Physiological Reaction to Burns - Essay Example

Burns Case study A 40 year old man was pulled from a collapsed building fully involved with fire. Initial observations of the patient at the scene show entire left arm and upper half of back showed raised wet blisters. The right arm and right leg were circumferentially brown, leathery, and insensitive to pain, with thrombosed blood vessels visible through the skin. The patient has great difficulty breathing; soot deposits are visible in both nostrils. Examination of the pharynx shows sooty deposits and visible sputum is red and black streaked. From this history it is evident that this 40 year old man suffered from thermal injury. The tissues involved are his skin and that of the oro- respiratory tract. Most of the burns are 2 and 3 rd degree burns. This patient has 45% burns along with inhalation injury. Introduction Damage to the tissues of the body as a result of heat, chemicals, electricity, sunlight or radiation is known as burns. Burns can cause swelling, blistering, scarring, shock and even death (Burns, Medline Plus). The most common type of burns is thermal burns. Burns are a common cause of mortality and morbidity. Injuries due to inhalation and subsequent pulmonary complications contribute to the mortality. It has been estimated that 50-60% of fire deaths are secondary to inhalation injury (Nettina 2006). Physiologic reaction to burns The response to burns is the one similar to inflammation. Burns causes the intact vessels to dilate causing redness and blanching with pressure. The vascular permeability of the vessels also increases. Cells like platelets and leukocytes adhere to the vascular endothelium in the early phases of burns, followed by influx of polymorphonuclear leukocytes and monocytes. There after, new capillaries, immature fibroblasts and new collagen fibrils appear within the wound as a part of regeneration activity (Nettina 2006). Tissues damaged in burn 1. Skin being the largest organ in the body is the most commonly and widely affected part in the body. Burns causes loss of functions of the skin. The main functions of the skin are thermal regulation, prevention of loss of fluid from the body by evaporation, barrier against infections from the environment, and perception of sensory information from the environment. Skin comprises of 3 layers, the dermis, epidermis and hypodermis. Epidermis is the outermost layer of the skin and consists of cornified epithelial cells. The middle layer is the dermis which is made up of mainly connective tissue. Embedded in the connective tissue are the capillaries that nourish the skin, nerve endings, and hair follicles. The innermost layer is the hypodermis which contains adipose tissue and some connective tissue. This layer differentiates the skin and the underlying tissues (Nettina 2006). 2. Other than skin, other tissues may also be damaged depending on the intensity and exposure of burns. The last to be damaged is the bone tissue. 3. Inhalation injury can occur as a result of burns. The upper airways and lower airways can get affected easily. Inflammation in the upper airways leads to epiglottitis and difficulty in breathing. Affectation of lower airways soon leads to adult respiratory distress syndrome (ARDS). ARDS causes defects in ventilation and perfusion of the lungs (Nettina 2006). Exposure to poisonous gases in inhalational injury 1. Carbon monoxide poisoning: Incomplete combustion of carbon containing materials results in the formation of carbon-monoxide. Since the affinity of hemoglobin to this gas is about 200 times more than that for oxygen, carbon monoxide easily displaces oxygen and causes hypoxemia. Infact, levels of 20% to 50% are known to cause headache, fatigue, arrhythmias, ataxia, vomiting, coma, hypotension, seizures, respiratory arrest and even death (Nettina 2006). 2. Sulphur dioxide and nitrous oxide: These gases are taken in along with soot. They form corrosive acids and alkalis along with water in the body and further damage the tissues (Nettina 2006). 