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Delayed death in burns and the allegations of medical negligence
Burns 32 (2006) 269–275 www.elsevier.com/locate/burns
Review
Delayed death in burns and the allegations of medical negligence B.R. Sharma * Department of Forensic Medicine and Toxicology, Govt. Medical College & Hospital, # 1156-B, Sector-32 B, Chandigarh 160030, India Accepted 13 January 2006
Abstract Burns and deaths due to burns to remain an important public health and social problem in India. Most of the victims, who survive the initial 24 h after burns, succumb to infection of the burnt area and its complications. Burns cause devitalization of tissues, leaving extensive raw areas, which usually remain moist due to the outflow of serous exudate. This exposed, moist area along with the dead and devitalized tissue provides the optimum environment favoring colonization and proliferation of numerous microorganisms, which is further enhanced by the depression of the immune response. All these factors, i.e., disruption of the skin barrier, a large cutaneous bacterial load, the possibility of the normal bacterial flora turning into opportunistic pathogens and the severe depression of the immune system, contribute towards sepsis in a burns victim, which usually is life threatening. Despite various advances in infection control measures, early detection of microorganisms and newer, broader spectrum antibiotics, management of burn septicemia still remains a challenge. Pulmonary, cardiac and other complications also contribute to the delayed deaths following severe burn. # 2006 Elsevier Ltd and ISBI. All rights reserved. Keywords: Burns; Septicemia; Toxic shock syndrome; Smoke inhalation injury; Cardiac complications; Multiorgan failure
Contents 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Introduction . . . . . . . . . Evolution of burn care . . Infections . . . . . . . . . . . Toxic shock syndrome . . Pulmonary complications Cardiac complications . . Electrolyte imbalance . . . Multiple organ failure. . . Total parenteral nutrition. Conclusion . . . . . . . . . . References . . . . . . . . . .
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1. Introduction Severe burn is a major problem in many areas of the world, but deaths due to burning are the problem of great * Tel.: +91 172 2622145. E-mail addresses: [email protected], [email protected]. 0305-4179/$30.00 # 2006 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2006.01.012
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concern in India. India was the only country in the world, where fire was classified among the 15 leading causes of death in 1998 [1]. It has been reported that in India, a dowry death (the unnatural death of a woman within 7 years of her marriage directly or indirectly due to any dispute over bridal dowry) usually by burning occurs every 1 h 42 min [2]. Apart from dowry deaths, a large number of suicides,
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particularly by married women in rural India, are reported by burning. This preference for a highly painful, active and violent method can be attributed to religious and sociocultural reasons. Traditionally, Hindu religion has given sanction to certain altruistic forms of suicide [3]. In historical times, some states in India, approved suicide under certain circumstances, as for example, ‘Sati’—the phenomenon of bride burning along with dead body of the husband was very common under British rule [4]. The legal ban on the practice although has made it almost extinct in modern days, but death by burning had been and continues to be recognized as a symbol of sacrifice. Apart from this, uninterrupted access to cooking fire, kerosene, and matches, for married women make burning the most preferred easily available and surest method to commit suicide [5]. In burn victims, invasion by the bacteria is not unexpected despite advances in chemotherapy because the skin that offers maximum resistance against infection is damaged and the host defense factors compromised. It has been reported that in the absence of topical chemotherapy, the superficial areas of burn wound contain up to 100 million organisms per gram of tissue within 48 h following the trauma [2]. In view of a delicate balance between the host and his surrounding environment being upset, antibiotic therapy may fail to bring about the desired results. Furthermore, like the patient with some chronic ailments, the traumatized (burnt) patient loses many host mechanisms which predispose him to infection with organisms of little violence and moreover, general nutrition of the subject, pre-existing disease, quantity of fluid loss, prolonged immobilization, seasonal factors, etc., may play a role in initiating the process leading to a fatal outcome. It has been noted that in alleged dowry deaths or alleged homicidal deaths, where the death of a victim occurred after a duration of few days or weeks of the burn, the defense counsel invariably asks a question to the doctor who treated the patient or who conducted the autopsy (while deposing in the court of law), ‘‘doctor, could septicemia or the infection reported to be the cause of death in the autopsy report be prevented by better management?’’ In case the doctor replying ‘yes’ some element of doubt is created about the standard of treatment provided to the victim. This question assumes a greater significance in homicidal burn deaths where charges, according to the Indian Law, need to be proved beyond any reasonable doubt for the conviction of the accused. In the case the doctor replies ‘no’, an endless discussion can be initiated by the defense counsel and the doctor finds it difficult to produce ample literature to support his version, firstly, because different studies report on a specific aspect of the burn and secondly, because textbooks focus on possible outcomes and their management or prevention and the language used as such, can be interpreted in favor as well as against the accused. The present paper, therefore, attempts to examine the various causes of delayed death in burn victims, with a forensic viewpoint.
