destruction
The traditional pathophysiological understanding of electric
injury was based on the assumption that the passage of
electric current produces heat and triggers tissue damage.5
Thus, tissue-specific susceptibility (and vulnerability) is con­
sidered to increase progressively from nerve to blood vessels,
muscle, skin, tendon, and fat to bone. As osseous tissue
shows the highest electrical resistance it will generate the
most heat. Electric current will preferentially take the path
of least resistance through the body, so that the current will
pass particularly along the neurovascular bundles. This
theory further postulated that the lesions produced by the
current would result in delayed vascular occlusion and
progressive tissue necrosis.6
In high-voltage injuries the internal milieu acts as a
single uniform resistance.7 Instead of conduction through
specific preferential tissues, the body conducts the current
with a composite resistance of all tissue components.8 The
crucial factor in determining the resistance and hence
the magnitude of tissue damage is the cross-sectional diam­
eter of the affected body part. Devastating injuries to the
extremities occur with a significantly higher frequency than
tissue damage to the thorax and abdomen9 (Fig. 39.1). As
muscle tissue occupies the largest cross-sectional area in the
limb it also carries the predominant electric current. As
joint areas are regions where the cross-sectional tissue
composition changes from low-resistance muscle to high-
resistance bone, tendon and skin, a proportionally higher
current and heat are produced in these areas according to
Ohm’s Law.9
Arcing describes the energy transmitted by a hot electri­
cally conducting gas. However, this requires a voltage of
more than 20 000 V to bridge even a short distance of 1 cm.10
Effects on tissue vary from minimal skin wounds to charring
and tissue vaporization.
The different trauma mechanisms of the burns induced
by the arcing phenomenon are often referred to as ‘flush
burns’, heat burns which are induced by the massive heat
generation. ‘Electrothermal burns’ are caused by current
passage through the body and the concomitant heat
production.
Electrical damage to a large artery represents a grave prog­
nostic sign for limb survival.11 The reported risk of amputa­
tion is high, between 37% and 65%.12–14
Further non-thermal mechanisms of cellular injury have
been defined. This includes a voltage-induced loss of cell
membrane semipermeability.15–17 When the integrity of the
cell membrane is lost, the impedance is markedly reduced,
leading to a simultaneous increase in the area exposed to
current flow.18 In addition to breakdown in cellular integrity
electrical fields also induce denaturation of membrane pro­
teins by altering their structural conformation and rendering
them non-functional.19 Both mechanisms are responsible for
©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00039-4
CHAPTER 39 
Access the complete reference list online at

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Clinical determination of tissue viability is based on
inspection and the demonstration of muscle contractility. As
yet, there are no other diagnostic tools available to accurately
assess the extent of tissue damage in the early phase follow­
ing electrical injuries. The value of magnetic resonance
imaging (MRI) for the detection of non-perfused non-
edematous muscle is debated.24–26 Angiography, although
not providing information on tissue viability, demonstrates
the absence of tissue perfusion and may lead to an early
indication for limb amputation.27
Rhabdomyolysis and myoglobinuria
Destroyed muscle cells release myoglobin, resulting in
myoglobinemia. Hemolysis also often occurs with electrical
injury. Serum levels of creatinine and creatinine phosphoki­
nase (CPK) are used as indicators of rhabdomyolysis. After
muscle injury CPK levels will peak by 24 hours and return
rhabdomyolysis and secondary myoglobin release, which
depends directly on the imposed electric current and is not
a thermal effect.20
The human body consists of about 60 % water. The intra-
and extracellular water content and their highly resistive
plasma membrane separate these two compartments from
each other.21 Change in the current transporters from elec­
trons to ions at the skin surface appears as metallic conden­
sations as dark-greyish skin lesions which resemble eschar.22
Another central factor of the cellular effect of electrical
current is its frequency, which can arbitrarily be divided into
low (<10 kHz) and high (>10 kHz, e.g. radio frequency,
microwave and ionizing frequencies).
Diagnosis and acute treatment
Diagnosis and acute treatment of electrical injury are
described in Chapter 38.
Assessment of tissue damage
Accurate assessment of the extent of tissue damage is diffi­
cult. The percentage of burned body surface area grossly
underestimates the injury to underlying tissue. Electrical
burns may appear as mere pinpoint marks. In contrast, fatal
electrocution may even take place without visible skin burns
in case of a large contact area (Table 39.1).
In contrast to thermal burns, deposition of metallic
iron and copper is found on the epidermis after electrical
injuries as electrolysis occurs in the extra cellular fluid of
the skin.24–26
Figure 39.1  Electrical burn from a domestic water heater (220 V). The 13-year-old girl manipulated the device while being immersed in the bathtub.
She sustained third- and fourth-degree burns to the digits (a). Debridement revealed full-thickness injuries involving tendons, nerves, and phalangeal bones
(b), which necessitated primary amputation (c).
A
B
cC
Table 39.1  Dependence of cutaneous resistance
on skin moisture
Resistance
Dry skin
100 000 Ω
Wet skin
2 500 Ω
Skin immersion
1 500 Ω
Rubber soles
70 000 Ω
Reproduced from Ohashi et al. Burns 1998;24:362–368.24

Electrical injury: reconstructive problems
443
Apart from specific therapeutic measures for cardiac com­
plications, acute treatment of patients with electrical injuries
adheres to guidelines of ABLS, ATLS and current practice of
intensive care medicine. The patient must be continuously
monitored for signs of neurovascular compromise, and
deranged tissue perfusion and oxygenation.
Surgical debridement
In recent decades the concept of progressive tissue necrosis
has led to the treatment strategy of early debridement and
fasciotomy, followed by serial debridement and delayed
wound closure.41 The observed changes may likely be
explained by vascular changes similar to ischemia–
reperfusion injury with immediate cessation of capillary
blood flow in response to current passage. This event is fol­
lowed by vascular spasms lasting for an extended period,
with subsequent vasodilatation and restoration of flow.43–45
Although still controversial, these findings may alter the
acute treatment paradigm.
Although there is little discussion about the early time
point of debridement, several recent studies question the
need for extensive and total necrectomy and advocate the
approach of delayed soft tissue coverage. ‘Conservative deb­
ridement’ consisting of removal of charred and obviously
necrotic tissue was promoted in a study on 40 patients.46 In
this study partially damaged tendons, muscles, and nerves
were preserved, and wound closure was achieved by immedi­
ate flap coverage. Patients treated in this manner with imme­
diate soft tissue coverage had a significantly better outcome
than a control group who underwent serial debridement
procedures. Similar results were found in a study using
early free-flap coverage for electrical injuries, suggesting that
careful limited initial debridement is an adequate measure.47,48
According to this study overly extensive and repeated debri­
dement to ensure viability of all remaining tissue appears
not only unnecessary but quite likely harmful. It appears safe
to abandon these strategies and to perform an early, exten­
sive but selective debridement in order to preserve continuity
of functionally important structures (Fig. 39.2). Limb salvage
with functional preservation of vital structures should be
attempted and may require revascularization using segmen­
tal vein grafts or segmental cable grafting of nerves. Pedicled
flaps should be considered in cases of suspected arterial
compromise.
Despite the encouraging results of the studies recommend­
ing early soft tissue reconstruction, by all means it should
be noted that for the extent of electrical injury no scoring
system has so far been established. Alternative approaches
to salvage upper extremity function, such as the temporary
ectopic implantation of an undamaged hand, have been
reported but cannot be considered standard of care.49
Compartment syndrome
Muscle compartment pressure should be monitored clini­
cally and by invasive pressure measurements. In contrast to
blunt trauma, pain is not a reliable indicator of increased
compartment pressure owing to the high incidence of
electrical nerve injury. When compartment pressures exceed
to baseline within 48–72 hours.28 This diminishes the diag­
nostic value of serum and urine chemistry testing.29,30
Renal failure
Myoglobinuria has traditionally been considered a major
risk factor for the development of acute renal failure. Recently,
patients with electrical injuries have been shown to have a
surprisingly low risk for renal failure.31 In 162 patients, only
14% had myoglobinuria and none developed renal failure.
Suggested criteria to evaluate the risk of acute renal failure
after electrical injury include prehospital cardiac arrest, full-
thickness burns, compartment syndrome, and high-voltage
injury. The presence of at least two of these criteria should
instigate immediate treatment, as the timeframe to prevent
progression to acute renal failure is limited to a few hours
post injury.
Cardiac monitoring
Among the estimated 1300 deaths that occur annually in the
United States from electrical injury (including lightning
strike), 30% of patients present with cardiac complications.
The majority of ECG abnormalities are sinus tachycardia and
non-specific changes in the ST-segment and T-wave.32 Death
from electric injury most commonly results from current-
induced cardiac arrest.
However, if an initial ECG shows no abnormalities the
delayed development of cardiac problems is very unlikely,
irrespective of whether the patient sustained high- or low-
voltage injuries.33–35
Conversely, the presence of dysrhythmias or conduction
abnormalities on initial presentation, electrical injury in
children, or the projected path of the current flow crossing
the thorax on initial presentation, warrant prolonged cardiac
monitoring.36–39 Depending on the nature of the current-
induced arrhythmia, pharmacotherapeutic and/or invasive
interventions may be necessary. Table 39.2 outlines recom­
mendations for cardiac monitoring of electrically injured
patients based on central clinical findings and specific fea­
tures of the trauma mechanism.42
Table 39.2  Recommendation for cardiac monitoring
in the absence of other injuries
Admission and cardiac
monitoring
Discharge
Loss of consciousness59
Asymptomatic patient60
Extensive burns50
Normal initial ECG61
Current passing through the
thorax52
Uneventful 4-hour observation62
Cardiac dysrhythmias59
Voltage less than 240/260 in adults60,61
Voltage less than 120/240 in children48,62
PP. 1257–1259