3. Toxic fumes from burning plastic: Noxious gases are produced when plastic is burned. These include hydrogen cyanide, hydrochloric acid, sulfuric acid, halogens and phosphene (Nettina 2006). Classification of burns First degree burns: The burns are limited to only the epidermis. There is erythema. The tissue blanches with pressure and is often painful. However tissue damage is minimal (Naradzay, eMedicine). Second-degree burns or partial-thickness burns: Epidermis and portion of dermis is affected. Though the adnexal structures like sweat glands and hair follicles may be involved, some parts of the tissue remain intact allowing proliferation and regeneration (Naradzay, eMedicine). Third degree burns: Burns in third degree involves destruction of all the layers and structures of the skin. There is evident scarring of the skin with a translucent white color. The vessels get coagulated and can be easily seen. Though there actually should be no pain in this type of burns, the patient often complains of pain due to second degree burns in the adjacent areas (Naradzay, eMedicine). Extent of burns Burns extent is calculated only on individuals with second-degree or third-degree burns. By extent of burns means the body surface area affected by burns. It is important to know the extent of burns because greater the extent of burns, the greater the morbidity and mortality rates and the difficulty in management (Naradzay, eMedicine). The most commonly used method of assessing the extent of burns in adults is the rule of nines. The head comprises of 9% BSA, each of the upper limbs comprises of 9%, each of the lower limbs is considered as 18%, the genitalia is attributed 1%, the front of the trunk is considered as 18% and same is the case with the back of the trunk (Naradzay, eMedicine). Indications for admission into burns ward According to the American Burn Association, the criteria for admission for burn center are as follows (Naradzay, eMedicine): 1. Third degree burns over 5% BSA 2. Second degree burns over 10% BSA 3. Second or third degree burns involving critical areas like face, hands, feet, genitals, perineum or skin over any major joint. 4. Circumferential burns of the thorax or extremities 5. Patients with significant medical history 6. Presence of inhalation injury Fluid and electrolyte imbalance in burns These changes occur because of increased loss of water due to evaporation, increased capillary permeability and increased interstitial osmotic pressure in burn tissue (Ramos 2000), in the first 24 to 36 hours of injury (Nettina 2006). Thus intravascular volume is lost. The fluid loss is accompanied by protein loss also due to weeping injuries which contain protein-rich fluid. Dehydration can occur quickly during this stage. After about 48 hours, the fluid will gradually start to move from interstitial spaces back to vascular compartment. Hyponatraemia is frequent and is due to extracellular sodium depletion following changes in cellular permeability. Hyperkalemia also occurs during the initial phase. It occurs due to release of potassium from the cells as a result of massive tissue necrosis and cell lysis (Ramos 2000). It is important to correct these derangements as soon as possible because these can lead to various complications as follows (Ramos 2000): 1. Change in hemodynamics: Decreased blood pressure, central venous pressure and glomerular filtration rate and increased heart rate. 2. Neurological changes: Altered consciousness, seizures, cerebral oedema and coma. 3. Gastrointestinal changes: Anorexia, nausea and vomiting. 4. Neuromuscular changes: Cramps and weakness. Hemodynamic changes The circulatory blood volume is decreased and there is decreased cardiac output and increased heart rate. There is also decreased stroke volume and marked rise in peripheral resistance due to constriction of arterioles and increased hemoviscosity. Ultimately, tissue perfusion is affected leading to acidosis, renal failure and shock (Nettina 2006). Hematologic changes Direct destruction of red blood cells can lead to anemia. There may be thrombocytopenia accompanied with defective platelet function, decreased fibrinogen levels and inhibition of fibrinolysis. Metabolic changes There is surge in the amount of catecholamines in the body as a result of acute stress. During the first week of burns injury, the patient suffers from burns fever. The temperature is usually around 102 deg. F to 103 deg. F and is dependent on the extent of injury. Glucose demand rises due to healing and excess glucose is derived from liver and muscle glycogen and gluconeogenesis. However, burns patients may demonstrate hyperglycemia due to decreased insulin production and increased gluconeogenesis. Skeletal and visceral proteins are metabolized to meet the demands and negative nitrogen balance ensues (Nettina 2006). The resting metabolic expenditure increases linearly with the extent of burns. Immunological changes Loss of skin barrier assists intrusion of infections front the environment. Hypoxia, acidosis and thrombosis impair immune defense mechanism. Added to this, several immunoglobins, complements and serum albumin are decreased (Nettina 2006). There is also depressed cellular immunity. Due to these aspects, bacteria can get colonized in the