2. Evolution of burn care Burn management has evolved substantially from the earliest documented treatment and burn care depicted in the cave paintings of Neanderthal man and the honey and resin salve used by the ancient Egyptians [6]. Until recently, burns were associated with tragic outcomes and sustained suffering. If burn shock did not claim the life of its victim during the immediate post-burn period, death came from wound sepsis or respiratory insufficiency due to poor understanding of pathophysiology [7]. It was not until 1924 when Berkow began to formally express size as a percentage of total body surface area that burn size as a crucial determinant of pathophysiological response was recognized. Lessons learnt from treating the casualties of disastrous accidents such as the Rialto Concert Hall fire of 1930 [8] and the Cocoanut Grove fire in 1942 [9] instilled the importance of fluid requirement in burn patients, whilst the experiences gleaned during World Wars stimulated burns surgeons to attain a better understanding of burn injury [10]. In the 1970s, early excision of small deep burns and immediate auto-grafting resulted in shortened hospital stays, reduced patient suffering, and better functional outcomes [11]. To extrapolate this to larger injuries required sophisticated intensive care and blood banking technologies. The principles of burn management evolved with improving technologies and rising sophistication of critical care medicine, including development of positive pressure ventilation, lung protective ventilation strategies, general critical care techniques, improved anesthetic procedures and innovative modes of support [12,13]. This resulted in the current gold standard of near total early excision with immediate autograft/allograft cover which markedly improved survival probabilities even with major burns (involving >80% total body surface area) [14–16]. However, optimal management of severely burned persons is enormously expensive, and even after survival is ensured, may require a protracted period of surgical, medical and psychological rehabilitative measures for many years [17]. In the mean time, the burn victim encounters a long list of complications that may lead to a fatal outcome.
3. Infections Infection in the burn patient is a leading cause of morbidity and mortality and continues to be one of the most challenging concerns for the burn team. According to reports, 75% of all deaths following burns are related to infection [18]. Several risk factors have been identified for burn infections that can be divided into: (A) patient factors, which include the extent of the burn, age of the patient, presence of pre-existing disease, wound dryness, temperature and secondary impairment of blood-flow and acidosis; and (B) microbial factors, which include virulence, number of organisms, motility, extra-cellular products such as
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proteinases, collagenases, hyaluronidases, exotoxins and antimicrobial resistance. In addition, burns also have a generalized immuno-suppressive effect, involving both the humoral and the cellular limbs, on the victims that further enhance the development of septicemia. Thermal injury destroys the skin barrier that normally prevents invasion by microorganisms, making the burn wound the most frequent origin of sepsis in these patients. Initially, the burned area is considered free of major microbial contamination, however, Gram-positive bacteria in the depths of sweat glands and hair follicles may survive the heat of the initial injury, and unless topical anti-microbial agents are used, these bacteria heavily colonize the wounds within the first 48 h after injury [19]. Gram-positive organisms are gradually superceded by Gram-negative opportunists that appear to have a greater propensity to invade [20]. Burn also causes depression of the immune response and severe catabolism proportional to the extent of injury [21]. The dysfunction of the immune system, a large cutaneous bacterial load, the possibility of gastro-intestinal bacterial translocation [22], prolonged hospitalization and invasive diagnostic and therapeutic procedures, all contribute to sepsis, making the burn wound different from other forms of trauma. Invasive devices, such as endotracheal tubes, intravascular catheters, and urinary catheters, bypass the body’s normal defense mechanisms. Infection from intravascular catheters is of particular concern in burn patients, as often these lines must be placed directly through or near burninjured tissue. Catheter associated blood stream infection is caused by organisms which migrate along the catheter from the insertion site and colonize the catheter tip [23]. Catheter tips are also susceptible to colonization from hematogenous seeding of organisms from the colonized burn wound. Catheter associated blood stream infection rates for burn intensive care units have been reported to be 8.8 per 1000 central venous catheter days, compared with pool mean rates of 7.4 for pediatric ICUs, 7.9 for trauma ICUs, and 5.2 for surgical ICUs [24]. Incidence of infection is also affected by the size of the burn (total body surface area involved). A study from Shriners Burn Hospital, Boston, reported that bloodstream infection increases dramatically as burn wound size increases [25]. Outbreaks of cross colonization and infection are a major challenge on burn units, requiring a clear understanding of how and why they occur. In almost all cases, the colonized patient is thought to be a major reservoir for the spread of infection, while other important sources include contaminated hydrotherapy equipment, common treatment areas, and contaminated equipment such as mattresses. Risks associated with care of the burn wound, such as hydrotherapy and common treatment rooms are related to the use of water sources that are frequently contaminated by Gramnegative organisms intrinsically and may also be contaminated by organisms from other patients [26]. This aquatic environment is difficult to decontaminate because of
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continuous reinoculation of organisms from the patient’s wound flora, and because of the organism’s ability to form a protective glycocalyx in water pipes, drains and other areas, making them resistant to the action of disinfectants. Adequate decontamination of this equipment (e.g. tanks, plinths, shower table, straps) is difficult to achieve between patients using this equipment on a daily basis. Furthermore, the patient’s own flora may be spread through the water and by care-givers to colonize other sites on the patients that are at increased risk of infection, as for example, the organisms from the wound may migrate to a central venous catheter site or bowel flora may be transferred to the burn wound. In addition to the difficulty in assuring that the common treatment room is appropriately cleaned between successive patients, necessity of stocking the room with dressing supplies for multiple patients also increases the risk of spread of infection. The other principal modes of transmission in burn units are via the hands of the personnel and contact with inadequately decontaminated equipment or surfaces. The two areas most likely to become contaminated when caring for the burn patient are the hands and apron area of the person, as the surfaces (beds, side rails, tables, etc.) are often heavily contaminated with organisms from the patient. Likewise all equipment used on the patient such as blood pressure cuffs, thermometers, wheel chairs, etc. are also heavily contaminated and may transmit infection to other patients if strict barriers are not maintained and appropriate decontamination not carried out [27].