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Figure 39.2  High-voltage injury from an overhead power line (30 000 V).
The teenager climbed a train and was struck by an arc without touching the
power line. The spectrum of injury included third- and fourth-degree burns
and deep tissue necrosis of the forearm (a). After fasciotomy because of
impending compartment syndrome (b). Coverage with free latissimus dorsi
flap after ‘conservative’ debridement. Significant functional deficits after 4
years (c).
A
B
C
30 mmHg surgical decompression by open fasciotomy
becomes necessary to prevent ischemic muscle injury. In case
of lower compartment pressure, progression may be pre­
vented by administration of non-steroidal anti-inflammatory
drugs (NSAIDs) and antioxidants, protective splinting, and
rest without elevation of the affected extremities. However,
general operative decompression in high-voltage injuries to
extremities appears not to be warranted. In a cohort study,
Mann et al. found an increased amputation rate of 45% with
immediate operative decompression compared to patients
undergoing selective fasciotomy, and they recommend fasci­
otomy only in cases of progressive peripheral nerve dysfunc­
tion, manifested compartment syndrome, or other major
injuries40 (Fig. 39.2 and Fig. 39.3) With a fixed neurological
deficit, however, surgical decompression shows no influence
on outcome.50 If the clinical situation remains doubtful,
however, the performance of open fasciotomy with early
debridement may be preferred.
Head: scalp, skull and mouth
Exposure and necrosis of osseous structures may lead to
osteomyelitis and epidural abscess formation. Treatment
strategies depend on the extent of the injury to the bone. In
case of only a partial necrosis of the bone the outer table of
the skull can be tangentially removed and the viable diploic
cavity exposed. In cases of sufficient vascularization the
exposed bone can be grafted immediately or, when blood
supply is questionable, grafted when suitable granulation
tissue has developed.51 Vacuum sealing of the wound can be
of significant efficacy in growing adequate amounts of gran­
ulation tissue. When the initial wound debridement is
delayed, necrotic and infected bone potentially becomes the
source of a full-thickness skull defect. Full-thickness injury
of the skull theoretically requires complete excision of the
necrotic bone to prevent infectious complications.69 Another
approach suggested is partial debridement followed by
definitive flap coverage of the exposed bone. This, however,
requires early debridement and the prevention of localized
bacterial colonization and infection.52,53
In a series of 10 male patients with non-viable cranial
bone after class IV electrical burns, 3 weeks after initial soft-
tissue debridement multiple burr holes in the non-viable
and preserved bone were made and scalp flap coverage
was performed.54 Leaving the necrotic osseous structures
in situ serves as a scaffold of substitution for bone
regeneration.55–57
Skull contour was maintained in all 10 patients, making a
secondary cranioplasty unnecessary. During a follow-up
period of at least 1 year no postoperative infection, osteo­
myelitis, or cranial bone sequestration occurred.54
Another option is the use of glycerol-preserved allografts
(GPA).58 The growth of spontaneous sufficient granulation
tissue is promoted by its angiogenetic capacity and split-skin
autografts can be performed at a later stage. Further benefi­
cial properties of GPA appear to be related to their perme­
able epidermal barrier, the subjacent network of dermal
collagen, and the protection of the bone by restoration of a
physical barrier that prevents drying out and reduces the risk
of infection. With these allografts the average healing time
could be shortened to 6 weeks.

Electrical injury: reconstructive problems
445
tightened lower lip, and consequent inhibition of normal
mandible growth.63,64
The conservative management approach, which we prefer,
performs the reconstructive procedure after maturation of
the burn wound scar. Thus the extent of the damage is more
apparent and the reconstruction can be performed elec­
tively.65 Oral splinting has been advocated during the initial
healing period to reduce the need for reconstructive surgery.
However, this more likely reduces scar contractures, so the
planned reconstructive procedure can be performed after
scar maturation.66–68
Thorax and abdomen
Electrical injury to the trunk is generally a minor concern.
However, high-tension injuries can cause damage to under­
lying parenchymatous organs such as the lung. Clinically
this may lead to atelectasis and edema, requiring aggressive
Fortunately, involvement of the dura occurs rarely. This
usually requires an extensive free flap procedure.59 We prefer
to use the latissimus flap connected to cervical vessels, occa­
sionally using interpositional vein grafts. This reduces the
risk of perfusion problems considerably. When these options
are not available, the use of acellular human dermis to recon­
struct the dural defect followed by split-thickness skin graft­
ing after vascularization may be an option.60
In children, especially toddlers, common sites of low-
tension injury include the mouth, usually in the area of the
oral commissure, affecting the commissure, the lips and the
tongue. The injury usually results in a localized partial necro­
sis of the lips and the commissure, and the subsequent
contracture results in microstomia. The treatment strategies,
conservative versus early surgical intervention, are debated.
The more aggressive early approach of excision and recon­
struction results in faster healing, a shorter hospital stay, and
fewer surgical procedures.61,62 However, in this sensitive age
group early excision and reconstruction may also result in a
Figure 39.3  High-voltage injury from a power line (50 000 V). Presentation with primary loss of perfusion, loss of function and compartment syndrome.
Initial operation with fasciotomy, revascularization of the radial artery and necrectomies. On the following days adequate perfusion with a patent radial artery
without coexisting veins. Coverage with groin flap on day 6. Venous congestion and subsequent malperfusion was temporarily treated with leeches.
Secondary amputation on day 10 due to late occlusion of the radial artery.
aA
bB
cC
dD

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Fascial flaps provide thin, pliable coverage for reconstruc­
tion of the dorsum of the hand.
The serratus fascia flap is the flap of choice for larger
defects; for smaller defects the temporoparietal fascial flap is
preferred.78
Other regions of selective destruction in the upper extrem­
ity are elbow and axilla. Debridement often leaves a vast
tissue defect, which may be covered by rotation flaps from
the anterior or posterior chest wall in the axilla. Microvascu­
lar free flaps at the level of the elbow are rarely used. For
extensive defects on the hand and forearm pedicled groin
flaps provide good coverage and an independent blood
supply. The groin flap also avoids a vascular ‘steal phenom­
enon’ as can be seen after microvascular free flaps in such
severely injured extremities.
Newer approaches comprising early wound excision,
coverage, and revascularization of damaged vasculature
with flow-through free flaps and aggressive endovascular
interventions will offer an opportunity to improve outcomes
for these devastating injuries.79–82
Saint-Cyr and Daigle compared the use of free flaps with
conventional multistage procedures and found a statistically
significantly reduction in the number of operations, the time
required to achieve wound closure, and duration of hospi­
talization in the microsurgical group.83
The flap survival rate as described in the current literature
is lower in the high-voltage injury group than in the burn
injury group. It ranges from 62% to 100% and is lowest
when performed early, within 5–21 days of trauma.83–85
In conclusion, free flaps play a key role in treating high-
voltage electrical injuries to the extremities by reducing mor­
bidity and functional impairment, which are characteristically
high after these injuries.83
Amputations
Although distressing to the patient, amputation often
remains the only option. As already mentioned, the amputa­
tion rates for electrical injuries affecting the upper extremi­
ties range from 24% to 49% in the current literature.73,74
Despite an increased awareness of the potential danger of
electrical burns, devastating outcomes with four-limb and
penis amputations are still presented in the literature.86–88
Although very rare, Haik and colleagues presented a case of
a 5-week-old girl undergoing MRI for evaluation of spina
bifida. She sustained a full-thickness burn encompassing her
right forearm and wrist in the area where a non-MR-compat­
ible pulse oximeter was attached. A possible cause for this
incident could have been an electrical injury due to an
exposed wire segment in direct skin contact. Even if immedi­
ate escharotomy was performed this injury led to amputa­
tion of the forearm and hand.89 The optimal level of
amputation is determined by the extent of remaining viable
tissue and the intention to create sufficient stump length for
function and cosmetic appearance of a prosthesis. In electri­
cal injury involving the lower extremity this often requires
higher amputation than initially anticipated in order to
achieve sufficient stability of the stump and thus allow early
prosthetic fitting and ambulation. However, open (guillo­
tine) amputation should be avoided whenever possible.
Split-thickness skin grafting onto open stumps is an
ventilator support. Intra-abdominal injuries are uncommon,
but may require treatment as for penetrating injury. When
exploration during escharectomy and debridement reveals
necrotic underlying muscle and fascia, exploratory laparot­
omy may be indicated. Reconstructive options for the closure
of chest or abdominal wall defects include direct closure or
placement of a synthetic mesh covered by local fasciocutan­
eous or musculocutaneous flaps. However, the potential
negative effects of direct closure on intra-abdominal pressure
and the subsequent development of an abdominal compart­
ment syndrome or compromise of respiratory function must
be considered.
Extremities
Electrical injuries to the extremities, especially to the arms
and hand, are more common in adult members of the work­
force. Electrical burns account for 3–5% of all admissions
to burn units and approximately 1000 deaths per year in
the United States.70 There are three patterns of injury: direct,
arc, and flash-type injury. Direct injuries are associated with
entry and exit wounds, and nearly 90% of these injuries
involve the upper extremity.71 As the resistance and hence
the local energy production are dependent on the tissue
mass and the cross-sectional diameter of the injured body
part high-tension injuries often lead to extensive tissue
damage and loss of the involved extremity. Despite aggres­
sive treatment strategies with early debridement and decom­
pression of neurovascular structures, the likelihood of
amputation is high.22–24,72 In the current literature the ampu­
tation rates for electrical injuries affecting the upper extremi­
ties range from 24% to 49%.73,74 Even if amputation can be
avoided the resulting outcome may be a non-functioning
extremity. With the phenomenon of ‘kissing’ lesions
extensive tissue damage may occur, with resulting thermal
necrosis of muscle, tendon, nerves, and blood vessel. The
superficial injury may appear innocuous, but debridement
shows deep tissue destruction often mandating limb ampu­
tation. The importance of initial debridement cannot be
overstated, as remaining non-viable tissue leads to infection
and tissue loss. In our view the early debridement of non-
viable tissue prevents this fatal development. When distal
limb ischemia becomes obvious one can assume that the
involved vessels have been severely injured. In these cases
early vascular grafting of upper extremity arteries may be
indicated to salvage an ischemic upper limb.75 Imminent or
suspected compartment syndrome should always trigger
open fasciotomy to prevent further compromise to the
involved extremity. Sometimes it appears wise to perform a
simple skin grafting procedure followed by elective second­
ary flap coverage and nerve cable grafting.
In high-voltage injuries (>1000 V) the point of entrance of
the electrical current is usually located on the distal extrem­
ity. Tissue destruction decreases from distal to proximal. Zelt
et al. described specific regions or so called ‘choke points’
such as the wrist and elbow. These are characterized by
smaller cross-sectional areas and highly resistant tissue com­
ponents (tendinous and bony configuration) which result in
increased heat production and more severe damage.76
The main area of reconstruction is the forearm, and limb
salvage is the sole cause of free flap coverage.77

