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failure. Vasodilatation and hyper perfusion caused by nitric oxide in the post-injury period may accentuate
the reperfusion injury; and (3) calcium influx injury, intra-cellular calcium levels increase due to energy
+
+
dependent Na K pump failure and thus, mitochondria act as calcium sinks [11,14,15] . Increased mitochondrial
2+
Ca leads to activation of calcium-dependent proteases and phospholipases. Increased mitochondrial
2+
Ca leads to opening of the permeability transition pore, and inner mitochondrial membrane channel.
This results in free passage of small molecules, osmotic swelling leading to outer membrane rupture, ATP
depletion and apoptotic mitochondrial cell death.
Mechanism of systemic secondary tissue injury
Systemic hypoxia: systemic hypoxia can cause tissue hypoxia of various organs/tissues. Cellular and tissue
[16]
hypoxia may lead to shock and various types of complications .

Delayed neurological changes in high voltage electric burns may be due to changes in the endothelium
of small vessels supplying nervous tissues . Kidney and heart muscle are damaged due to the release of
[17]
[18]
various intracellular chemicals, hemoglobin and myoglobin .

SIRS: follows major trauma, leading to a phase of inflammatory response which involves the synthesis of
acute phase proteins by the liver, complement activation and the release of pro- (IL-1, TNF alpha, IL- 6, IL-8)
and anti-inflammatory cytokines (IL-10, IL-13). If the balance between the pro- and anti-inflammatory
cytokines is disrupted, it leads to the development of SIRS and increases morbidity and mortality [19-22] [Figure 1].

The auto amplification of cytokine production following major trauma/surgery can occur due to
overwhelming multiple organ dysfunction syndrome (MODS) and/or severe infection, leading to a
[23]
cytokine storm [Figure 2]. Infection with exaggerated inflammatory responses induce more cells that
produce cytokines and act as catalysts to the cytokine storm [24,25] .

Very high level of circulatory pro-inflammatory cytokines, as in a cytokine storm, may cause uncontrolled,
auto destruction that leads to life threatening MODS.

Immune depression: cytokines are known to cause immune depression in musculoskeletal trauma .
[26]
Microvascular dysfunction and increased tissue pressure can occur following musculoskeletal trauma and
[27]
lead to secondary soft tissue damage and compromised skeletal muscle function .

Clinical implications of secondary injury
Repeated debridement and consequent exposure of vital structures - due to secondary injury following
initial and surgical trauma, new necrosis occurs, requiring repeated debridement.

Complex reconstructive procedures are required on several occasions to cover vital exposed structures
following repeated debridement.

SIRS - Pro-inflammatory cytokines are produced due to tissue damage that increase several times following
infection, and if absorbed in large quantities, may produce SIRS, MODS and multiple organ failure.

[28]
Immobilization, edema and inflammation lead to functional loss and stiff joints .
[29]
Missed injuries like spinal injuries may lead to serious crippling injuries .

Clinical strategy against secondary damage in trauma
[30]
In the management of complex surgical problems, a surgeon has three options : (1) avoidance (laissez-
faire); (2) aggressive approach; or (3) temporizing maneuvers.