Belba M.

Clinic of Burns and Plastic Surgery, University Centre Hospital, Tirana, Albania

SUMMARY.The Author describes the experience of the medical staff at the hospital where she works as regards the treatment of post-burn complications. After presenting the statistics of the previous year, she indicates the incidence of complications in the phase of shock and in sepsis. The criteria for admission to the Intensive Care Unit in question on the basis of the percentage of burn area are indicated, together with the more frequent complications in survivors and in deceased patients. The mortality rate was 13%. The Author’s main intention was the introduction of new concepts in the evaluation of the clinical situation, especially during the septic period of the illness. A definition is given of SIRS (Systemic Inflammatory Response Syndrome) and a description is made of how this gradually proceeds, according to the severity of the illness, up to septic shock.

Introduction

Nearly all patients hospitalized in a burns Intensive Care Unit (ICU) are patients with a reserved prognosis who are subject to complications. The classification of the severity of a burn patient’s illness depends on certain factors, the most important of which are: 1) the extent, depth, and location of the burn injury; 2) the patient’s age; 3) the aetiological agents involved; 4) the presence of inhalation injury; and 5) co-existing illnesses. This classification creates three categories of burn injury (major, moderate, and minor) and defines the optimal setting for the management of each. The first and the second category necessarily require hospitalization, intensive treatment, and rigorous observation during all phases of the burn illness.

In its clinical and therapeutic protocol, our University Service for the treatment of burns uses the following criteria for the hospitalization and treatment of patients in its ICU:

1. adults with partial-thickness burns in more than 15% TBSA or full-thickness burns in more than 10% TBSA;
2. children over 4 years old with partial-thickness burns in more than 10% TBSA or full-thickness burns in more than 5% TBSA;
3. children under 4 years old with partial-thickness burns in more than 5% TBSA or full-thickness burns in more than 1% TBSA;
4. adults and children with burns involving critical regions (face, hands, feet, perineum), patients with electrical or chemical burns, and elderly patients with accompanying diseases.

In view of the fact that numerous complications of a widely varying nature can occur during the burn illness, we classified the complications in two major groups - complications caused by massive loss of liquids and complications due to a variety of infections.

Burn injury is immediately followed by considerable loss of liquids. This loss reaches a maximum after 2 h and according to the clinical situation may persist for 8 to 36 h. In adult patients with burns in more than 15% TBSA and children with burns in more than 10% TBSA, the liquid deficit and incorrect treatment may lead to hypovolaemic shock. The physiological changes seen after thermal injury are a response to diminished circulating blood volume. The main features of hypovolaemic shock are an increase in the heart rate, a decrease in arterial and venous blood pressure, and a high haematocrit level, causing a significant reduction in diuresis. Within the first 48 h the reduction of circulating mass diminishes by up to 10% of body weight.

Bacterial invasion occurs in a burn patient because the skin no longer acts as a barrier impeding the entrance of micro-organisms. Damage to the stratum corneum not only “opens the doors” to micro-organisms but allows them to multiply. Destruction or malfunction of the Langerhans cells aggravates the situation through alteration of the local immune response. Because of the reduction at the same time of the systemic immune response, severely burned patients are susceptible to life-threatening infections. Concretely, the most important consequences for the immune system are specific deficits in neutrophil chemotaxis, phagocytosis, and intracellular bacterial killing. The results of this condition of compromised cell-mediated immunity are a decrease in lymphocyte activation and suppressive mediators, and above all a reduction in immunoglobulin synthesis.

The prevention and successful treatment of complications after severe burns require knowledge of the clinical periods of burn illness and a precise theoretical methodology for the evaluation of prognosis. Thus, instead of the phase of liquid loss, we speak of the period of therapeutic rehydration, which lasts up to 3 days. On the third day the patient enters the hyperdynamic and hypercatabolic period, with a high probability of infection.2 The patient should be treated intensively, with strong nutritional support, in order to combat the risk of septic complications during the convalescent period until complete recovery.

In addition to considering the clinical complications of severely burned patients, we evaluate the patient according to contemporary nomenclature. Some newly developed concepts provide a series of determinations for clarifying the terminology used in the description of the haemodynamic impairment seen in severe infections. This terminology includes the term SIRS (Systemic Inflammatory Response Syndrome), which will be considered later in this article.