4. Toxic shock syndrome The mortality associated with ‘toxic shock syndrome’ (initially described in menstruating women using tampons and subsequently shown to be associated with other conditions including surgery, wounds, viral illness, skin infections, etc. [28,29]) can be high, especially if there is delay in recognition and subsequent management of the disease [30]. The center for disease control (CDC) [31] devised a strict set of criteria to define cases of toxic shock syndrome with a high degree of specificity as tabulated below: 1. Fever—temperature >38.9 8C, 102 8F 2. Rash—diffuse macular erythroderma 3. Desquamation—particularly of palms and soles, 1–2 weeks after onset of illness 4. Hypotension—systolic blood pressure <90 mmHg for adults or <5th percentile by age for children <16 yr of age or orthostatic syncope 5. Involvement of three or more of the following organ systems: Gastro-intestinal—vomiting or diarrhea at onset of illness Muscular—severe myalgia or creatin phosphokinase level twice upper limit of normal for laboratory Mucus membrane—vaginal, oropharyngeal, or conjunctival hyperemia Renal—blood urea nitrogen or creatinine level > twice upper limit of normal for laboratory or >5 white blood cells per high power field in absence of urinary tract infection
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Hepatic—total bilirubin, serum glutamic oxaloacetic transaminase or serum glutamic pyruvic transaminase > twice upper limit of normal for laboratory Hematological—platelets <100,000/mm3 Central nervous system—disorientation or alteration in consciousness without focal neurological signs when fever and hypotension are absent 6. Negative results on the following: Blood, throat or cerebrospinal cultures Serological tests for Rocky Mountain Spotted Fever, leptospirosis or measles
This case definition identifies patients with toxic shock syndrome based mainly on clinical grounds and is very useful when retrospectively analyzing suspected cases. It is widely accepted and utilized definition although it lacks sensitivity that may lead to cases of toxic shock syndrome not being diagnosed, especially in early stages. However, once toxic shock syndrome is suspected, its subsequent management should be aggressive and performed in a high dependency setting or intensive therapy unit. Circulatory support may necessitate the infusion of vast amounts of fluids, inotropes and the correction of cardiac dysfunction. Ventilatory support is often needed and biochemical and hematological abnormalities must be corrected. Appropriate antimicrobial therapy to stop further staphylococcal colonization and toxin production is advocated, however, this does not neutralize the toxins already produced. A synthetic peptide that can block the ability of the toxins to activate T-cells and thus suppress their effects even when the process of toxic shock syndrome has begun, gives hope for the future management [32]. However, to date, there is no test or set of criteria in widespread use that can reliably, with a high degree of specificity and sensitivity, diagnose toxic shock syndrome promptly and the management is guided by strong clinical suspicion.
5. Pulmonary complications Pulmonary complications occur in 15–20% of hospitalized burn victims and have been reported to account for as much as 70% of all deaths after thermal injury [33]. Chronic obstructive pulmonary dysfunctions, which may develop secondary to a single episode of smoke inhalation are reactive airway dysfunction syndrome, bronchiolitis obliterans, chronic bronchitis, and bronchiectasis [34]. Products of kerosene combustion like SO2, CO2, aldehydes and aromatic compounds are known pulmonary irritants. In the presence of water they form corrosive acids and bases that cause extensive mucosal injury leading to tracheo-bronchitis and chemical pneumonia [35]. Long-term pathological consequences can be mucosal gland hyperplasia, basement membrane thickening, smooth muscle hypertrophy, saccular bronchiectasis and bronchiolitis obliterans [36]. These changes can lead to increased small airway reactivity and asthma like syndrome resulting from chronic nonspecific inflammatory response, altered neural tone of bronchial smooth muscles, decreased
threshold of subepithelial irritant receptor and increased permeability of the pulmonary epithelium [34]. Diagnosis of smoke inhalation is largely clinical [37], although, currently bronchoscopy and xenon scans can contribute significantly. It has also been shown that presence of carbonaceous sputum correlates very well with abnormal scans [38]. Kinsella et al. [36], assessed the severity of smoke inhalation on the basis of clinical examination, history and presence of carboxyhemoglobin levels. The impact of inhalation injury on pneumonia is clinically important [39]. Onset of pneumonia can either be early, generally within 7 days of the burn injury, or later in the burn course when it usually accompanies generalized systemic sepsis. Diagnosis includes clinical features such as hyperthermia, cough, chest pain, wheezing, etc. or, in incubated patient, progressive respiratory deterioration with a change in the character of sputum (purulent), with changes on the chest radiograph showing a new or progressive infiltrate, consolidation, cavitation, or pleural effusion. Sputum culture is also helpful in diagnosis.