Electrical injury: reconstructive problems
447
depending on cross-sectional resistance and the proximity of
peripheral nerves to underlying bone. The local thermal
effect affects vascularity and perfusion of perineural tissue by
producing thrombosis, necrosis or hemorrhage of epineural
vessels. Delayed development of fibrosis and therefore a
delayed onset of symptoms are not uncommon. Especially
in areas of minimal cross-sectional area, the peripheral nerve
is in close proximity to bone and fibrous tissue which results
in perineural fibrosis and symptoms of a compressive periph­
eral neuropathy. The treatment of choice to gain nerve recov­
ery is decompressive corrective surgery.93 Other mechanisms
of nerve injury are the development of focal axonal degen­
eration following axonal excitation,94 or electroporation,
which more likely affects myelinated axons, and collagen
type I deposition.95–98
Complications
Central nervous system
Approximately 60% of all patients with high-voltage injury
present with immediate neurological complications, pre­
dominantly loss of consciousness.99Involvement of the
spinal cord has been described in 2–27% of patients with
an entry point of the current located in the head region.100–102
The incidence of a delayed paralysis progressing to tetraple­
gia followed by partial remission has been described.103
Although mortality in patients with neurological complica­
tions from electrical burns is not high, these patients are at
great risk of permanent disability. The neurological sequelae
were classified in 1964 by Silverside into immediate, second­
ary and late effects.104
Immediate spinal cord injury is transient and symptoms
usually clear within 24 h after the accident. The late effects
are characterized by progressive traits where complete recov­
ery is not the rule. The ischemic injury in the distal area of
the sulcal branch, the longest branch originating from the
anterior spinal artery, is due to the susceptibility of the ante­
rior horn cell and the spinal cord at T4–T8 to ischemic
injury. Early administration of prostaglandin E1 or steroid
treatment is recommended to reduce ischemic spinal cord
injury in cases of electrical burns.105 The neuropsychological
effects of electric injury have been described, mainly in case
reports and retrospective studies. Typical consequences
and complaints are related to physical, cognitive, and emo­
tional changes.106,107 In a study on 481 professional electri­
cians, 97% reported having experienced an electrical shock
at some point in their career.108 The low incidence of neu­
ropsychological dysfunction in this study differed from
other findings about the nature and progression of a
characteristic neuropsychological syndrome of electrical
injury.107,109 Although the development of transient and pro­
gressive neuropsychiatric complications is possible and
undisputed, the actual specific effects of electrical injury are
difficult to determine.
Ocular manifestations of electrical injury
An increased incidence of cataract formation has been
described after electrical injury, varying from 1% to 8% in
different reports.110,111 Patients with head and neck wounds
additional but less preferable approach, as skin breakdown
occurs more often in grafted areas, especially at graft borders
or at point where grafts adhere to underlying bone, and
further surgical interventions will be required. However, if
valuable stump length can be maintained by skin grafting it
should be attempted, as secondary plastic surgical correction
and specific prosthetic fitting are available.
In the upper extremity more length should be preserved,
as the resulting weightbearing load on the stump is less than
in the lower extremity. This allows for better control of the
prosthesis by the patient and thus enhanced functionality.
In the forearm the muscle length of the flexor–extensor
system should be preserved to improve function. In long
forearm stumps, atraumatic handling of tendons and muscles
is necessary to preserve pronation and supination. Upper
arm amputations should preserve as much length as possible
as this eases subsequent kineplastic procedures for a func­
tional prosthesis. As in the forearm muscular length of the
flexor–extensor system is maintained by joining them over
the bone end. Although it is technically feasible to maintain
extremity length by coverage with a free flap, this appears
only useful in upper extremity amputation where the func­
tional implications warrant such large-scale surgery and the
load on the stump is reduced.
Despite the availability of sophisticated modern myoelec­
tric prostheses the old techniques of surgical rehabilitation
should be kept in mind. This includes the Sauerbruch
kinemato-myoplasty of the biceps humeri muscle and the
Krukenberg plasty of the forearm, which provides sensible
chopstick-like stumps. Especially for upper arm amputations
distraction osteogenesis procedures (Ilizarov technique)
provide a valuable option to lengthen a short amputation
stump.
Peripheral nerve injury
Peripheral nerves are very sensitive to electric alterations, and
even minor injury may cause transient dysfunction. Clinical
findings may be anesthesia, paresthesia, or dysesthesia of
usually short-term duration. In rare cases minor electrical
injury may cause temporary autonomic dysfunction and
trigger a complex regional pain syndrome (sympathetic
reflex dystrophy). Treatment for reflex sympathetic dystro­
phy should be initiated early and include elevation of
the extremity to reduce edema formation, active exercise,
non-steroidal anti-inflammatory drugs, and adequate pain
relief. The autonomic dysfunction may be influenced by
α-adrenergic antagonists, calcium-channel blockers, and
low-dose diazepam, or may require intravenous regional
blocks and sympathetic ganglion blockade.90
Electrical injury to the upper extremity commonly results
in peripheral nerve injury to the median and ulnar nerves.
The clinical findings may resemble upper extremity compres­
sion syndromes or peripheral neuropathy.91,92 Nerve lesions
may be caused by secondary factors such as incorrect
positioning and splinting, constricting dressings, or delayed
inadequate escharotomy or fasciotomy. Owing to the accom­
panying severe muscle loss and scarring the extent of pure
nerve damage is sometimes difficult to determine.
Direct damage to peripheral nerves occurs following the
above-mentioned mechanisms of local heat production,

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joints, especially the elbows. Causative factors include forced
passive mobilization, secondary articular bleeding, and
calcium precipitation and deposition in damaged or
degenerating muscle and connective tissue. Particularly for
electrical injury, heterotopic bone formation also occurs
in amputation stumps of long bones. This, as well as the
common formation of bone cysts in the amputation stump,
may lead to secondary skin erosion, inflammation, and dif­
ficult adjustment to a prosthesis. In both situations surgical
excision and wound closure may be adequate therapy.126
Summary
Electrical injuries result in deceptively large tissue loss, often
leading to amputation of involved extremities. After initial
resuscitation, early debridement, necessary decompression
of neurovascular structures, and early wound closure are
essential to successful restoration of function. Extensive sur­
gical procedures including free soft-tissue transfer may be
necessary to achieve wound closure, and to save and restore
limb function. Sometimes, however, early amputation
may provide easier and earlier recovery and reintegration
into daily life. Long-term complications such as central
nervous sequelae, cataracts, and heterotopic ossification
must be considered and addressed early in the rehabilitation
process.
Further reading
Brumback RA, Feedback DL, Leech RW. Rhabdomyolysis following
electrical injury. Sem Neurol. 1995;15:329-334.
Saint-Cyr M, Daigle JP. Early free tissue transfer for extremity
reconstruction following high-voltage electrical burn injuries.
J Reconstr Microsurg. 2008;24(4):259-266.
Sauerbier M, Ofer N, Germann G, et al. Microvascular
reconstruction in burn and electrical burn injuries of the severely
traumatized upper extremity. Plast Reconstr Surg. 2007;119(2):
605-615.
Smith M, Muehlberger T, Dellon AL. Peripheral nerve compression
associated with low-voltage electrical injury without associated
significant cutaneous burn. Plast Reconstr Surg. 2002;109:137-143.
Spies C, Trohman RG. Narrative review: electrocution and life-
threatening electrical injuries. Ann Intern Med. 2006;145:531-537.
appear to be most at risk. However, the path of the current
and the location of the entry point were not related to the
development of ocular sequelae. Cataracts may also occur
without injury to the head and appear even years after injury.
Common initial complaints are blurred vision or dimin­
ished visual acuity.112
Cataracts usually develop from 1 month to 2 years after
injury but may occur as soon as within several hours.113 The
mechanisms for formation are debated and several theories
have been proposed, such as decreased permeability of the
lens capsule, direct coagulative effect on the lens proteins, a
disturbance in nutritional mechanisms of the lens cells due
to iritis or impaired circulation, and exposure to ultraviolet
and infrared radiation.114
Lightning strikes are a common cause of ophthalmic inju­
ries and the most common permanent sequela by far is
lightning-induced cataract.115 The lens of the eye is seemingly
very sensitive to electrical current or the resultant heat, and
prompt evaluation by an ophthalmologist is imperative.116
Iritis and uveitis have also been described as possible seque­
lae after electrical injury.117 Visual prognosis in patients with
lightning-induced ocular injury will depend on the extent of
irreversible retinal damage and optic nerve damage. Long-
term follow-up of these patients is recommended according
to the late onset of pigmentary changes at the fovea and
papillomacular bundle, which may further prevent visual
improvement.118
Patients should undergo serial ophthalmologic examina­
tions and treatment should be started immediately when
abnormalities are recognized.
Skeletal injury
Besides direct tissue destruction through electrical energy,
additional trauma can be indirectly inflicted by electric
current. Fractures occur due to secondary falls or with force­
ful tetanic muscle contractions. These are mostly seen in the
shoulder,119 wrists,120,124,125 femurs,121,123 and spine,122 and
may require open reduction and internal fixation. Late
sequelae of electrical injury similar to severe thermal burns
include major joint contractures and limited function of the
extremities.
Another common late complication of electrical burns are
heterotopic calcifications in periarticular tissue of large
 