Clinical material

During the year 2000, 219 patients were hospitalized in the ICU of our service, of whom 38 died (mortality rate, 13%). The average burned body surface area in patients treated in the ICU was 25%, while in deceased patients the average was 38%.

Twelve patients suffered from complications in the shock phase, all of whom died. Of these, six had acute pulmonary oedema after inhalation burn, three had cardiac congestive insufficiency, and three suffered cardiovascular arrest.

Before we present our statistics regarding complications in the septic phase, we think it may be useful to provide the definitions for classification according to the Consensus Conference of the American College of Physicians and the Society of Critical Care Medicine.3

1. SIRS (Systemic Inflammatory Response Syndrome) is regarded as a clinical situation in which the patient presents two or more of the following conditions:
   • temperature > 38 °C or < 36 °C
   • heart rate > 90 beats/min
   • respiration > 20/min or PaCO2 < 32 mm Hg
   • leukocyte count > 12,000/mm3, < 4,000/mm3, or > 10% immature (band) cells.
2. Sepsis is evaluated as SIRS plus a documented infection site (i.e., with a positive culture for micro-organisms from that site). The blood culture does not need to be positive.
3. Severe sepsis is regarded as sepsis associated with organ dysfunction, hypoperfusion abnormalities, or hypotension. Hypoperfusion abnormalities include
   • lactic acidosis
   • oliguria
   • an acute alteration in mental status.
4. Septic shock is sepsis-induced hypotension, despite fluid resuscitation, plus hypoperfusion abnormalities.
5. MODS (Multiple Organ Dysfunction Syndrome) is the presence of altered organ function in an acutely ill patient in whom homeostasis cannot be maintained without intervention.

Mortality increases with an increase in number of SIRS symptoms and in the severity of the disease process.

In our 219 cases, SIRS was present in 80 patients (36%). Of these 80 cases, only 59 were complicated with sepsis (equivalent to 22% overall and to 74% of the cases with SIRS). Positive blood cultures were found in 48 patients; 27 of these referred to Pseudomonas aeruginosa (Table I).

Severe sepsis was evident in 47 patients, and 28 presented septic shock. We would underline the fact that there was a continuum of clinical manifestations from SIRS to sepsis to severe sepsis to septic shock to MODS. In all, 26 patients died from complications after following the clinical situations described.

Table II presents details of the types of septic complications in survivors and in deceased patients.

Discussion

In our discussion we shall concentrate on the development of the main complications after severe burns in the two phases of the illness. We shall begin with the complications that occur in the period of liquid losses corresponding to therapeutic resuscitation, i.e., the phase of burn shock.

1.Complications during the phase of burn shock

We consider these in a range that begins with pulmonary complications, which are the most problematic and most frequent and require special, close attention. In each group we describe the pathophysiological changes in the organs and systems where the complication occurs.

-Lungs

The severely burned patient presents a decrease in pulmonary function caused by humoral factors such as histamine, serotonin, and thromboxane A2. A manifestation of this reduction is the diminishing of pulmonary and tissue compliance.5 The situation is more aggravated in patients with inhalatory burn injury, which damages the lungs and gives rise to three possibilities:

• carbon monoxide intoxication accompanied by deep hypoxia, which is responsible for immediate death even at the site of the accident. The effects of carbon monoxide poisoning range from altered judgement, confusion, disorientation, and lethargy to respiratory arrest and death;6
• inhalation injury above the glottis that occurs as a result of the thermal effect of particles of smoke and progresses towards the total obstruction of the respiratory tract due to laryngeal oedema. The development of oedema and the increase in oral and nasal secretions caused by smoke irritation lead to symptoms of obstruction: stridor, dyspnoea, increased labour in breathing, and eventually cyanosis. These are present in the immediate post-burn period or up to 12 h post-burn;
• inhalation injury below the glottis, which causes acute respiratory failure as a result of damage to the bronchioles and alveoli. This group of systems includes bronchorrhoea, wheezing, coughing, dyspnoea, increased labour in breathing, and impaired gas exchange. This is mainly caused by inhalation of smoke and prognosis is poor.7

-Heart

The cardiovascular response to thermal injury is a reduction in cardiac output accompanied by an increase in peripheral vascular resistance. Burn patients therefore present cardiac failure as a result of two factors:

• direct action in myocardial contractility owing to the release of the inflammatory cytokine tumour necrosis factor-·;8
• indirect action of tissue hypoxia that happens as a consequence of the reduction in O2 perfusion in peripheral tissues. The initiation of appropriate therapy manifestly alleviates the influence of this factor in cardiac activity.