6. Cardiac complications The early impact on the heart of severely burnt patients (total body surface area >50%), includes myocardial suppression resulting in a decreased cardiac output, increased cardiac workload, myocardial ischemia and cardiac decompensation during large fluid shifts and wound sepsis [40]. The decreased cardiac output can be attributed to: (1) increased sympathetic activity and concomitant inadequate sympathetic-adrenal medullary response associated with a major burn; (2) hypovolemia and venous pooling resulting in myocardial ischemia; (3) myocardial damage by toxic substances such as myocardial depressant substance [41] called tumor necrosis factor-alpha (TNF-alpha) released partially from myocytes stimulated by endotoxin or thermal injury [42,43]. The diverse effects of TNF-alpha on cardiac function include reversible biventricular dilation, decreased ejection fraction, decreased response to fluid resuscitation and catecholamine stimulation, myocarditis, cardiac failure and dilated cardiomyopathy especially during septic shock. The effects of TNF-alpha are enhanced by serum interleukin-1 beta (IL-1 beta) [44]. Acute cardiac infection occurs in approximately 2% of such patients. Pathogens enter the vasculature by way of the burn wound via thrombophlebitis related to central lines or from the lungs and subsequent systemic dissemination results in cardiac involvement. The myocardium is the principle site involved leading to a high mortality rate [45,46], especially combined with burn induced immunosuppression and acute myocardial dysfunction seen with the effect of burn or infection induced TNF-alpha and IL-1 beta [44]. Recovery from this complication is rare and those who survive such an ordeal typically need to undergo a series of wound debridement procedures, skin grafting,
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and reconstructive surgical procedures that make for a long period of hospitalization [47]. A deficiency in special nutritional elements such as selenium and taurine may also result in dilated cardiomyopathy. Repeated wound debridement, blood loss and chronic anemia requiring a large volume of blood transfusion, with blood hemolysis and hemosiderin deposits occurring within the general circulation and myocardium may finally elicit secondary irreversible pathological changes to the heart. Under such circumstances, electrolyte imbalance may also arise that may lead to dilated cardiomyopathy. Other causes may include a prolonged clinical course, myocardial lesions, or a previous history of congestive heart failure [48].
7. Electrolyte imbalance Patients with major burns are particularly prone to hypernatremia. When the initial fluid resuscitation is carried out with hypertonic saline, hypernatremia may develop early on the first or second day due to an increase in the sodium load but may manifest later on the fourth or fifth day, when water loss exceeds sodium excretion [49]. The burn surface, particularly with higher total body surface area involvement, itself provides a vast area for free water loss leading to dehydration and subsequent hypernatremia. Furthermore, the burn patients who suffered a combination of inhalation injury and cutaneous burns have been reported to have a higher fluid requirement with the increment amounting to 35–44% in excess of that predicted by Parkland formula [50]. Burn patients are perpetually in a catabolic state and therefore, require hyper-caloric feeds to shift them to an anabolic phase. They may also need frequent administration of blood, plasma, albumin, sodium bicarbonate to counter acidosis, total parental nutrition solutions, and antibiotics; all of which can increase the sodium load. Pyrexia in the septic patient also causes increased free water losses, both cutaneous and respiratory. Urea diuresis from protein loading and breakdown of proteins from burn catabolism liberating osmotically active particles add further to free water losses. Low levels of antidiuretic hormone have been suggested to contribute to the development of hypernatremia [51]. Burn patients may present with a high output despite impaired renal tubular function and diminished concentration ability, thus promoting free water losses via kidney contributing to the development of hypernatremia [52]. Dudley et al. [53] reported a case of fatal hypernatremia related to a mannitol induced osmotic diuresis used in the management of hemoglobinuria in extensive burns. Burns as well as septicemia tend to induce stress hyperglycemia leading to solute diuresis that promote hypernatremia [54]. Hypernatremia has also been shown to depress the normal fat metabolism thereby preventing the formation of osmotically free water that is normally released during fat metabolism, consequently leading to a breakdown of proteins with release
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of an excess of osmoles causing this hyperosmolar state to be self-perpetuating and resistant to therapy [55]. It has been reported that the presence of severe septicemia simultaneously overwhelms all homeostatic mechanisms that help to maintain normal serum sodium levels promoting hypernatremia, which may impromptu, appear in a burn patient signaling the presence of septicemia [56].