Access the complete reference list online at

Electrical injury: reconstructive problems
448.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00040-0
Cold-induced injury: frostbite
Amalia Cochran, Stephen E. Morris, Jeffrey R. Saffle
History of frostbite
Frostbite is a traumatic injury caused by the failure of normal
protective mechanisms against the thermal environment,
resulting in local tissue temperatures falling below freezing.
The preponderance of documented experience with frostbite
has come from military campaigns, where the success of
many of these campaigns hinged on the incidence of cold
injury. Cold-induced injury remains a relatively frequent
injury in the United States owing to increasing interest in
outdoor winter recreational activities as well as the common
presence of homeless and socioeconomically disadvantaged
individuals in large urban centers.1,2
The incidence of and circumstances surrounding frostbite
have been documented in numerous military histories.3
Hannibal lost nearly half of his army of 46 000 soldiers
during a 2-week crossing of the Alps due to frostbite injury.
During the Revolutionary War, Dr James Thatcher recorded
that Washington lost 10% of his army to cold-related casual­
ties during the winter of 1778. Baron Dominique Jean Larrey
produced the first systematic medical observations of frost­
bite while serving as Surgeon General of Napoleon’s forces
during the ill-fated invasion of Moscow in the Fall of 1812
and the subsequent retreat in a harsh Russian winter.4
Because of the epidemic nature of frostbite in this campaign,
Larrey was able to create seminal descriptions of frostbite
and to identify the debilitating effects of daily refreezing that
occurred with bonfire thawing and subsequent marching in
frigid conditions; in addition, many soldiers would burn
their insensate frostbitten feet while attempting to rewarm
them over bonfires. Larrey became convinced that the
optimal therapeutic management consisted of friction
massage with snow or ice, resulting in slow rewarming.4
These recommendations were maintained as the standard
of care for frostbite in military medicine for more than
100 years.
In the winter of 1941–1942, German troops sustained an
estimated 250 000 frostbite injuries in the attempt to take
Moscow, constituting the largest reported number of related
frostbite injuries in history.5 Although American troops per­
sisted with the practice of slow rewarming, both German and
Russian troops had moved to a philosophy of rapid rewarm­
ing; the Russian paradigm shift was based on work con­
ducted at the Kirov Institute in the 1930s.5,6 Following World
War II existing Russian and German works were translated
into English and became the basis for rapid rewarming
as the predominant Western paradigm. In 1960, Mills
published the first major clinical experience with rapid
rewarming and included a philosophy of total care for
frostbite with this report.7 Meryman subsequently edited a
seminal text elucidating the scientific bases for frostbite
injury.8 Both military and civilian cold-induced injury data
continued to accrue over the subsequent three decades in the
absence of any significant clinical advances in the care of
frostbite.9–16 Frostbite continues to present a tremendous
clinical challenge, with the greatest clinical advance coming
only in the last decade with the use of thrombolytic therapy
in early management.17–19
Pathophysiology and classification of frostbite
The injury associated with frostbite is attributed to two broad
mechanistic categories: the first is that of direct cellular
damage and death due to the cold insult, and the second
is the delayed process mediated by progressive tissue
ischemia.20–23 The immediate effects of frostbite are evi­
denced by formation of extracellular ice crystals. These cry­
stals cause direct injury to the cell membrane, resulting in
cellular dehydration due to a change in the osmotic gradi­
ent.24 The rate of cooling is reported to have an effect on the
development of extracellular or intracellular ice crystals.
Rapid cooling results in intracellular freezing, causing more
severe cellular damage and cell death, while a slower rate of
cooling produces extracellular ice crystals. This slower process
results in a transmembrane osmotic shift that draws water
from within the cell and produces intracellular dehydration.
This dehydration causes changes in protein and lipid
conformation as well as changes in biochemical processes
that are deleterious to intracellular homeostasis.25–29 As the
temperature continues to fall, intracellular crystals develop
regardless of cooling rate, with a loss of the linear relation­
ship of temperature to metabolism, decreased DNA syn­
thesis, and histamine response with skin flushing and
development of a fluid-filled wheal (the triple response of
Lewis).13,30–33
Microvascular pathophysiology may be even more impor­
tant to outcome than the direct thermal injury to the cell.
This was suggested by studies showing the survival of
full-thickness skin subjected to freezing and thawing that
progressed to necrosis when left in situ but survived
when transplanted to a normal, uninjured recipient site.23
Zacarian identified a number of processes that may play a
role in the microcirculatory changes of frostbite. Transient
CHAPTER 40 
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IN THIS CHAPTER
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Total Burn Care
40
450
involves some degree of dermal and soft tissue injury. Clini­
cal appearance evolves over a period of time after rewarming,
although the initial appearance may be deceptive because of
the hyperemia present in both frostbite and frostnip.9,51 The
development of skin blebs is time dependent and may
require hours to days from the time of injury. After 12–24
hours the character of the blebs usually becomes apparent
and an assessment of the degree of involvement can allow
for planning of management of the injury.
Traditional classification of frostbite is similar to that of
the burn injury. First-degree injury is superficial, without
formation of vesicles or blebs. There may initially be an
area of pallor with surrounding erythema that evolves into
general edema and erythema without long-term sequelae.
Second-degree injury has associated light-colored blisters
and subsequent epidermal sloughing. This may correlate
with partial dermal involvement but has a generally favo­
rable prognosis. Third-degree frostbite typically has dark or
hemorrhagic blisters that evolve into thick, black eschar over
1–2 weeks. Fourth-degree injury involves bone, tendon or
muscle and uniformly results in tissue loss. Precision in
depth of injury cannot be expected and some favor a
more general classification of superficial (first- and second-
degree injury) or deep (third- and fourth-degree) frostbite
injury;52,53 clinically these can be delineated by clear vesicles,
present with superficial injury, or hemorrhagic blisters,
indicative of structural damage to the subdermal tissues.53,54
Cauchy most recently proposed an alternative classification
system based on risk of amputation that includes the extent
of the lesion immediately after rewarming, findings from
bone scan on day 2, and the presence of blisters on day 2.55
Although this system has not come into widespread use, the
relationship of objective findings to prognosis may prove
helpful for future therapeutic trials in the management of
frostbite.
Initial management of freezing cold injury
Prevention is obviously the ideal means of treatment for
frostbite. Frostbite continues to be a relatively frequent
injury in the United States owing to increasing interest in
wilderness activities, even during inclement weather. Further,
the incidence of frostbite among homeless and mentally ill
individuals persists, with these groups representing the most
frequently seen local cold-injury patients; alcohol and drug
intoxication heightens these risks.1,2,49,56,57 Although the cases
of frostbite that occur in intoxicated, mentally ill, and home­
less individuals are truly preventable only through broader
social interventions, simple techniques exist for those who
sustain frostbite secondary to involvement in cold-weather
wilderness activities. Frostbite prevention measures in cold-
weather wilderness activity include, but are not limited to,
wearing appropriate clothing, which may include layers,
keeping that clothing dry (particularly clothing over acral
areas, such as gloves and socks), responding appropriately
to changing conditions, and performing ‘cold checks’ of
at-risk or suspect areas.58
If frostbite is identified in the field, the greatest manage­
ment priority is to not incur further injury. Jewelry should
be removed if present in the affected area; rubbing the area
vasoconstriction of both arterioles and venules with subse­
quent resumption of capillary blood flow appears to occur,
and concomitant microemboli are present.34 With thawing,
the capillaries demonstrate restoration of blood flow that
diminishes within minutes. Complete cessation of blood
flow is often seen within 20 minutes of rewarming frozen
tissue. Similar changes have been seen with random skin
flap models after reperfusion, suggesting reactive oxygen
species as mediators of injury.35 Within 72 hours significant
de-endothelialization and deposition of fibrin in the capil­
lary bed occurs. Examination of the endothelial ultrastruc­
ture demonstrates swelling, fluid extravasation, endothelial
cell dilation, and significant projection of the cell into the
vascular lumen prior to cell lysis.36 There is regional variation
in the extent of injury, with venules being most profoundly
affected, resulting in the hypothesis that, as evidenced by
lower flow present in venules, stasis must play a role in this
pathophysiologic process.32
The pathobiochemistry of frostbite has been closely com­
pared to the inflammatory response in the burn wound.37
Inflammatory mediators such as eicosanoids in burn blister
fluid as well as bradykinin and histamine release in the
region of injury draw parallels with findings in cold-induced
injury.38–45 This has prompted investigators to hypothesize a
frostbite model similar to that of Jackson’s for burns, includ­
ing zones of necrosis and stasis.46 Similar to their burn blister
analysis, Robson and Heggers examined the fluid in frostbite
blisters and found high levels of prostaglandin F2 and throm­
boxane B2.37 These agents or their precursors have been
implicated in vasoconstriction and leukocyte adherence. In
addition, when refreezing follows thawing the cellular
damage caused by ice crystals and the subsequent inflamma­
tory response are exaggerated.47,48
Clinical findings and classification
of frostbite injury
In many situations, the patient is unaware that frostbite is
occurring. The presence of hypothermia and the frequent use
of mind-altering substances by frostbite patients may con­
tribute to this problem. Typical distribution of injury is acral,
with injuries to ears, nose, cheeks and penis also being fairly
common.9,14,49 The patient may note insensitivity and clum­
siness of the affected part. This complex of symptoms rapidly
reverses upon rewarming. Severe pain occurs during and
immediately after the rewarming process, is often described
as throbbing in character, and typically requires parenteral
opioids for relief.50 This may evolve into severe neuropathic
pain that can be aggravated by warm environments and
dependent positioning of the injured body part.
Because of the nature of freezing injury, classification has
traditionally been based on physical examination findings
and adjunct imaging that occurs after rewarming. A condi­
tion often termed ‘frostnip’ may be present in which there
is not true injury to the underlying dermis or soft tissues.
The most common presentation of frostnip is numbness and
pallor of exposed skin. Rewarming results in near-complete
resolution of symptoms and physical findings, with the pos­
sible exception of minimal hyperemia, edema, and tingling
in the region. True frostbite, on the other hand, always

Cold-induced injury: frostbite
451
blisters because hemorrhage results from damage to subder­
mal structures, implying that debridement of these blisters
would extend the soft tissue damage in these areas.53,54 A
more practical justification for debridement of blisters is that
it improves the visualization of underlying tissue, allowing
the clinician to better assess the status of the wounds.65
Aloe vera has properties that counter the arachidonic acid
cascade and therefore benefit the local care of frostbitten
areas. Heggers demonstrated that the use of systemic NSAIDs
and local aloe vera to address the inflammatory chemokines
coupled with systemic penicillin as prophylaxis against
Gram-positive infection resulted in demonstrably less tissue
loss, a lower amputation rate, and shorter hospital stay
versus patients managed with traditional topical antimicro­
bials.13 Topical aloe vera alone was credited with clinically
significant tissue salvage in these patients, resulting in pref­
erential management with aloe vera rather than topical anti­
microbials such as silver sulfadiazine or sulfamylon.13,58,66
Topical wound care, including gentle daily cleansing, also
should address mechanical protection of the affected areas,
with careful padding, splinting, and elevation to manage
edema formation.52,54,66
Non-surgical therapies
Pharmacologic management of the frostbite patient also
includes systemic blockade of the arachidonic acid pathway
to ameliorate the inflammatory response to the local cold
injury. Historically aspirin was used and did demonstrate
tissue survival improvement >20% in a rabbit ear model.13
However, aspirin blocks all arachidonate metabolites, includ­
ing those that are beneficial for wound healing. Therefore,
more recent recommendations center on the use of ibupro­
fen and the specific blockade of TXA2.1,64,67
Pentoxifylline, a phosphodiesterase inhibitor that is pri­
marily used in claudication, has been shown to synergisti­
cally improve tissue viability in conjunction with topical
aloe vera.68 Pentoxifylline improves red blood cell flexibility,
which may limit microvascular sludging and thereby dimin­
ish thrombus formation in small vessels. In addition, pen­
toxyfilline may reduce blood viscosity, again contributing to
improved tissue survival.69 When pentoxifylline is used for
post-thaw pharmacologic management, the current recom­
mendation, based on a study of pedal frostbite, is 400 mg
TID for 2–6 weeks following injury.69 Both reserpine and
tolazoline have been used as vasodilators in hopes of dimin­
ishing the vasospasm associated with freezing cold injury,
with poor results for both.50,58 Iloprost, a prostacyclin analog
that also serves as a vasodilator, has interesting features that
may be of benefit, although all data on its use are prelimi­
nary.58 Although studies of pentoxifylline and iloprost are
ongoing in Europe, current data are inadequate to recom­
mend their use.
Thrombolytics have demonstrated the most notable clini­
cal advances in the management of frostbite in the last 50
or more years. The first demonstration of possible utility for
thrombolytics in frostbite management was an animal
model using IV urokinase.70 In 1992 a preliminary account
was shared showing that thrombolytics were potentially
better than slow rewarming for reducing amputations
following frostbite injury.71 Subsequent publications by the
with ice or snow, although consistent with historical recom­
mendations, is now known to incur further damage to
fragile, injured tissue.4,50,52,59,60 Injured areas should be
mechanically protected from trauma because they are typi­
cally insensate and are at high risk for further injury.50,52,59,61
The key decision that must be made in the field is whether
thawing should be pursued prior to transfer to a facility that
can provide definitive care for the frostbite injury. Based on
the work of Mills at the Arctic Aeromedical Laboratory dem­
onstrating the deleterious effects of thawing and refreezing
on clinical outcomes from frostbite, rewarming in the field
should not be pursued unless the ability to maintain the
affected tissue in a thawed state is certain.7,59,62,63 Systemic
cold injury in the form of hypothermia often accompanies
local frostbite injury, mandating that patients be carefully
evaluated to verify that they are normothermic prior to com­
mencement of definitive frostbite management. Hypother­
mia causes peripheral vasoconstriction and diminished
blood flow, processes that are exacerbated by the local cold
injury. Most importantly, hypothermia can be life-threatening,
as opposed to the limb or digit threat posed by frostbite.
Moderate to severe hypothermia, defined as a core tempera­
ture <32°C, should therefore be addressed prior to initiation
of frostbite treatment.50,52,59,64 The traditional recommenda­
tions for rapid rewarming favor a water bath temperature of
40–42°C.50,54,59,62 The State of Alaska guidelines recently
changed the water bath recommendation to a temperature
of 37–39°C, as this does not substantially increase the time
to rewarming but causes less pain for the patient during that
process.52,58 The water bath for thawing should be main­
tained in this range with the water circulating around the
involved tissue. The duration of rewarming is approximately
30 minutes, although clinical findings to determine the
length of time for rewarming include the return of sensation
(often resulting in significant discomfort to the patient) and
presence of flushing at the most distal aspect of the involved
tissue.52 Administration of narcotics is appropriate at the
time of definitive rewarming because of the pain associated
with the thawing process.50 In addition, because these are
tetanus-prone wounds, the patient’s tetanus immunization
should be verified and updated as appropriate. Finally, sys­
temic antibiotics are recommended by some authors in
patients with marked edema because of loss of the anti­
streptococcal properties of the skin when edema is
present.48,54,58,64–66
Post-thaw evaluation and management
Following rewarming of frostbitten tissue, local care of the
involved tissue is the first priority. Unroofing of blisters has
been, and remains, a matter of controversy.66 The work of
Heggers’ group showed that high levels of PGF2α and TXB2,
as well as diminished levels of PGE2, are present in blister
fluid following both burns and frostbite.13,37,40 The result of
these alterations in local chemokines is vasoconstriction of
the involved area, increased leukocyte adherence, and
increased platelet aggregation, all of which result in progres­
sive dermal ischemia.37,44 This would suggest that debride­
ment of blisters might help limit further tissue damage.
However, concern exists about removal of hemorrhagic