-Kidneys

Renal failure is caused by a prolonged reduction in renal blood flow. In most cases it is a consequence of insufficient resuscitation. In severe burns there may be damage to the kidneys (acute tubular necrosis).

-Brain

During the phase of rehydration there is the risk of hyponatraemia, which can lead to the syndrome of post-burn encephalopathy. This syndrome is especially present in burns in critical areas such as the head and neck.

-Digestive tract

Two forms of complications occur:

• in the form of a haemorrhagic syndrome caused by the disturbing action of gastric acids on the mucosa. The last stage of this syndrome is Curling’s ulcer;
• in the form of paralytic ileus, which is caused by a decrease in intestinal motility and integrity. This occurs in the first two days of hypovolaemic shock. In burns in more than 25% TBSA, the first sign is gastroparesis, which in severe forms assumes the clinical condition of ileus.

-Haemopoetic system

Burn shock can be complicated by acute erythrocyte haemolysis caused both by direct heat damage and by a decreased half-life of damaged red blood cells. In major burns, the red blood cell mass can be reduced by 3-15%.

2. Complications during the hyperdynamic and hypercatabolic phase (septic phase)

-Lungs

Pulmonary problems remain a major cause of morbidity and mortality during this phase. In the early post-resuscitation period (days 2-6), five major abnormalities impair pulmonary function:

• continued upper airways obstruction;
• decreased chest wall compliance;
• tracheobronchitis due to inhalation injury;
• pulmonary oedema;
• surgery- and anaesthesia-induced lung dysfunction.

These abnormalities are predisposal factors for aggravation of the clinical situation and for creation of the premises for real pulmonary complications that are evident after the first week post-burn. These abnormalities are:

• nososocomial pneumonia. The pathophysiology of this complication is related to colonization of the naso-oropharynx by pathogens, aspiration of infected tracheobronchial secretions, and impairment of immune defences;
• hypermetabolic-induced respiratory fatigue. This is characterized by shortness of breath, increasing respiratory rate, decreasing tidal volume, use of accessory muscles, weakness, coughing, hypercapnia, and diffuse atelectasis on x-ray. Pathophysiology explains the increase in O2 consumption and carbon dioxide production, which will require an increase in gas exchange. A 50-100% increase in carbon dioxide is therefore seen in burn patients with over 50% TBSA burns;
• adult respiratory distress syndrome, which is a clinical situation characterized by dyspnoea, severe hypoxaemia, and decreased lung compliance, with radiographic evidence of diffuse bilateral of pulmonary infiltrates. ARDS is mainly caused by severe infection.10

-Heart

In every severe burn patient, as a consequence of significant catabolism and the action of toxins, there is the possibility of the development of cardiac failure. The clinical form is known as congestive cardiac insufficiency.

Hypertension is another cardiac complication that is relatively frequently present in adult patients and nearly always present in elderly patients. This complication is treatable and early detection prevents the development of threatening problems.

Vascular complications are present in the form of thrombophlebitis. The main causes are venous stasis, damage to the endothelium of blood vessels, and a tendency for hypercoagulation. These are considered risky complications and should not be neglected, as they cause secondary ischaemic disorders in the extremities.

-Kidneys

Evidence of renal failure in a state of sepsis is usually the final symptomatology before septic shock. The parenchyma of the kidneys is irreversibly damaged by septic thrombi. The treatment is complex and prognosis generally depends on treatment of the burn sepsis.

-Brain

Complications manifest themselves in the form of damage to the meningeal membrane and cerebral matter. Meningeal membrane damage is evident in the early period of sepsis, while cerebral matter damage manifests late and has a bad prognosis. Septic encephalitis is a major complication that may generalize very rapidly, leading to the patient’s death. It may alternatively focus in the form of a cerebral abscess of uncertain prognosis.