8. Multiple organ failure Multiorgan failure, reported to be responsible for 67% of burn deaths, is felt to be caused by several possible engines including infection [57], tissue injury [58], bacterial translocation from the gut [59], and inadequate oxygen delivery [60]. These mechanisms are of particular significance in burnt patients, with their frequent wound-related bacteremias, high oxygen delivery needs and their possible enhanced gut permeability, perhaps explaining the frequent occurrence multiorgan failure as the proximate cause of death.
9. Total parenteral nutrition Total parenteral nutrition can also contribute to organ dysfunction. Total parenteral nutrition-associated alterations in hepatic function with intrahepatic cholestasis and fatty infiltration are common and so are glucose intolerance, and ventilatory impairment. Animal studies demonstrate that total parenteral nutrition is associated with a loss of gut barrier function and increased rates of bacterial translocation [61]. Prophylactic control of gastric pH to prevent stress ulceration may lead to gastric overgrowth with Gramnegative organisms and is likely to increase the rate of nosocomial pneumonia [62]. Gastric colonization with common ICU pathogens is frequent and is significantly correlated with the development of invasive infection at multiple sites, including the lungs, the urinary tract and the blood [63,64].
10. Conclusion In an increasingly litigious society, where public demands for accountability within the health-care system are becoming the norm, it is important to be aware of the medicolegal aspects of trauma in general. There being a large list of complications following burn, some of them having even a fatal outcome, allegations of negligence may not be unusual. What a medical man is required to do, is to maintain the standard of care, and the standard of care which, the law requires, is not assurance of good outcomes but such a degree of care as a normally skillful member of the profession may reasonably be expected to exercise in the actual circumstances of the case in
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question. The law permits taking chances of some measure of risks in public interest so that various kinds of activities should go on. The purpose to be served, if sufficiently important, justifies the assumption of an abnormal risk. A balance has, therefore, to be drawn between the importance and usefulness of an act and the risk created thereby. The kind of risk involved, in turn, determines the precautions to be taken.
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[23] Goldman DA, Pier GB. Pathogenesis of infection related to intravascular catheterisation. Clin Microbiol Rev 1993;6:176–92. [24] National Nosocomial Infections Surveillance (NNIS) System Report. Data summary from Jan 1992–June 2002. Am J Infect Control 2002;30:458–75. [25] Weber J, McManus A. Infection control in burn patients. Burns 2004;30:A16–24. [26] Weber JM. Epidemiology of infections and strategies for control. In: Carrougher GJ, editor. Burn care and therapy. St Louis, MO: Mosby Inc; 1998. p. 185–211. [27] Sharma BR, Singh VP, Bangar S, Gupta N. Septicemia: the principal killer of burn patients. Am J Infect Dis; in press. [28] Parsonnet J. Nonmenstrual toxic shock syndrome: new insights into diagnosis, pathogenesis and treatment. Cur Clin infectDis 1996;16:1–20. [29] Edwards-Jones V, Shawcross SG. Toxic shock syndrome in the burned patient. Br J Biomed Sci 1997;54(2):110–7. [30] Brown AP, Khan K, Sinclair S. Bacterial toxicosis/toxic shock syndrome as a contributor to morbidity in children with burn injuries. Burns 2003;29:733–8. [31] Center for Disease Control (CDC) follow-up on toxic shock syndrome. MMWR 1980;29:442. [32] Siegel-Itzkovich J. Scientists build a peptide to stop toxic shock syndrome. BMJ 2000;320:958. [33] Ahuja RB, Bhattacharya S, Sethi GR. Late residual pulmonary sequel following kerosene burns. Burns 2004;30:188–91. [34] Brooks SM, Weiss MA, Bernstein IL. Reactive airway dysfunction syndrome (RADS). Chest 1985;88:376–84. [35] Sadtomo T, Minoru K, Masaki M, Fujshima S. Long-term course of bronchiectasis and bronchiolitis obliterans on late complications of smoke inhalation. Respiration 1995;62:40–2. [36] Kinsella J, Carter R, Reid WH, Campbell D, Clark CJ. Increased airway reactivity after smoke inhalation. Lancet 1991;337:595. [37] Stone HL. Management of respiratory injury according to clinical phase. In: Polk HC, Stone HH, editors. Contemporary burn management. Boston: Little Brown; 1971. p. 111. [38] Petroff PA, Hander EW, Clayton WH, Pruitt BA. Pulmonary function studies after smoke inhalation. Am J Surg 1976;132:346. [39] Weber JM, Sheridan RL, Pastermack MS, Tompkins RG. Nosocomial infection in pediatric patients with burns: proposed definitions and benchmark rates. Am J Infect Control 1997;25:195–201. [40] Hoshi VV. Effects of burns on heart—a clinicopathological study in children. JAMA 1970;211:2130–4. [41] Reilly JM, Cunnion RE, Burch-Whitman C, Parker MM, Shelhamer JH, Parrillo JE. A circulating myocardial depressant substance is associated with cardiac dysfunction and perepheral hypoperfusion in patients with septic shock. Chest 