Burns

Question 1

Describe the local response to burn in terms of 3 zones

Answer 1

1. Zone of coagulation –> This is the region that has experienced maximal damage. Proteins have undergone coagulation. Coagulative necrosis. Irreversible/ non-viable. Requires debridement or grafting.
2. Zone of stasis –> Characterized by ischemia caused by reduced blood flow/ vasoconstriction. Accounts for the systemic effects of burn injury. Potentially salvageable with prompt fluid therapy to re-perfuse tissue.
3. Zone of hyperemia –> Characterized by vasodilation and inreased blood flow. The tissue is fully viable as long as there are no secondary insults or infection.

Question 2

Define burn and give examples of 4 different types of burn that can occur

Answer 2

A burn is a tissue injury that is caused by chemical, electrical, radiation, frictional or thermal energy leading to coagulative necrosis and potential systemic complications.

Types of burn: chemical, electrical, thermal, frictional, radiation

Question 3

Explain the primary systemic response in severe burn

Answer 3

The primary systemic response to burn injury is driven by a massive release of inflammatory cytokines (TNF-a, IL-1, IL-6) and vasoactive mediators (histamine, NO, prostaglandins), leading to increased vascular permeability. This causes significant fluid loss into the interstitial space, resulting in intravascular hypovolemia and edema. While vasodilation may occur, the dominant issue in the acute phase is capillary leak and subsequent burn shock.

The initial 48-hour “ebb” phase is characterized by a hypometabolic state. Cardiac output drops due to a combination of myocardial depression (caused by cytokine release) and reduced preload (due to fluid shifts out of the intravascular space). Despite compensatory catecholamine release, perfusion remains inadequate. Aggressive fluid resuscitation is critical to restoring intravascular volume and preventing organ failure.

By approximately 48 hours, the “flow” phase begins, characterized by a hypermetabolic state that can persist for months—or even over a year in severe burns. This phase is driven by increased catecholamine and cortisol release, resulting in tachycardia, hyperglycemia, massive catabolism, muscle wasting (due to proteolysis), insulin resistance, and immunosuppression, increasing the risk of infection and sepsis. Splanchnic vasoconstriction, which can impair gut barrier function and promote bacterial translocation, should be mitigated with early enteral feeding to maintain gut integrity and reduce septic complications.

Question 4

Outline 4 causes of anemia in a burns patient

Answer 4

1. Acute blood loss from the injury itself and/or surgical intervention.
2. Inflammatory cytokines suppress erythropoeisis by inhibiting erythoid precursor proliferation and inhibiting EPO synthesis in kidney.
3. Depletion of iron, folate, B12 due to hypermetabolic state.
4. Increased hepcidin production in liver in response to inflammation; inhibits iron absorption from the gut and release of iron from intracellular stores –> further hinders erythropoeisis.
5. Increased RBC sequestration in damaged tissue and haemophagocytosis.
6. Hemodilutional anemia due to fluid replacement therapy

Question 5

Outline 4 reasons why burns victims may be predisposed to infection

Answer 5

1. Effect on Lymphocytes
   –> T and B cell proliferation is inhibited, particularly due to excessive release of TGF-β, which suppresses immune cell function post-burn.
   –>A shift from a Th1 to a Th2-dominated response impairs pathogen clearance. IL-4 and IL-10 promote Th2 responses, which suppress cytotoxic T-cell and macrophage activation, weakening cell-mediated immunity and increasing susceptibility to infections.
2. Effect on Innate Immune Response
   –>Initial hyperinflammatory phase (cytokine storm) with TNF-α, IL-1, and IL-6 leads to immune dysregulation, followed by compensatory anti-inflammatory response syndrome (CARS), which causes immune suppression.
   –>Neutrophils, macrophages, and dendritic cells exhibit impaired chemotaxis, phagocytosis, and antigen presentation, reducing pathogen clearance.
   –> Complement dysfunction weakens opsonization, further impairing innate immune defense.
3. Hormonal and Metabolic Changes
   –> Elevated cortisol and catecholamines contribute to immunosuppression by downregulating pro-inflammatory cytokines and impairing leukocyte function.
   –> These stress-induced changes weaken both adaptive and innate immune responses, making infections more likely.
4. Loss of Skin Barrier
5. Burn-induced gut permeability
   –>Splanchnic vasoconstriction and elevated systemic inflammatory mediators contribute to gut mucosal atrophy and increased permeability.
   –>This allows bacterial translocation from the gut into the bloodstream, leading to sepsis and systemic infections.

