Burn Shock: Definition, Causes, Treatment in First Aid and Emergency

By Cristiano Antonino On Apr 30, 2023

Burn shock is defined as non-haemorrhagic hypovolaemic shock (shock from decreased circulating blood volume NOT caused by haemorrhage) that occurs when the patient is subjected to a large area of the body being burned

Burn shock is hypovolaemic non-haemorrhagic shock (shock from decreased circulating blood volume NOT determined by haemorrhage) that occurs when the patient is subjected to a large-area burn of the body.

Why does burn shock occur?

Burn shock is related to an alteration in capillary tone and permeability produced by toxins that are formed in burnt tissue by the breakdown and reabsorption of necrotic protein substances.

Initially, the lymphatic system drains excess fluid but soon its absorption capacity becomes saturated and oedema appears.

The altered permeability of the capillaries results in the passage of plasma from the vessels to the interstitium, which causes oedema, dehydration and hypoprotidemia, leading to a decrease in circulating blood volume and an increase in its viscosity.

The amount of fluid lost depends on the extent of the burn.

Fluids are also lost directly through phlegm and secretions from the burned surface.

The altered capillary permeability is also more pronounced in the burn area, but in reality the phenomenon appears generalised, i.e. liquids are also lost in areas far away from the burned area.

The fluid that collects in the interstitium through the vessels can account for a considerable proportion of the extracellular fluid.

Fluid loss is greatest in the first 24 hours after the thermal trauma, after which capillary permeability returns to normal after 48 hours and reabsorption of the oedema begins.

In reality, not all the fluid in the third compartment (oedema) can be reabsorbed.

In fact, about half of it remains bound to interstitial proteins and this share may increase in relation to alterations in the acid-base balance.

The fluid in the oedema consists of water, salts and proteins. The salts are the same as in plasma and interstitial fluid (NaCl).

Signs and symptoms of burn shock

Severe disturbances of the general condition generally occur in burns shock, with some characteristic signs and symptoms, such as:

vomiting;
convulsions;
drowsiness;
loss of consciousness;
hypotension (lowering of blood pressure);
hypothermia;
symptoms of circulatory failure;
haemorrhages in the mucous membrane of the nose and bronchi;
lowered central venous pressure;
elevation of haematocrit;
decreased diuresis;
albuminuria;
haematuria.

Alterations in protein balance caused by burn shock

In the first week after the burn, protein loss is 25-50 g/day, of which 12-30 g is lost through hypercatabolism after the first 5-10 hours (during which there is no catabolic activity), and 10-20 g is lost through exudate and in the oedema fluid.

It has been shown that plasmapheresis, i.e. the loss of proteins from the plasma unaccompanied by losses of mineral salts and water, does not cause shock.

Moreover, part of the plasma proteins return to the circulation via lymphatic drainage.

In contrast, the sudden loss of sodium can cause shock and cardiovascular collapse.

Alterations in haematological balance

The number of red blood cells decreases in proportion to the extent and degree of the burn for four reasons

direct haemolysis by heat
formation of vessel thrombi in the burned area that trap and destroy red blood cells;
destruction by the reticuloendothelial system of partially altered haematous cells;
the phenomenon of intravascular agglutination, also called ‘sludging’, which corresponds to an agglutination of blood cells that occurs within the circulatory stream: they form a semi-solid mass within the blood vessels that can even impede circulation.

The phenomenon of sludging is aggravated by haemoconcentration due to fluid loss

Erythrocyte deficiency reduces blood flow in the microcirculation worsening the perfusion and oxygen deficit.

This state is then maintained by the erythropoietic deficit (due to reduced iron utilisation, altered porphyrin metabolism and decreased erythropoietin as a result of renal damage) and loss in granulation tissue.

The total loss during the entire course of the disease can be up to 85% of normal values.

Despite this, transfusions are not recommended in the first 72 hours.

Since plasma depletion is greater than erythrocyte depletion, transfusion of whole blood would only increase blood viscosity and thus sludging.

Alterations in acid-base balance

The normal pH of arterial blood is maintained at 7.4 by buffer systems.

The most important buffers include:

phosphates and proteins (haemoglobin) in the intracellular compartment;
bicarbonate – carbonic acid system in the extracellular compartment.

In the burn victim, there is an increase in organic and inorganic acids for three reasons

increase in anaerobic metabolism due to tissue hypoxia (increase in pyruvate and lactate)
increase in protein catabolism and tissue necrosis (increase in urates and sulphates);
increased catabolism of fatty acids to meet energy needs (increase in ketone bodies). These acids, after being neutralised by buffer systems, are eliminated by increasing respiratory activity and renal excretion. However, the lungs are often damaged and diuresis is reduced due to renal hypoperfusion (see below).