Total Burn Care
40
452
promising, allowing direct visualization of occluded vessels
and possible better delineation of viable tissue than 99Tc
scanning.83 However, a subsequent study demonstrated that
MRI was no better than bone scanning to identify anatomic
sites for amputation, and that the limited soft tissue present
in digits hampered the utility of MRI.64
Because of a historical bias based on data showing that
early surgery was potentially associated with worse out­
comes, the adoption of scintigraphy with early operative
intervention has been limited.74 However, Greenwald devel­
oped a protocol with early scintigraphy followed by opera­
tive intervention at 7–10 days following injury.82 Cauchy
makes a plausible argument for intervention at 10–15 days
post injury with a bone scan, based on a shorter waiting
time for the patient, lower infection risk, and earlier progres­
sion to rehabilitation; of note, Cauchy advocates repeat
scanning at 7–10 days post injury if the injury is not clearly
delineated on an early (<48 hours) bone scan.65 Neverthe­
less, the prevalent clinical practice remains to time surgery
anywhere from 4 weeks to 3 months following injury,
once tissues have clearly demarcated to an experienced
clinical eye.50,66
Summary
Frostbite has a long clinical history but remains a modern
clinical challenge. Although the pathophysiology of freezing
cold injury is well delineated, few advances from the tradi­
tional ‘frostbite in January, amputation in July’ management
approach have occurred in the last 50 or more years. Throm­
bolytic therapy has shown benefit in digital salvage but
requires early use and has unclear long-term functional out­
comes. Hyperbaric oxygen has shown promise in terms of
salvage and functional outcomes but so far has only been
evaluated in case series. Vasodilation with pentoxifylline or
iloprost is under ongoing study as a potential therapy for
frostbite. Scintigraphy may provide a means to expedite the
surgical management of frostbitten digits and extremities,
but again has only been studied in limited settings. Large-
scale multicenter evaluation of these varied evaluation and
management techniques is required to demonstrate whether
any of these practices will ultimately improve tissue salvage
and functional outcomes.
Further reading
Bruen KJ, Ballard JR, Morris SE, et al. Reduction of the incidence of
amputation in frostbite injury with thrombolytic therapy. Arch
Surg. Jun 1 2007;142(6):546-551; discussion 551-553.
This retrospective, single-center review presented the largest series of frostbite
patients managed with thrombolytic therapy. A reduction in incidence of
digital amputation rates from 41% to 10%.
State of Alaska. State of Alaska Cold Injury Guidelines. Juneau: State of
Alaska; 2005.
These represent the most comprehensive guidelines for the management of
all forms of cold injury. Frostbite guidelines include the spectrum of care,
from management in the field through arrival at a hospital that can
provide definitive care.
Cauchy E, Marsigny B, Allamel G, Verhellen R, et al. The value of
technetium 99 scintigraphy in the prognosis of amputation in
severe frostbite injuries of the extremities: A retrospective study of
Minneapolis group and the Utah group have shown signifi­
cantly improved digit salvage with the use of tissue plas­
minogen activator (t-PA).17,19,72 Unfortunately, t-PA only
appears to be efficacious within 24 hours of thaw, meaning
that this may not be an option for patients who are injured
in extremely remote environments. Additionally, although
digit salvage has been improved with thrombolytics, the
actual long-term functional results of this salvage have not
been documented.
Sympathectomy, both surgical and chemical, has largely
fallen out of favor owing to clinical results that are mixed at
best. Early studies of sympathectomy demonstrated that it
had the potential to reverse vasospasm, although this was at
the cost of increased edema if undertaken too early following
injury.72 Most importantly, sympathectomy has not shown
any improvement in tissue preservation in frostbite and may
ultimately result in more proximal injury demarcation.73,74
Perhaps the two best-documented benefits to sympathec­
tomy affect long-term function, with improved cold
tolerance and amelioration of the neuropathic pain and par­
esthesias that often present one of the greatest clinical chal­
lenges following freezing cold injury.73,75 Therefore, the best
use of sympathectomy may be in the longer-term manage­
ment of disabling complications of frostbite.
Studies of hyperbaric oxygen (HBO) are limited but have
some of the most promising functional results of an adjunc­
tive therapy for frostbite. One of the early documented uses
of HBO for therapy in frostbite involved four Alpine
mountaineers, all of whom presented 10 or more days fol­
lowing injury and all of whom demonstrated good tissue
preservation with HBO.76 A more recent case report, again
with delayed therapy, involved a patient with deep injury
to multiple digits; this patient had complete preservation
with 14 days of HBO treatment and did not sustain the
neuropathic sequelae commonly seen with freezing cold
injury.77 In an additional case study in the last decade,
improved nutritive skin flow was demonstrated 2 weeks fol­
lowing injury.78 The utility in delayed presentations com­
bined with the potential for improved functional outcomes
make HBO an extremely attractive therapy in frostbite,
although definitive evidence in its favor has not yet accu­
mulated. Multicenter trials of HBO would provide substan­
tial progress toward understanding the role for this therapy
in frostbite management.
Imaging and surgical management
Both scintigraphy and MRI/ MRA have been recommended
as diagnostic aids to improve the process of surgical manage­
ment of frostbite. Over 20 years ago, Mehta identified three
different patterns in triple-phase bone scanning that were
useful indicators of outcome within 48 hours of injury.79
Specifically, he found that perfusion and blood pooling
phases demonstrated at-risk tissue and the bone phase
showed deep tissue and bone infarction. Several studies have
demonstrated excellent correlation between scintigraphic
findings and surgical outcomes, although some authors
claim that bone scan findings best correlate with surgical
findings at 7–10 days following injury.65,80,81 Confidence in
scintigraphic findings by some practitioners has been ade­
quate for them to derive a protocol using the findings to
direct early surgery.55,82 The use of MRI/ MRA initially seemed

Cold-induced injury: frostbite
453
McCauley RL, Hing DN, Robson MC, et al. Frostbite injuries: a
rational approach based on the pathophysiology. J Trauma. Feb
1983;23(2):143-147.
This seminal article describes a limited single-center experience with
frostbite. The University of Chicago Frostbite Protocol that is included
is the foundation for multiple protocols that have been published
subsequently.
92 severe frostbite injuries. J Hand Surg Am. Sep 2000;25(5):
969-978.
The Chamonix group provides a twelve-year review including 92 patients,
demonstrating the value of 99Tc scanning in frostbite evaluation and
management. They use their experience to delineate an algorithm with
potential use in future research on medical and surgical management of
frostbite.
 
Access the complete reference list online at

Cold-induced injury: frostbite
453.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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oxygen treatment in deep frostbite of both hands in a boy. Burns.
Jun 2001;27(4):404-408.
78. Finderle Z, Cankar K. Delayed treatment of frostbite injury with
hyperbaric oxygen therapy: a case report. Aviat Space Environ Med.
Apr 2002;73(4):392-394.
79. Mehta RC, Wilson MA. Frostbite injury: prediction of tissue
viability with triple-phase bone scanning. Radiology. Feb
1989;170(2):511-514.
80. Cauchy E, Chetaille E, Lefevre M, et al. The role of bone scanning
in severe frostbite of the extremities: a retrospective study of 88
cases. Eur J Nucl Med. May 2000;27(5):497-502.
81. Salimi Z, Vas W, Tang-Barton P, Eachempati RG, et al. Assessment
of tissue viability in frostbite by 99mTc pertechnetate scintigraphy.
AJR Am J Roentgenol. Feb 1984;142(2):415-419.
82. Greenwald D, Cooper B, Gottlieb L. An algorithm for early
aggressive treatment of frostbite with limb salvage directed by
triple-phase scanning. Plast Reconstr Surg. Sep 1998;102(4):
1069-1074.
83. Barker JR, Haws MJ, Brown RE, et al. Magnetic resonance imaging
of severe frostbite injuries. Ann Plast Surg. Mar 1997;38(3):
275-279.

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©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00041-2
Chemical burns
Itoro E. Elijah, Arthur P. Sanford, Jong O. Lee
Introduction
Many compounds have the potential to induce chemical
burns. Individuals are exposed in both occupational and
personal environments. The American Association of Poison
Control Centers’ (AAPCC) National Poison Data System
(NPDS) 2008 annual report demonstrated 224 884 cases of
exposure to cosmetic/personal care products, 213 595 house­
hold cleaning substances, 93 998 pesticides, 46 418 hydro­
carbons, and 44 736 unspecified chemicals.1 In 2007, 137 055
cases of exposure were specific to acids, alkalines, peroxide,
bleach, and phenol products alone.2 The reality concerning
the ease of access to toxic products is evident in the presence
of a rising number of pediatric exposures to chemical inju­
ries. Most chemical burns involving children are secondary
to common household products. Domestic chemical burn
injuries are often due to poor labeling and storage, as well
as secondary to intentional assault and suicide attempts. The
most commonly affected areas of the body are the face, eyes,
and extremities. Chemical burn injuries compose only 3%
of all burns, yet they are the etiology behind approximately
30% of burn deaths. As a result, length of hospital stay and
duration of healing tend to be greater with chemical burns.
The majority of these deaths are related to the ingestion of
chemical substances.3 This chapter will provide general prin­
ciples for the treatment of chemical injuries.
Pathophysiology
All burn wounds, whether due to chemical or thermal
sources, have in common the denaturation of proteins. The
structure of biological proteins involves not only a specific
amino acid sequence, but also a three-dimensional structure
dependent on weak forces, such as hydrogen bonding or Van
der Waals’ forces. These three-dimensional structures impart
biological activity to the proteins, and are easily disrupted
by outside influences. Heat energy breaks these weak bonds
to unfold and denature proteins. In addition, changes in pH
or dissolution of surrounding lipids may stabilize a protein
and disrupt its function. Direct chemical effects on a reactive
group in a protein will similarly render it ineffective.
The severity of a chemical burn injury is determined by
several factors:
•
concentration
•
quantity of chemical agent
•
manner and duration of skin contact
•
extent of penetration
•
mechanism of action
•
phase of agent (liquid, solid, gas).
There are six mechanisms of action for chemical agents in
biological systems:4
1. Reduction: Reducing agents act by binding free
electrons in tissue proteins, causing denaturation.
Examples include hydrochloric acid, nitric acid, alkyl
mercuric compounds, ferrous iron, and sulphite
compounds.5
2. Oxidation: Oxidizing agents are oxidized on contact
with tissue proteins. Byproducts are often toxic and
continue to react with the surrounding tissue. Examples
of oxidizing agents are sodium hypochlorite, potassium
permanganate, chromic acid, and peroxide.
3. Corrosive agents: Corrosive substances denature
tissue proteins on contact and form eschar and a
shallow ulcer. Examples of corrosive agents include
phenols, cresols, white phosphorus, dichromate
salts, sodium metals, lyes, sulphuric acid, and
hydrochloric acid.
4. Protoplasmic poisons: These agents produce their
effects by binding or inhibiting calcium or other
organic ions necessary for tissue viability and function.
Examples of protoplasmic poisons include ‘alkaloidal’
acids, acetic acid, formic acid, and metabolic
competitors/inhibitors such as oxalic, hydrofluoric, and
hydrazoic acid.
5. Vesicants: Vesicant agents produce ischemia
with necrosis at the site of contact. There is
associated tissue cytokine release and blister formation.
Examples include cantharides, dimethyl sulfoxide
(DMSO), mustard gas (sulphur and nitrogen), and
Lewisite.
6. Desiccants: These substances cause damage by
dehydrating tissues and exothermic reactions causing
the release of heat into the tissue. Examples include
sulfuric acid, muriatic acid, calcium sulphate, and
silica gel.
Within these groups there are different categories of com­
pound. Chemical burns are often described as acidic or alka­
linic.6 Acids act as proton donors in the biological system,
and strong acids have a pH < 2. Alkali, or basic material,
capable of producing injury typically have a pH > 11.5.7
In general, alkaline materials cause more injury than
CHAPTER 41 
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IN THIS CHAPTER
PowerPoint Presentation Online