Question 6

Summarise how a burn injury affects (i) cardiovascular (ii) respiratory and (iii) immune systems

Answer 6

Cardiovascular system
-Increased vascular permeability due to inflammatory cytokine release (e.g. TNF-α, IL-1) → fluid shifts from the intravascular space to the interstitial space (third spacing).

-Reduced cardiac contractility (burn shock phase) due to myocardial depressant factors and systemic inflammatory response.

-Peripheral and splanchnic vasoconstriction occurs to maintain perfusion of vital organs (brain, heart).

-Hypovolemia results from plasma loss and reduced venous return, contributing to decreased cardiac output and organ perfusion.

Respiratory system
-Bronchoconstriction due to inflammatory mediator release (e.g. histamine, prostaglandins, leukotrienes).

-Airway and pulmonary edema can occur from systemic capillary leak and inhalation injury; may lead to respiratory distress or failure.

Immune system
-Suppression of innate and adaptive immunity (both cell-mediated and humoral) due to massive systemic inflammation, lymphocyte dysfunction, and apoptosis.

-Burn patients are at increased risk of infections and sepsis due to loss of skin barrier and impaired immune response.

Question 7

Classify burns based on depth and give the clinical features of each

Answer 7

(1) Superficial thickness - Epidermis
-erythema
-blanchable
-painful
-dry
-No blisters

(2) Superficial partial thickness (papillary dermis)
-erythema
-blanchable
-wet
-painful
-blisters with clear fluid

(3) Deep partial thickness (reticular dermis)
-Mottled
-sluggish or absent blanching
-painless
-easily deroofed blisters

(4) Full thickness (hypodermis)
-dry, waxy, leathery
-no blanching
-painless
-visualization of muscle/tissue if deep enough

Question 8

Define sepsis and give 4 clinical features

Answer 8

Sepsis is defined as a life threatening organ dysfunction caused by a dysregulated host response to an infection.

Clinical features:
(1) Temperature >38°C (fever) or <36°C (hypothermia)
(2) Tachypnea
(3) Tachycardia
(4) Altered mental status.
(5) Hypotension

Question 9

Define septic shock

Answer 9

Septic shock occurs in the setting of sepsis and is characterized by circulatory, cellular and metabolic abnormalities.
There is typically co-existence of:

(1) Persistent hypotension requiring vasopressors to maintain mean arterial pressure (MAP) ≥65 mmHg, despite adequate fluid resuscitation, and

(2) Serum lactate >2 mmol/L, indicating tissue hypoperfusion and metabolic dysfunction.

Question 10

What forms can candida albicans take and what form is best suited for invasion of tissues?

Answer 10

Yeast, pseudo-hyphal and hyphal form.

Hyphal form is most suitable for invading tissues.

Hyphae can release hydrolytic enzymes to penetrate tissues/ through endothelium to enter blood stream.

C.A can form biofilms on mucosal surfaces increasing its resistance to antifungals. It can also change cell wall composition to avoid an immune attack.

Question 11

Briefly describe the pathogenesis of septic shock

Answer 11

(1) Innate immune response is activated against microbes via PAMP-TLR interaction –> hyperinflammatory response with ++ inflammatory cytokine release + nitric oxide release –> vasodilation and hypotension

(2) Endothelial dysfunction occurs and causes vascular leakage, oedema, more hypotension, increased adhesion molecules, increased leukocyte infiltration.

(3) Pro-coagulable state can occur due to increased tissue factor and plasminogen activator inhibitor plus decreased anti-thrombin III and protein C –> disseminated intravascular coagulation –> microvascular thrombosis and hypoxia/ischemia.