Alterations in potassium balance in burn shock

There is an increase in potassiemia because

the damaged cells release their potassium content;
acidosis is partly buffered by exchanging extracellular H+ for intracellular K+;
K+ is poorly eliminated by the kidney.

Alterations in calcium balance

Initial hypocalcaemia occurs due to:

calcium loss in the burnt area
metabolic acidosis;
adrenocortical hypereactivity (increased secretion of ACTH which stimulates the adrenal cortical to produce cortisol etc.);
corticosteroid treatment.

Cortisol reduces intestinal calcium absorption both by reducing vitamin D formation and by exerting an antagonistic action on it, increasing urinary calcium secretion.

Late hypercalcaemia occurs due to:

initial hypocalcaemia;
forced immobility.

These factors affect the reabsorption of calcium from the bones.

Alterations in magnesium balance

Sometimes magnesium values are within the normal range, other times there is hypomagnesaemia associated with psychic changes, delusions and hallucinations.

Causes are:

direct loss from the burned area;
secondary hyperaldosteronism (aldosterone production is stimulated by the kidney via renin secretion, renin-angiotensin-aldosterone system, whenever hypovolaemia occurs).

Within a few days, infection with gram-negatives (which find the burnt tissue a favourable breeding ground for their development) may occur, leading to endotoxic shock.

The shock can lead to death of the patient, if left untreated, even without serious injury to vital organs or complications from wound infection.

Among the most dreaded complications of burns is septicaemia, which can occur between days 4 and 10 and greatly worsens the prognosis.

Burn shock therapy

Correct therapy first requires a proper assessment of the severity of the clinical picture and changes in the main haemato-clinical parameters.

Various parameters have to be taken into consideration, including:

age and general state of health of the patient;
PVC (central venous pressure);
hourly diuresis;
body weight;
Ht (haematocrit) and other blood parameters;
systolic and diastolic blood pressure;
volaemia (blood volume);
globular mass;
ionogram;
plasma and urinary osmolarity;
acid-base balance.

Burn shock is a non-haemorrhagic hypovolaemic shock characterised by low PVC and high Ht (haematocrit), the first therapeutic measure is therefore to re-establish adequate tissue perfusion by adjusting the blood volume to the changed capacity of the vascular bed.

A qualitatively and quantitatively correct infusion therapy is required, which is gradually adjusted according to the following laboratory tests: Ht, electrolytes (Na+, K+, Cl-, Mg-, Ca++), pH, pO2, pCO2, HCO3-, PVC, diuresis, osmolarity.

They should be checked six times a day.

If during infusion therapy the Ht remains above 45% then the administration rate is low, if it falls below 35% then it is too high.

In general, the Ht should be lower than normal especially if the kidney is functioning well and can therefore eliminate excess H2O on its own.

The PVC informs us of the pressure in the right atrium; if it is less than 9 cmH2O the infusion therapy is insufficient if it is more than 12 cmH2O it means either that the therapy is excessive or that there is a left heart deficit.

The volume of fluid to be infused varies according to the author

Hourly diuresis: this is a sufficiently reliable index of renal perfusion (it is performed with a catheter in the bladder)

Urine values between 0.5 and 1 mg/Kg body weight/hour indicate good renal perfusion.

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Plasma and urinary osmolarity: these are indicative for assessing renal function and the ionic concentration of infused fluids.

If lower than 290-300 then the fluids administered are hypotonic if higher there is a danger of hyperosmolar coma.

The drugs and aids used are generally

cortisone;
heparin (prevents disseminated intravascular coagulation or DIC);
proteolytic enzyme inhibitors (trasylol);
dopamine (increases renal output);
targeted antibiotic therapy (repeated antibiogram);
parenteral nutrition (during burns of the respiratory tract;
tetanus prophylaxis.

Pain therapy

Even a small burn (1st or 2nd degree) can be very painful as it leaves the nerve endings intact while a severe burn (3rd degree) destroys them and is therefore less painful.

The dose of sedation must be well judged because it aims to be

high enough to guarantee the least pain for the patient;
as low as necessary to avoid depressions of cardio-pulmonary and sensory activity.

The route of administration must be intravenous because the physiopathological changes to the skin circulation and muscle tissue alter the dynamics of absorption.

The most reliable drugs are morphine and pyseptone.

Pedimix (paediatric mixture) is given to children who can hardly tolerate pain.

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