Total Burn Care
41
456
observation that chemical burns tend to be deeper than
they initially appear. As a result, they tend to heal more
slowly.
Specific agents
Acids
Acetic acid
Acetic acid, also known as ethanoic acid, ethylic acid, and
methane carboxylic acid, is a mild chelating agent. Solutions
diluted to <40% concentrations, such as table vinegar and
hair-wave neutralizing products, are usually harmless, but if
used inappropriately may cause injuries such as partial-
thickness burns. In such cases, initial treatment involves
irrigation.13,14
Carbolic acid (phenol)
Carbolic acid is a hydrocarbon derived from coal tar, which
acts to cause damage secondary to its ability to induce dena­
turation and necrosis.15,16 The most common adverse effects
are dermatitis, abnormal pigmentation, and burns to the
skin.17 Concentrated amounts of phenol are caustic; there­
fore, prolonged skin contact causes partial- or full-thickness
burns. These burns tend to become extensive prior to detec­
tion, secondary to the local anesthetic properties of phenol.
Ingestion of as little as 1 g may cause death. Systemic
effects include ventricular arrhythmias,18 pulmonary edema,
stridor, and tachypnea. Locally, conjunctivitis, corneal
edema/necrosis, and skin necrosis result.15
Acute poisonings are potentially fatal, hence prompt
action is necessary with copious irrigation.19 Polyethylene
glycol (PEG molecular weight 300 or 400 Da) has been
shown to be of potential benefit,20,21 but large-volume lavage
should not be delayed while PEG application is begun.
Reports in the literature indicate that intravenous sodium
bicarbonate may be of use to prevent some of the systemic
effects of phenol.22
Chromic acid
This acid causes non-painful but corrosive ulcers upon
contact with the skin.23,24 Ulceration of the nasal septum and
bronchospasm can also occur with inhalation. This agent
will cause protein coagulation. Peak blood levels are thought
to be achieved within 5 hours of exposure. Symptoms may
occur with just 1% total body surface area (TBSA) burn, but
a 10% burn or greater is often fatal owing to its systemic
effects. Irrigation is the primary treatment for exposure, but
in an industrial setting, washing with a dilute solution of
sodium hyposulfite or water, followed by rinsing in a
buffered phosphate solution, may be a more specific anti­
dote. Dimercaprol may be used at 4 mg/kg IM every 4 hours
for 2 days, followed by 2–4 mg/kg/day for 7 days in total to
treat the systemic effects. Dialysis in the first 24 hours is a
reasonable means to remove circulating chromium and to
address existing electrolyte imbalances. Exchange transfu­
sion may be necessary. Various ointments containing prod­
ucts such as 10% calcium EDTA or ascorbic acid are available
for small superficial burns.14,25 There have been case reports
acidic compounds. Acids cause coagulation necrosis with
precipitation of protein, whereas the reaction to alkali is
‘liquefaction’ necrosis allowing the alkali to penetrate deeper
into the injured tissue.8 The presence of hydroxyl ions
within these tissues increases their solubility, allowing
alkaline proteinates to form when the alkalis dissolve the
proteins of the tissues.9 Organic solutions tend to dissolve
the lipid membrane of cell walls and cause disruption
of cellular architecture as their mechanism of action. Inor­
ganic solutions tend more to remain on the exterior of
cells, but may act as vehicles to carry the above-mentioned
agents that denature proteins, or form salts with proteins
themselves.
General principles of management
The most important aspects of first aid for chemical burns
involve removal of the offending agent from contact with
the patient. This requires removal of all potentially contami­
nated clothing and copious irrigation. Irrigation of chemical
burns requires protection of healthcare providers to prevent
additional injuries. Further, the wounds should not be irri­
gated by placing the patient into a tub, thereby containing
the chemical and spreading the injurious material. Irrigation
should be large volume and drained ‘to the floor,’ or out of
an appropriate drain. Immediate copious irrigation has been
shown to reduce the extent and depth of injury, especially
to eyes.10 No measure of adequacy of lavage has been devel­
oped, but monitoring the pH from the effluent can provide
quantifiable information as to adequacy of lavage. Thirty
minutes to 2 hours of lavage may be necessary.
Material Safety Data Sheets (MSDS) are mandated to be
available for all chemicals present in the workplace. These
can be valuable resources for potential systemic toxicity and
side effects of an agent. Further assistance is available from
regional poison control centers for household chemicals or
unidentified agents.
The use of neutralizing agents is discouraged. The practical
problems encountered with their use are exothermic reac­
tions causing further thermal damage. When the burning
agent is known and an appropriate antidote is known, some
benefit to its use has been demonstrated.11 Despite this, no
agent has been found to be more effective than plain water
for irrigation.12
Burn and trauma patients should be managed with the
same principles in mind. After airway patency is assured,
adequate air movement and hemodynamics should be
maintained. Conventional thermal burn formulas are used
for resuscitation. Monitoring of urine output remains
paramount to assessment of adequacy of end-organ per­
fusion and hence resuscitation. Systemic disturbances of
pH are potential complications and must be monitored
until acid–base disorder and electrolyte abnormalities are
corrected.
The typical large-volume lavage required to adequately
dilute chemical exposures puts the patient at potential
risk for hypothermia, both from evaporative cooling losses
and from the use of unwarmed lavage fluid. Principles of
wound care for chemical burns are typically the same as for
thermal burns. Early excision and grafting of obviously
non-viable tissue is advocated, particularly in light of the

Chemical burns
457
up to 80–99%.14 Muriatic acid is the commercial grade of
concentrated hydrochloric acid. Once in contact with the
skin, it denatures proteins into their chloride salts. Copious
irrigation and early excision are the treatments of choice.41
Hydrochloric acid fumes can cause inhalation injury with
acute pulmonary edema. (Figs 41.2 and 41.3).
Hydrofluoric acid
Hydrofluoric acid is a corrosive that is commonly used in
industrial applications. It is used as a cleaning agent in the
petroleum industry, in the production of high-octane fuel,
glass etching, germicides, dyes, tanning, and fireproofing
material, as well as in rust removal.14 Hydrofluoric acid is
particularly lethal owing to its properties both as an acid and
supporting the early excision of chromic acid burn to assist
in preventing systemic toxicity.26,27
Epichlorohydrin acid
Epichlorohydrin is a rare, corrosive carcinogen that is color­
less and exudes a garlic-like odor. It is used in the production
of glues, plastic, glycerols and resins, as well as in paper
reinforcement and water purification.28 It can also be con­
verted into a binder used in the production of explosives.29
At our burn center in Galveston, Texas, four patients were
exposed to epichlorohydrin after an industrial accident. The
TBSA burned ranged from 10% to 60%, with the largest burn
showing rapid progression to a full-thickness wound within
hours. Management of these patients was commenced with
copious irrigation and hemodynamic monitoring (Fig. 41.1).
Formic acid
Formic acid is a strong inorganic acid used by glue makers
and tanning workers. After contact, it creates an eschar which
does not prevent systemic absorption. Once it is absorbed,
metabolic acidosis, intravascular hemolysis with hemoglob­
inuria, renal failure, pulmonary complications, and abdomi­
nal pain with necrotizing pancreatitis usually occur.30,31 All
patients injured by formic acid should be hospitalized
because of this multitude of potential systemic effects.
Formic acid is the acid most commonly used in assaults,
especially in developing countries, because of its easy
availability.14,32
Hydrochloric acid/muriatic acid/sulfuric acid
Hydrochloric acid is one of the most commonly treated
chemical burns. Hydrochloric acid and sulfuric acid are
proton donors,33 which cause the pH in local tissues to drop
to zero as hydrogen ions disassociate. Coagulation necrosis
and tissue ulceration occur, leading to consolidation of con­
nective tissue and thrombosis of intramural vessels, ulcera­
tion, fibrosis, and hemolysis.5 Many household cleaners
contain dilute hydrochloric acid (3–6%), sulfuric acid and
its desiccant precursor (sulphur trioxide) in concentrations
Figure 41.1  Epichlorohydrin acid burn 3 days after admission.
Figure 41.2  Hydrochloric acid burn to the hand before blister removal.
Figure 41.3  Hydrochloric acid burn to the hand after blister removal.