1989;95:1072–80. [42] Odeh M. Tumor necrosis factor-alpha as a myocardial depressant substance. Int J cardiol 1993;42:231–8. [43] Torre-Amione G, Kapadia S, Lee J, Durand JB, Bies RD, Young JB, et al. Tumor necrosis factor-alpha and tumor necrosis factor receptors in the failing human heart. Circulation 1996;93:704–11. [44] Kumar A, Haery C, Parrillo JE. Myocardial dysfunction in septic shock. Crit Care Clin 2000;16:251–87. [45] Munster AM, DiVincenti FC, Foley FD, Pruitt BA. Cardiac infections in burns. J Surg 1971;122:524–7. [46] Pruitt BA, Flemma RJ, Divincenti FC. Pulmonary complications in burn patients. J Thorac Cardiovasc Surg 1970;59:7–20. [47] Mukherjee GD, Basu PG, Roy S, Seal M. Cardiomegaly following extensive burns. Ann Plast Surg 1987;19:378–80. [48] Chen TJ, Shen BH, Yeh FL, Lin JT, Huang CH, Fang RH. Delayed dilated cardiomyopathy for major burn injuries. Burns 2003;29:343–8. [49] Harada T, Izaki S, Tsutsumi H, Kobayashi M, Kitamura K. Apoptosis of hair follicle cells in the second-degree burn wound under hypernatremic conditions. Burns 1998;24:464–9. [50] O’Neill JA. Inhalation injury in children. In: Haponik EF, Munster AM, editors. Respiratory injury: smoke inhalation and burns. 1st ed., New York: McGraw-Hill; 1990. p. 305–18.
B.R. Sharma / Burns 32 (2006) 269–275 [51] Kahn T. Hypernatremia with edema. Arch Intern Med 1999;159:93–8. [52] Eklund J. Studies on renal function in burns. Hyperosmolal states in burned patients related to renal osmolal regulation. Acta Chir Scand 1970;136:741–5. [53] Dudley HAF, Batchelor ARD, Sutherland AB. The management of hemoglobinuria in extensive burns. Br J Plast Surg 1957;9:275–85. [54] Hogan GR. Hypernatremia—problems in management. Pediatr Clin North Am 1976;23:569–74. [55] Eklund J, Hallberg D. Hyper-osmolality and lipolysis. An experimental study with reference to hypernatremia in burned patients. Acta Chir Scand 1970;136:91–3. [56] Ebrahim MK, George A, Bang RL. Only some septicemic patients develop hypernatremia in burn ICU: why? Burns 2002;28:543–7. [57] Goodwin CW. Multiple organ failure, clinical overview of the syndrome. J Trauma 1990;30:S163–5. [58] Roumen RM, Redl H, Schlag G. Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma. Crit Care Med 1995;23:474–80.
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[59] Ryan CM, Yarmush ML, Burke JF, Tompkins RG. Increased gut permeability early after burns correlates with the extent of burn injury. Crit Care Med 1990;20:1508–12. [60] Shoemaker WC, Appel PL, Kram HB. Role of oxygen debt in the development of organ failure, sepsis and death in high risk surgical patients. Chest 1992;102:208–15. [61] Alverdy JC, Aoys E, Moss GS. Total parenteral nutrition promotes bacterial translocation from the gut. Surgery 1988;104: 185–9. [62] Cook DJ, Laine LA, Guyatt GH. Nosocomial pneumonia and the role of gastric pH: a meta analysis. Chest 1991;100:7–15. [63] Marshall JC, Christou NV, Meakins JL. The gastrointestinal tract: the undrained abscess of multiple organ failure. Ann Surg 1993;218: 111–4. [64] Marshall JC, Nathens AB. Multiple organ dysfunction syndrome. In: Wilmore DW, Cheung LY, Harken AH, Holcroft JW, Meakins JL, Soper NJ, editors. ACS surgery-principles and practice. USA: WebMD Corporation; 2002. p. 1473–94.
Review
Delayed death in burns and the allegations of medical negligence B.R. Sharma * Department of Forensic Medicine and Toxicology, Govt. Medical College & Hospital, # 1156-B, Sector-32 B, Chandigarh 160030, India Accepted 13 January 2006
Abstract Burns and deaths due to burns to remain an important public health and social problem in India. Most of the victims, who survive the initial 24 h after burns, succumb to infection of the burnt area and its complications. Burns cause devitalization of tissues, leaving extensive raw areas, which usually remain moist due to the outflow of serous exudate. This exposed, moist area along with the dead and devitalized tissue provides the optimum environment favoring colonization and proliferation of numerous microorganisms, which is further enhanced by the depression of the immune response. All these factors, i.e., disruption of the skin barrier, a large cutaneous bacterial load, the possibility of the normal bacterial flora turning into opportunistic pathogens and the severe depression of the immune system, contribute towards sepsis in a burns victim, which usually is life threatening. Despite various advances in infection control measures, early detection of microorganisms and newer, broader spectrum antibiotics, management of burn septicemia still remains a challenge. Pulmonary, cardiac and other complications also contribute to the delayed deaths following severe burn. # 2006 Elsevier Ltd and ISBI. All rights reserved. Keywords: Burns; Septicemia; Toxic shock syndrome; Smoke inhalation injury; Cardiac complications; Multiorgan failure
Contents 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Introduction . . . . . . . . . Evolution of burn care . . Infections . . . . . . . . . . . Toxic shock syndrome . . Pulmonary complications Cardiac complications . . Electrolyte imbalance . . . Multiple organ failure. . . Total parenteral nutrition. Conclusion . . . . . . . . . . References . . . . . . . . . .