-Digestive tract

In conditions of severe sepsis, gastrointestinal complications begin with septic diarrhoea, which is a disorder of the normal intestine bacterial flora. Aggravation of the patient’s clinical condition creates the premises for paralytic ileus. This is the moment of the onset of septic shock. Severe sepsis always results in the appearance of septic infarcts of the intestine with or without liver insufficiency. The clinical situation of meteorism and icterus indicates a very poor prognosis.

-Haemopoetic disorders

Haemolytic microangiopathic anaemia is a common ongoing complication that in the septic phase has a high frequency and persists until epithelialization or closure of the wound. It is very aggressive in the phase of burn shock and requires the use of considerable amounts of blood. It is more frequent in paediatric patients.

-Endocrine disorders

Burn patients frequently present disorders of glucose metabolism, including post-burn pseudo-diabetes.11 In such cases glycaemia is high, reaching levels treatable only with insulin. The wrong treatment can cause non-ketotic hyperosmolar hyperglycaemic coma. It is important to note that this type of pseudo-diabetes clears up in the early phases of recovery and does not recur.

After describing the complications of severe burns in the phase of burn shock and sepsis, we would stress the fact that the pathophysiology of these complications has SIRS as its cause, initiating not only from non-infectious causes but more frequently from infectious causes.12

SIRS is mainly triggered by various bacterial products of gram-negatives (endotoxins, formyl peptides, exotoxins, and proteases) but also by products of gram-positives (exotoxins, superantigens, and enterotoxins). These products bind to cell receptors on the host’s macrophages and activate regulatory proteins. As a result the patient presents a biphasic inflammatory response: pro-inflammatory and anti-inflammatory. This is caused by various cytokines that can act either directly, affecting organ function, or indirectly, through secondary mediators (nitric oxide, thromboxanes, leukotrienes, prostaglandins, and complement). Together they activate the coagulation cascade and the complement cascade, and in general damage the endothelial cells. Clinically, this moment corresponds to the development of threatening complications such as ARDS and DIC. Further damage to the cellular endothelium leads to a decrease in profusion of the organs, causing MODS.

Conclusions

1. Recognition of complications in their two phases (shock phase and septic phase) is indispensable for clinicians working in a burn unit in order for them to take the necessary steps to resolve the various situations that arise. On the basis of the incidence and frequency of complications, it is possible to formulate for each patient a prognosis of the disease and to take the appropriate measures in order to ensure that the prognosis is favourable. It is not inevitable that these complications should occur in every case, but in view of their potential danger the vigilance of all the medical staff - physicians and nurses alike - must be at a maximum to contribute to early detection and successful treatment.

2. The standardization of scientific ideas and the evaluation of complications are permanent duties of medical staff. The introduction of new concepts in the denomination of the clinical situations of burn illness is of great importance for clinical observation and treatment following contemporary standards. Apart from the objections of medical staff to the realization or not of genuine scientific studies, the acceptance of ready-made, advanced concepts gives positive results in diagnosis and recognition of the pathophysiology of complications.

3. This article, parallel to theoretical views, presents data regarding the incidence of complications in our severely burned patients during the last year. The most important complications were pulmonary, renal, gastrointestinal, and cardiac. We regard complications not as separate phenomena but in relation to the whole burn illness, with special features in each individual patient. We have therefore paid close attention to the description of the patient’s clinical situation and given a concrete definition of SIRS and its evolution towards sepsis, severe sepsis, and septic shock.

RESUME. L’Auteur décrit l’expérience du personnel médical de son hôpital pour ce qui concerne le traitement des complications après les brûlures. Après avoir présenté les statistiques de l’année passée, l’Auteur indique l’incidence des complications dans la phase du choc et de la sepsis. Selon les critères pour l’hospitalisation dans l’Unité de Réanimation sur la base du pourcentage de la surface corporelle brûlée, les complications les plus fréquentes des patients décédés et guéris sont décrites. Le taux de mortalité était de 13%. L’intention principale de l’Auteur est de présenter les nouvelles théories dans l’évaluation de la situation clinique du patient, particulièrement pendant la phase septique de la maladie. La condition de SIRS est définie, comme aussi la progression graduelle jusqu’au choc septique.

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