Total Burn Care
41
458
casting iron and steel, and engraving. Upon skin contact a
yellow-brown stain develops, with an eschar. Demarcation
tends to occur slowly, causing difficulty in discerning burn
depth. Initial treatment involves irrigation and the use of
topical treatment.46
Oxalic acid
This is a potent metabolic poison that combines with
calcium to limit its bioavailability, thereby limiting muscle
contraction.14 It is used industrially to remove rust and in
bleaching products. Treatment consists of water irrigation
and intravenous calcium, with continuous cardiopulmonary
monitoring, as well as measurements of serum electrolytes
and renal function.14
Phosphoric acid
Phosphorus is an incendiary agent found in hand grenades,
artillery shells, fireworks and fertilizers.47 White phosphorus
ignites in the presence of air and burns until the entire agent
is oxidized or the oxygen source is removed. The wounds are
irrigated with water and easily identifiable pieces of phos­
phorus are removed. Soaked dressings are applied for trans­
port. Ultraviolet light can be used to identify embedded
particles through phosphorescence. In addition, a solution
of 0.5% copper sulfate can be applied which will impede
oxidation and turn the particles black to aid in their identi­
fication and removal. Hypocalcemia, hyperphosphatemia,
and cardiac arrhythmias have been reported with phospho­
rus burns.48
Alkalis
Strong alkalis have a pH ≥12. Wounds caused by alkalis
initially appear superficial, but may often become full thick­
ness in 2–3 days. This chemical creates a soluble protein by
binding with lipids and proteins, thus allowing passage of
hydroxyl ions into the tissue. Eventually, a soft, brownish,
gelatinous eschar is created. Alkalis are very corrosive
in nature and penetrate deeply. Examples of strong
alkalis (lyes) include barium, sodium, ammonium, calcium,
lithium, and potassium hydroxides. They are present in
many household cleaning solutions, and have historically
been ingested in suicide attempts, causing death secondary
to airway occlusion.14 Management of these burns necessi­
tates immediate and copious irrigation.
Dry residues of alkali (e.g. lime) must be brushed away,
and then copious irrigation is undertaken. Attempts to neu­
tralize alkali are not recommended. Alkaline injury to the
eye is particularly devastating. These compounds rapidly
penetrate the cornea, causing scarring and opacification,
with associated perforation.49
Cement
Cement acts both as a desiccant and an alkali. Cement is
calcium oxide, which becomes calcium hydroxide upon
exposure to water. It usually contains lime, sand and other
metal oxides. The dry powder is very hygroscopic and will
cause desiccation injury if not hydrated or washed away.
Injury results from the action of the hydroxyl ion.50
as a metabolic poison. The acid component causes coagula­
tion necrosis and cellular death. Fluoride ion then gains a
portal of entry that chelates positively charged ions such as
calcium and magnesium, resulting in hypocalcemia and
hypomagnesemia.34 This causes an efflux of intracellular
calcium with resultant cell death. The fluoride ion remains
active until it is completely neutralized by the bivalent
cations. This may exceed the body’s ability to mobilize
calcium and magnesium rapidly enough, causing muscle
contraction and cellular function to become dysfunctional.
Fluoride ion also acts as a metabolic poison by inhibiting
Na-K ATPase, allowing efflux of potassium.35 Excess potas­
sium subsequently causes shifts at nerve endings and is
thought to be the cause of the extreme pain associated with
hydrofluoric acid burns.36
Hydrofluoric acid burns are classified based on the con­
centration of the exposure.37 Concentrations >50% cause
immediate tissue destruction and pain. Concentrations of
20–50% result in a burn becoming apparent within several
hours of exposure. Injuries from concentrations <20% may
take up to 24 hours to become apparent.
Death from hydrofluoric acid exposure is usually second­
ary to systemic toxicity. Systemic symptoms are secondary to
acidosis, hypocalcemia, hypomagnesemia, and hyperkale­
mia, which can lead to ventricular fibrillation. Thus, electro­
lytes and cardiac rhythm should be monitored closely.38
Once cardiac dysrhythmias develop, it is difficult to restore
a normal rhythm.39 Compounding the problem of hypocal­
cemia, the fluoride ion may be acting as a metabolic poison
in the myocardium to promote the irritability. The typical
electrocardiographic change seen is Q-T interval prolonga­
tion. The fluoride ions can be removed by hemodialysis or
cation exchange resins.40,41
Treatments for hydrofluoric acid exposure are designed to
neutralize the fluoride ion and prevent systemic toxicity. Pri­
marily, the wound should be copiously irrigated for 30
minutes. If the concentration of exposure is <20%, or the
duration of exposure is minimal, this may serve as the extent
of treatment. For more serious exposures, topical, subcutane­
ous, or intra-arterial mixtures of calcium gluconate can be
used as a first option. The topical gel is a mixture of 3.5 g of
2.5% calcium gluconate and 5 oz of water-soluble lubricant.
It should be applied to the wound 4–6 times each day for 3–4
days.42 The mixture’s penetration into the dermis is limited by
its calcium component. This is improved with the use of
DMSO, which has its own associated toxicity. Calcium gluco­
nate injections into the area of the wound (0.5 mL/cm2 of
10% calcium gluconate subcutaneously or intradermally)
have also been used, with good results.14,43 Intra-arterial injec­
tions into the radial artery (10 mL 10% calcium gluconate and
40 mL D5W infused over 2–4 hours) can be used for manage­
ment of burns to the hand,44 but in severe cases palmar fasci­
otomy may be needed.45 This injection should be performed
within 6 hours of exposure, to prevent tissue necrosis and
minimize pain. It should continue until the patient is
symptom free.
Nitric acid
This is a strong oxidizing agent that can combine with
organic proteins to produce organonitrates, which act as
metabolic poisons. It is used in fertilizer management,

Chemical burns
459
from the skin immediately. Once cooled, the tar produces
liquefaction injury and should be debrided from the skin,
especially if obvious burn, blister, or tissue loss is apparent.
Antibiotic ointments and household items such as baby oil,
mineral oil, mayonnaise, and butter have been found to aid
in its removal14,54 (Fig. 41.5).
Vesicant chemical warfare agents
(mustard, lewisite, nitrogen)
These agents affect all epithelial tissues, including skin, eyes,
and respiratory epithelium. Symptoms described after expo­
sure to mustard gas include burning eyes, burning throat,
and a feeling of suffocation.42 This is followed by erythema
of the skin within 4 hours and blister development within
12–48 hours. Severe pruritus develops, particularly in moist
areas such as the axilla and perineum. When the blisters
rupture, they leave painful, shallow ulcers. Exposure to larger
quantities of these agents produces coagulative necrosis of
the skin, with either no blistering or ‘doughnut blisters’ sur­
rounding a central necrotic zone.43
Lewisite (2-chlorovinyl-dichloroarsine) is the best known
arsine. It is more powerful than the mustards and the symp­
toms occur sooner.
Phosgene oxime is another common agent in chemical
warfare. It is the most widely used halogenated oxime and
has the immediate effect of stinging, likened to contact with
a stinging needle.44 Affected areas quickly become swollen
with blister formation, and eschars develop over the ensuing
week. Wound healing is slow, typically over 2 months. Eye
involvement is extremely painful and can result in perma­
nent blindness. Inhalation leads to hypersecretion and pul­
monary edema.
Clothing must be removed from the victim and large-
volume lavage of the skin is undertaken. Eyes are irrigated
with water or ‘balanced salt solution.’ Symptomatic relief of
itching is provided with benzodiazepines, antihistamines,
or phenothiazines. Blisters are debrided and dressed with
topical antimicrobials. Dimercaprol is a chelating agent that
is an antidote for lewisite poisoning. There is no specific
antidote for nitrogen mustard, but sodium thiosulfate and
Metals
Occupational injuries often occur to workers using molten
metal, such as elemental metals, sodium, lithium, potas­
sium, magnesium, aluminum, or calcium. After exposure,
the use of water is contraindicated as it may result in an
explosive exothermic reaction. Class D fire extinguishers or
sand are ideal for management, but mineral oil is also an
option14 (Fig. 41.4).
Hydrocarbons
Hydrocarbons are corrosive agents, often contained within
plants, animal fats, and fuel oils.51 Prolonged contact with
petroleum distillates results in dissolution of lipid cell mem­
branes, leading to cell death.52 These burns tend to be super­
ficial. Systemic toxicity usually involves respiratory depression.
Heat loss from rapid evaporation of gasoline can cause the
development of frostbite and dehydration.14 Early decon­
tamination is most efficiently achieved with soap and water.51
Hypochlorite solutions
These are potent oxidizers delivered in alkaline solution
used as bleaches and household cleaners. Exposure to 30 mL
of 15% solution is potentially fatal. Systemic manifestations
of toxicity include vomiting, confusion, dyspnea, airway
edema, cyanosis, cardiovascular collapse, and coma.53 Treat­
ment consists of copious irrigation.
Alkyl mercuric compounds
Skin reaction with these substances releases free mercury,
which can be found in blister fluid. With time, mercury is
absorbed, leading subsequently to systemic effects. After blis­
ters are debrided, repeat washing to lavage the blister fluid
is necessary.
Tar
Tar, crude oil, and asphalt are various names for mineral
products created from long-chain petroleum and coal or
fossil hydrocarbons. This compound should be removed
Figure 41.4  Sodium hydroxide burn to the face and tongue.
Figure 41.5  Crude oil burn to the face.

Total Burn Care
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460
literature. J Burn Care Res. 2007 Nov-Dec;28(6):827-834. (General
overview of cement burns.)
Devereaux A, Amundson DE, Parrish JS, et al. Vesicants and nerve
agents in chemical warfare. Decontamination and treatment
strategies for a changed world. Postgrad Med. 2002 Oct;112(4):
90-96. (General overview of vesicant chemical warfare agents.)
Harchelroad FP, Rottinghaus DM. Chemical Burns. In: Emergency
Medicine: A Comprehensive Study Guide, 6th ed. 2004:200.
(General review of chemical burns.)
Kuckelkorn R, Schrage N, Keller G, Redbrake C. Emergency treatment
of chemical and thermal eye burns. Acta Ophthalmologica
Scandinavica. 2002 Feb;80(1):4-10. (General review of chemical
burns to eyes.)
Stuke LE, Arnoldo BD, Hunt JL, et al. Hydrofluoric acid burns: a
15-year experience. J Burn Care Res. 2008 Nov-Dec;29(6):893-896.
(General overview of hydrofluoric acid burns.)
N-acetylcysteine may be helpful to reduce the effects if
administered early.45 The blister fluid from nitrogen mustard
injuries does not contain active agent and is hence harm­
less.46 Agranulocytosis or aplastic anemia can result from
exposure to these agents.47 In the appropriate setting, bone
marrow transplantation may be considered.
Conclusion
Many chemical compounds can cause burn injury. The prin­
cipal idea behind the treatment of chemical burns is early,
copious irrigation. Wound care is the same as for thermal
burns. Chemical burns tend to be deeper than they initially
appear, often requiring skin grafting for management.
Further reading
Chung JY, Kowal-Vern A, Latenser BA, et al. Cement-related injuries:
review of a series, the National Burn Repository, and the prevailing
 