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1. Introduction Severe burn is a major problem in many areas of the world, but deaths due to burning are the problem of great * Tel.: +91 172 2622145. E-mail addresses: [email protected], [email protected]. 0305-4179/$30.00 # 2006 Elsevier Ltd and ISBI. All rights reserved. doi:10.1016/j.burns.2006.01.012
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concern in India. India was the only country in the world, where fire was classified among the 15 leading causes of death in 1998 [1]. It has been reported that in India, a dowry death (the unnatural death of a woman within 7 years of her marriage directly or indirectly due to any dispute over bridal dowry) usually by burning occurs every 1 h 42 min [2]. Apart from dowry deaths, a large number of suicides,
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particularly by married women in rural India, are reported by burning. This preference for a highly painful, active and violent method can be attributed to religious and sociocultural reasons. Traditionally, Hindu religion has given sanction to certain altruistic forms of suicide [3]. In historical times, some states in India, approved suicide under certain circumstances, as for example, ‘Sati’—the phenomenon of bride burning along with dead body of the husband was very common under British rule [4]. The legal ban on the practice although has made it almost extinct in modern days, but death by burning had been and continues to be recognized as a symbol of sacrifice. Apart from this, uninterrupted access to cooking fire, kerosene, and matches, for married women make burning the most preferred easily available and surest method to commit suicide [5]. In burn victims, invasion by the bacteria is not unexpected despite advances in chemotherapy because the skin that offers maximum resistance against infection is damaged and the host defense factors compromised. It has been reported that in the absence of topical chemotherapy, the superficial areas of burn wound contain up to 100 million organisms per gram of tissue within 48 h following the trauma [2]. In view of a delicate balance between the host and his surrounding environment being upset, antibiotic therapy may fail to bring about the desired results. Furthermore, like the patient with some chronic ailments, the traumatized (burnt) patient loses many host mechanisms which predispose him to infection with organisms of little violence and moreover, general nutrition of the subject, pre-existing disease, quantity of fluid loss, prolonged immobilization, seasonal factors, etc., may play a role in initiating the process leading to a fatal outcome. It has been noted that in alleged dowry deaths or alleged homicidal deaths, where the death of a victim occurred after a duration of few days or weeks of the burn, the defense counsel invariably asks a question to the doctor who treated the patient or who conducted the autopsy (while deposing in the court of law), ‘‘doctor, could septicemia or the infection reported to be the cause of death in the autopsy report be prevented by better management?’’ In case the doctor replying ‘yes’ some element of doubt is created about the standard of treatment provided to the victim. This question assumes a greater significance in homicidal burn deaths where charges, according to the Indian Law, need to be proved beyond any reasonable doubt for the conviction of the accused. In the case the doctor replies ‘no’, an endless discussion can be initiated by the defense counsel and the doctor finds it difficult to produce ample literature to support his version, firstly, because different studies report on a specific aspect of the burn and secondly, because textbooks focus on possible outcomes and their management or prevention and the language used as such, can be interpreted in favor as well as against the accused. The present paper, therefore, attempts to examine the various causes of delayed death in burn victims, with a forensic viewpoint.
2. Evolution of burn care Burn management has evolved substantially from the earliest documented treatment and burn care depicted in the cave paintings of Neanderthal man and the honey and resin salve used by the ancient Egyptians [6]. Until recently, burns were associated with tragic outcomes and sustained suffering. If burn shock did not claim the life of its victim during the immediate post-burn period, death came from wound sepsis or respiratory insufficiency due to poor understanding of pathophysiology [7]. It was not until 1924 when Berkow began to formally express size as a percentage of total body surface area that burn size as a crucial determinant of pathophysiological response was recognized. Lessons learnt from treating the casualties of disastrous accidents such as the Rialto Concert Hall fire of 1930 [8] and the Cocoanut Grove fire in 1942 [9] instilled the importance of fluid requirement in burn patients, whilst the experiences gleaned during World Wars stimulated burns surgeons to attain a better understanding of burn injury [10]. In the 1970s, early excision of small deep burns and immediate auto-grafting resulted in shortened hospital stays, reduced patient suffering, and better functional outcomes [11]. To extrapolate this to larger injuries required sophisticated intensive care and blood banking technologies. The principles of burn management evolved with improving technologies and rising sophistication of critical care medicine, including development of positive pressure ventilation, lung protective ventilation strategies, general critical care techniques, improved anesthetic procedures and innovative modes of support [12,13]. This resulted in the current gold standard of near total early excision with immediate autograft/allograft cover which markedly improved survival probabilities even with major burns (involving >80% total body surface area) [14–16]. However, optimal management of severely burned persons is enormously expensive, and even after survival is ensured, may require a protracted period of surgical, medical and psychological rehabilitative measures for many years [17]. In the mean time, the burn victim encounters a long list of complications that may lead to a fatal outcome.