wounds and result in sepsis. It is not possible to treat these infections with antibiotics because of altered pharmacokinetics and decreased delivery of drugs. Renal changes The glomerular filtration rate decreases in burns. Without proper resuscitation, oliguric renal failure may ensue. This can lead to decreased creatinine clearance (nettina 2006). Gastrointestinal changes The peristalsis of the tract decreases due to increased catecholamines. This can lead to gastric distension, nausea, vomiting and paralytic ileus (Nettina 2006). Gradually gastric and duodenal ulcers can be formed due to relative ischemia. Management of burns Stabilization of airway The first and foremost in the management of a patient with burns is stabilization of airway. This is because airway edema can rapidly occur due to causes mentioned above. The emergency personnel should maintain a high index of suspicion for airway injury and a low threshold for intubation because; intubation may be extremely difficult once edema forms (Naradzay, eMedicine). Fluid and electrolytes management The next step is to assess the extent of burns and establish atleast 2 large bore intravenous access and start fluid resuscitation. Resuscitation must be started with crystalloids like normal saline or Ringers lactate. The requirements for fluids in the acute phase can be calculated using Parkland formula as below (Naradzay, eMedicine): (4 cm3 of crystalloid) X (% BSA burn) X (body weight in kg) 50% of the estimated fluid is administered in the first 8 hours, and the balance is given over the remaining 16 hours (Naradzay, eMedicine). During fluid therapy the patients vital signs, neurological status and urine output must be continuously monitored. Foleys catheter must be placed to determine accurate urine output. Hyponatremia and hypokalemia must be treated appropriately. Sodium replacement is given in the form of normal saline or Ringers lactate. The deficit is calculated using the formula (Ramos 2000): (140-Na+) x 0.6 x weight (kg) If necessary, the osmolality of the fluids may be increased by adding further sodium lactate into the fluids. If a hypertonic solution is used to restore serum sodium, it should not be allowed to increase above 160 mEq/1 and the rate of increase should not exceed 1.5 mEq/h (Ramos 2000). Hyperkalemia must be dealt with appropriately and with caution. The potassium effects in the cellular membrane must be reversed with calcium chloride 10% which should be given as infusion over 10 minutes. The extra cellular potassium must be transferred into the cells using glucose- insulin therapy, sodium bicarbonate or hyperventilation. Potassium can be removed from the body by means of diuretics, potassium exchange resins or in serious cases, haemodialvsis (Ramos 2000). The most important aspect of managing hyperkalemia is monitoring for serious cardiac complications like heart block, atrial asystole, ventricular tachvcardia, ventricular fibrillation, asystole and cardiac arrest (Ramos 2000). These can be prevented by monitoring by ECG. The changes that are seen in ECG in hyperkalemia are T waves changes, decreased P waves and PR prolongation (Ramos 2000). Pain management Pain is managed with opiates like morphine which give considerable relief. Other drugs which can be used to mange pain are meperidine, hydrocodone bitartrate, acetaminophen and non-steroidal anti-inflammatory drugs (Naradzay, eMedicine). Control of infections The burns patient must be managed in a separate isolated ward. The treating staff and health personnel must take all measures to prevent infections. Some topical antibiotics which may be useful are neomycin, polymyxin B and silver sulfadizine (Naradzay, eMedicine). Care of burns wounds Burns of areas such as the face are best treated by an open technique. The wounds are washed cleanly, the open blisters are debrided and topical antibiotics are applied. Intact blisters should be left alone. As far as inhalational injuries are concerned, the patient must be managed according to the severity of respiratory and pulmonary complications. References Burns. Medline Plus. http://www.nlm.nih.gov/medlineplus/burns.html [Accessed 1 December 2007]. Naradzay, J.F.X., 2006. Burns, Thermal. eMedicine from WebMD. http://www.emedicine.com/emerg/topic72.htm [Accessed 1 December 2007]. Nettina, S.M., 2006. Lippincott Manual of Nursing Practice. 8th ed. Philadelphia: Lippincott Williams and Wilkins. Ramos, C.G., 2000. Management of fluid and electrolyte disturbances in the burn patient. Annals of Burns and Fire Disasters, 4 (4), http://www.medbc.com/annals/review/vol_13/num_4/text/vol13n4p201.htm [Accessed 1 December 2007]. Read More