Access the complete reference list online at

Chemical burns
460.e1
© Copyright 2012 Elsevier, Inc. All rights reserved.
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24. Ogawa M, Nakajima Y, Endo Y. Four cases of chemical burns
thought to be caused by exposure to chromic acid mist. J Occup
Health. 2007;49(5):402-404.
25. Terrill PJ, Gowar JP. Chromic acid burns; beware, be aggressive,
be watchful. Br J Plast Surg. 1990 Nov;43(6):699-701.
26. Cason JS. Report on three extensive industrial chemical burns.
Brit Med J. 1959;1(5125):827-829.
27. Matey P, Allison KP, Sheehan TM, et al. Chromic acid burns: early
aggressive excision is the best method to prevent systemic toxicity.
J Burn Care Rehabil. 2000 May-Jun;21(3):241-245.
28. (
batch-lot-2/106–89–8_e.html).
29. Gould RF. Advanced Propellant Chemistry. ACS Chemistry Series
54. 1966.
30. McIvor ME. Delayed fatal hyperkalemia in a patient with acute
fluoride intoxication. Ann Emerg Med. 1987 Oct;16(10):
1165-1167.
31. Chan TC, Williams SR, Clark RF. Formic acid skin burns resulting
in systemic toxicity. Ann Emerg Med. 1995 Sep;26(3):383-386.
32. Karunadasa KP, Perera C, Kanagaratnum V, et al. Burns due to
acid assaults in Sri Lanka. J Burn Care Res. 2010 Sep-Oct;31(5):
781-785.
33. Reilly DA, Garner WL. Management of chemical injuries to the
upper extremity. Hand Clin. 2000 May;16(2):215-224.
34. Stuke LE, Arnoldo BD, Hunt JL, et al. Hydrofluoric acid burns: a
15-year experience. J Burn Care Res. 2008 Nov-Dec;29(6):893-896.
(General overview of hydrofluoric acid burns.)
35. Mayer TG, Gross PL. Fatal systemic fluorosis due to hydrofluoric
acid burns. Ann Emerg Med. 1985 Feb;14(2):149-153.
36. McIvor ME, Cummings CE, Mower MM, et al. Sudden cardiac
death from acute fluoride intoxication: the role of potassium.
Ann Emerg Med. 1987 Jul;16(7):777-781.
37. Yolken R, Konecny P, McCarthy P. Acute fluoride poisoning.
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38. Anderson WJ, Anderson JR. Hydrofluoric acid burns of the hand:
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39. Vance MV, Curry SC, Kunkel DB, et al. Digital hydrofluoric acid
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40. Caravati EM. Acute hydrofluoric acid exposure. Am J Emerg Med.
1988 Mar;6(2):143-150. (Excellent review of hydrofluoric acid
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41. McCulley JP, Whiting DW, Petitt MG, et al. Hydrofluoric acid
burns of the eye. J Occup Med. 1983 Jun;25(6):447-450.
42. Miller FG. Poisoning by Phenol. Can Med Assoc J. 1942
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43. Saunders A, Geddes L, Elliott P. Are phenolic disinfectants toxic to
staff members? Aust Nurses J. 1988 May;17(10):25-26.
44. Schutz W. Phenoldermatosen. Berufsdermatosen. 1959;7:266.
45. Devereaux A, Amundson DE, Parrish JS, et al. Vesicants and nerve
agents in chemical warfare. Decontamination and treatment
strategies for a changed world. Postgrad Med. 2002 Oct;112(4):
90-96. (General overview of vesicant chemical warfare agents.)
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50. Chung JY, Kowal-Vern A, Latenser BA, et al.
Cement-related injuries: review of a series, the National
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Toxicologic Emergencies, 8th ed. 2006.
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©2012 Elsevier Ltd, Inc, BV
DOI: 10.1016/B978-1-4377-2786-9.00042-4
Radiation injuries and vesicant burns
Stephen M. Milner, Michael J. Feldman
Introduction
In the aftermath of 9/11, with the threat of constant and
unrelenting terrorism, the possibility of employment of
nuclear weapons, or crude nuclear devices, of attacks on
nuclear facilities and use of chemical agents cannot be
ignored. Such attacks may result in types of injuries in previ­
ously unimaginable numbers. Given the devastating medical
consequences that would follow the use of such weapons,
the training of medical personnel will be a crucial factor in
the effective management of such casualties, should the
unthinkable ever occur.
Only 4 months after Roentgen reported the discovery of
X-rays, Dr John Daniel observed that irradiation of his
colleague’s skull caused hair loss. Since this finding was
reported in 1896, many biomedical effects of radiation have
been described.1 Knowledge of nuclear physics was rapidly
amassed in the early part of the 20th century, leading eventu­
ally to the Manhattan project and the development of the
atomic bomb. The last 50 years has also seen widespread
deployment of energy-generating nuclear reactors, and the
expanding use of radioactive isotopes in industry, science,
and healthcare.2 More recently, major industrial accidents of
note at Three Mile Island in Pennsylvania, Chernobyl in the
Ukraine and at Goiania, Brazil have resulted in potential or
real radiation injuries to hundreds of people. According to
the latest NCRP report on radiation exposure to United
States citizens, the most significant increase in ionizing radi­
ation exposure, over the last 20 years, has been through
medical imaging.3 Health professionals have become more
aware of the cumulative effects of radiation. This has become
a common topic for debate in regards to ionizing radiation
exposure during the treatment of breast cancer patients and
children.
Exposure to ionizing radiation can follow one of three
patterns:
1. Small-scale accidents, or cumulative exposures, as
might occur in a laboratory or from an X-ray device in
a hospital setting.
2. Large industrial accidents (such as those mentioned
above), stretching the need for treatment beyond
available resources.
3. Detonation of a nuclear device in a military conflict
where resources are totally overwhelmed or unavailable
and associated multiple and combined injuries also
exist.
This chapter first describes the terminology used in stand­
ard measurement of radiation exposure and discusses the
frequency of radiation accidents, injuries and fatalities. The
effects of exposure to ionizing radiation and triage and care
protocols are considered according to known and projected
prognostic factors. The complications that arise specifically
with this injury and the supportive measures that need to be
taken will be addressed.
Vesicant agents are characterized by their ability to pro­
duce cutaneous blisters resembling ‘burns.’ Although most
physicians are unlikely to encounter casualties of chemical
weapons, the proliferation of these agents has increased the
risk to both military and civilian populations. They are
likely to require the expertise found in burn centers and for
this reason an account of the management of these injuries
is included in this text.
Radiation injuries
Terminology
Damage to biological tissue by ionizing radiation is medi­
ated by energy transference. This can be the result of expo­
sure to electromagnetic radiation (e.g. X-rays and gamma
rays) or particulate radiation (e.g. alpha and beta particles
or neutrons). The severity of tissue damage is determined by
the energy deposited per unit track length, known as linear
energy transfer (LET).4 Electromagnetic radiation passes
through tissue almost unimpeded by the skin and are called
low LET since little energy is left behind. In contrast, neutron
exposure has high-LET, resulting in significant energy absorp­
tion within the first few centimeters of the body. Alpha and
low-energy beta particles do not penetrate the skin, and
represent a hazard only when internalized by inhalation,
ingestion or absorption through a wound.
The biological effect of ionizing radiation is measured by
the radiation absorbed dose (rad). The newer SI unit of
absorbed dose is the gray (1 Gy = 100 rads). Not all radiation
is equally effective in causing biological damage, although it
may cause the same energy deposition in tissue. For example,
1 Gy of neutron radiation will not have the same effect as
1 Gy of gamma or X-radiation. For this reason, a unit of dose
equivalence was derived that allows radiations with different
LET values to be compared. One such unit is the rem
(acronym of roentgen equivalent man). The dose in rem is
equal to the dose in rads multiplied by a quality factor (QF).5
CHAPTER 42 
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IN THIS CHAPTER
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Total Burn Care
42
462
of 128 fatalities recorded by the Registry worldwide.6 The
majority of the radiation deaths occurred as a result of the
Chernobyl accident in 1986 (>40). The classification of radi­
ation accident by device for the period 1944 until June 2010
is shown in Table 42.2.6
The majority of radiation accidents are due to radiation
devices. This may be an accelerator; however, most devices
involved in accidents are encapsulated, highly radioactive
sources used for industrial radiography. Next most frequent
accidents are radioisotope accidents involving radioactive
materials which are unsealed, such as tritium, fission pro­
ducts, radium and free isotopes used for diagnosis and
therapy. Uncommon criticality accidents occur when enough
fissionable material, such as enriched uranium, is brought
together to produce a neutron flux so high that the material
undergoes a nuclear reaction (becomes critical).
The most devastating radiation injuries and fatalities yet
seen, however, resulted from detonation of nuclear weapons
at Hiroshima and Nagasaki during World War II. Since 1945,
nuclear weapon technology has developed enormously
and current strategic thermonuclear warheads dwarf those
weapons used in Japan.7 Keep in mind that the bombs
dropped on Japan still contained the same energy equivalent
to 12–15 thousand tons of TNT (Hiroshima) and 20–25
thousand tons of TNT (Nagasaki).8 The majority of radiation
exposure in this case occurred within the first minute of the
explosion. There were no deaths attributed to the products
left behind by the atomic explosions. As detailed by Kucan
in 2004, the majority of radioactive fallout from these
weapons were dispersed into the atmosphere, as both were
detonated several thousand feet in the air.8
The QF takes into account the linear energy transfer and has
a different value for different radiations; for X-rays it is 1.0,
for neutrons 10. The international unit, now more widely in
use, is the sievert (Sv). One sievert equals 100 rem; 1 rem
equals 10 mSv. This allows radiations with different LET
values to be compared, since 1 Sv of neutron radiation has
the same biological effect as 1 Sv of low LET gamma or
X-radiation.
Incidence
A significant radiation accident is one in which an individual
exceeds at least one of the following criteria:6
•
Whole body doses equal to or exceeding 25 rem
(0.25 Sv)
•
Skin doses equal to or exceeding 600 rem (6 Sv)
•
Absorbed dose equal to or greater than 75 rem
(0.75 Sv) to other tissues or organs from an external
source
•
Internal contamination equal to or exceeding one-half
the maximum permissible body burden (MPBB) as
defined by the International Commission on
Radiological Protection (this number is different for
each radionuclide)
•
Medical misadministrations provided they result in a
dose or burden equal to or greater than the criteria
already listed above.
Radiation accidents within the United States should be
reported to the federally funded Radiation Emergency Assist­
ance Center/Training Site (REAC/TS). This is operated by
Oak Ridge Institute for Science and Education (ORISE)
at Oak Ridge, Tennessee and can be contacted by calling
(865) 576–1005 (website: ). A
radiological emergency response team of physicians, nurses,
health physicists, and support personnel provides consulta­
tive assistance on a 24-hour basis and has the capability
of providing medical treatment, whenever a radiation acci­
dent occurs. REAC/TS also maintains a Radiation Accident
Registry System.
The number of accidents, number of persons involved, as
well as the number of fatalities, in the United States and
worldwide is shown in Table 42.1. There have been a total
Table 42.1  Major radiation accidents: human experience
(1944–June 2010)
Location
No. of
accidents
No. of
persons
involved
Significant
exposuresa
Fatalities
US
250
1358
796
26
Non-US
184
132 461
2287
102
Former
Soviet
Unionb
(137)
(507)
(278)
(35)
Total
434
133 819
3083
128
aDOE/NRC dose criteria. bFormer Soviet Union Registry Data (not included in totals
– data incomplete). Source: REAC/TS Registry.
Table 42.2  Major radiation accidents worldwide (1944–June
2010): ‘classification by device’
Radiation devices
320
Sealed sources
212
X-ray devices
83
Accelerators
25
Radar generators
1
Radioisotopes
96
Diagnosis and therapy
40
Transuranics
28
Fission products
11
Tritium
2
Radium spills
1
Other
13
Criticalities
20
Critical assemblies
8
Reactors
6
Chemical operations
6
Total
435
Source: REAC/TS Registries.