The 6 phases of the clinical course of a burn: patient management

By Cristiano Antonino On Apr 15, 2023

Clinical course of a burn patient: a burn is a lesion of the integumentary tissues (skin and skin appendages) caused by the action of heat, chemicals, electric current or radiation

Classification of the phases of a burn

They can be of various entities according to the intensity of the temperature, the duration of the contact and the physical state of the burning substance (solid, liquid or gaseous); in relation to the severity they are divided into groups (1st, 2nd, 3rd and 4th degree).

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The clinical course of a burn can be divided into 6 phases:

phase of nervous shock from terrible pain;
hypodynamic phase or phase of hypovolemic shock (first 48 hours);
catabolic phase (before burn closure);
phase of exudate absorption toxicosis;
stage of sepsis by infection of the sores;
stage of synchratic dystrophy or convalescence.

1) Nervous shock phase

It lasts a few hours, and is characterized by: psychic excitement, intense pain, intense thirst, sweating, polypnoea (breathing frequency above normal), insomnia (sometimes delirium and convulsions), little or no diuresis, gastrointestinal atony, sudden changes in blood pressure.

2) Phase of hypovolemic shock

It is characterized by: small and frequent pulse, low blood pressure (especially systolic), peripheral cyanosis, cold sweat, low temperature (36-35 °C), shallow and frequent breathing, nervous hyperexcitability alternating with periods of depression with drowsiness, apathy, adynamia; continuous need to urinate with emission of a few drops or anuria, bowel closed with faeces and gas, haemodynamic crisis that lasts from a few hours to 3-4 days.

The patient may die of heart failure. Hemodynamic changes include:

tachycardia;
hypotension;
reduction in cardiac output;
vasoconstriction.

Cardiac output may decrease to 30-50% of normal due to hypovolemia and myocardial depressant factor.

Cardiac output often tends to normal levels only after several days, even if infusion therapy is correct.

Changes in renal function are due to:

hypovolemia;
vasoconstriction;
opening of arteriovenous shunts bypassing the kidney;
adrenal imperative.

The juxtaglomerular cells of the kidney release renin into the circulation in response to sodium deprivation, low blood pressure (hypovolemia), and a sympathetic nerve stimulus (due to hypovolemia).

Renin causes, through angiotensin, the release of hormones from the adrenal cortex (cortisol, mineralocorticoids e.g. aldosterone, glucocorticoids, etc.) which act on renal reabsorption.

Following these occurs:

oliguria (more or less severe);
reduction of glomerular filtration;
sodium retention (aldosterone);
increased secretion of potassium (aldosterone).

If the therapy is adequate, these manifestations may not appear, otherwise, renal insufficiency similar to hemorrhagic shock may occur.

After 2-3 weeks there may be gram-negative septic shock which further aggravates renal function, with the possible onset of an often fatal irreversible acute renal failure.

Several theories explain oliguria, which could be due to:

a nervous reflex that causes spasm of the afferent arterioles;
the introduction into the circulation of toxic substances released from the burnt area which would act either at the glomerular level or by producing the spasm of the afferent arterioles which blocks filtration;
a renal attempt to compensate for the hydrometabolic alterations through a greater tubular reabsorption of sodium and water by reducing urinary elimination. In the first phase, an activation of the renin-angiotensin system was also highlighted, which causes sodium retention.

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3) Catabolic phase

The third phase is characterized by:

decreased general reactivity of the organism;
negative nitrogen balance;
decline in defensive capabilities.

If septic shock occurs in this phase, renal failure leads to death.

The most reliable data for monitoring renal function is plasma and urinary osmolarity.

If this continues to increase (progressive hyperosmolarity) the prognosis becomes poor.

The symptoms of progressive hyperosmolarity are: intense thirst, changes in consciousness, orientation disturbances, hallucinations, coma, convulsions, death.

The negative nitrogen balance and the energy deficit are partly related to the lack of increase in evaporative water.

The duration and intensity of the catabolic phase are related to:

extent and degree of burn;
severity of any infectious processes;
nutritional regimen;
duration of the open phase of wounds.

During this phase the energy requirement of calories is greater than 4000cal/day.

Despite the introduction of appropriate therapies, the positivization of the nitrogen balance is achieved only in the convalescent phase.

4) Phase of toxicosis (autotoxic shock)

Appears after 3-4 days.

The reabsorption of transudate and exudates from the burned areas puts toxic substances into circulation.

After a period of apparent well-being (characterized by normalization of pulse, pressure and temperature), they determine new symptoms such as: high fever (39-40°C), headache, nausea and haemorrhagic ulcers.

This phase can last from 15 to 20 days.

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5) Stage of sepsis

It is due to infection of the burned areas facilitated by immunosuppression.

The temperature begins to rise again with continuous and remitting fever preceded or accompanied by chills, headache, nausea.

The pulse is frequent and the pressure is lowered. There is virulence of cutaneous saprophytic germs which pollute the surface of the granulation tissue during the period of sepsis (they are gram-negative: Pseudomonas, Serratia, Klebisiella, Candida, etc.)