3. Infections Infection in the burn patient is a leading cause of morbidity and mortality and continues to be one of the most challenging concerns for the burn team. According to reports, 75% of all deaths following burns are related to infection [18]. Several risk factors have been identified for burn infections that can be divided into: (A) patient factors, which include the extent of the burn, age of the patient, presence of pre-existing disease, wound dryness, temperature and secondary impairment of blood-flow and acidosis; and (B) microbial factors, which include virulence, number of organisms, motility, extra-cellular products such as
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proteinases, collagenases, hyaluronidases, exotoxins and antimicrobial resistance. In addition, burns also have a generalized immuno-suppressive effect, involving both the humoral and the cellular limbs, on the victims that further enhance the development of septicemia. Thermal injury destroys the skin barrier that normally prevents invasion by microorganisms, making the burn wound the most frequent origin of sepsis in these patients. Initially, the burned area is considered free of major microbial contamination, however, Gram-positive bacteria in the depths of sweat glands and hair follicles may survive the heat of the initial injury, and unless topical anti-microbial agents are used, these bacteria heavily colonize the wounds within the first 48 h after injury [19]. Gram-positive organisms are gradually superceded by Gram-negative opportunists that appear to have a greater propensity to invade [20]. Burn also causes depression of the immune response and severe catabolism proportional to the extent of injury [21]. The dysfunction of the immune system, a large cutaneous bacterial load, the possibility of gastro-intestinal bacterial translocation [22], prolonged hospitalization and invasive diagnostic and therapeutic procedures, all contribute to sepsis, making the burn wound different from other forms of trauma. Invasive devices, such as endotracheal tubes, intravascular catheters, and urinary catheters, bypass the body’s normal defense mechanisms. Infection from intravascular catheters is of particular concern in burn patients, as often these lines must be placed directly through or near burninjured tissue. Catheter associated blood stream infection is caused by organisms which migrate along the catheter from the insertion site and colonize the catheter tip [23]. Catheter tips are also susceptible to colonization from hematogenous seeding of organisms from the colonized burn wound. Catheter associated blood stream infection rates for burn intensive care units have been reported to be 8.8 per 1000 central venous catheter days, compared with pool mean rates of 7.4 for pediatric ICUs, 7.9 for trauma ICUs, and 5.2 for surgical ICUs [24]. Incidence of infection is also affected by the size of the burn (total body surface area involved). A study from Shriners Burn Hospital, Boston, reported that bloodstream infection increases dramatically as burn wound size increases [25]. Outbreaks of cross colonization and infection are a major challenge on burn units, requiring a clear understanding of how and why they occur. In almost all cases, the colonized patient is thought to be a major reservoir for the spread of infection, while other important sources include contaminated hydrotherapy equipment, common treatment areas, and contaminated equipment such as mattresses. Risks associated with care of the burn wound, such as hydrotherapy and common treatment rooms are related to the use of water sources that are frequently contaminated by Gramnegative organisms intrinsically and may also be contaminated by organisms from other patients [26]. This aquatic environment is difficult to decontaminate because of
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continuous reinoculation of organisms from the patient’s wound flora, and because of the organism’s ability to form a protective glycocalyx in water pipes, drains and other areas, making them resistant to the action of disinfectants. Adequate decontamination of this equipment (e.g. tanks, plinths, shower table, straps) is difficult to achieve between patients using this equipment on a daily basis. Furthermore, the patient’s own flora may be spread through the water and by care-givers to colonize other sites on the patients that are at increased risk of infection, as for example, the organisms from the wound may migrate to a central venous catheter site or bowel flora may be transferred to the burn wound. In addition to the difficulty in assuring that the common treatment room is appropriately cleaned between successive patients, necessity of stocking the room with dressing supplies for multiple patients also increases the risk of spread of infection. The other principal modes of transmission in burn units are via the hands of the personnel and contact with inadequately decontaminated equipment or surfaces. The two areas most likely to become contaminated when caring for the burn patient are the hands and apron area of the person, as the surfaces (beds, side rails, tables, etc.) are often heavily contaminated with organisms from the patient. Likewise all equipment used on the patient such as blood pressure cuffs, thermometers, wheel chairs, etc. are also heavily contaminated and may transmit infection to other patients if strict barriers are not maintained and appropriate decontamination not carried out [27].
4. Toxic shock syndrome The mortality associated with ‘toxic shock syndrome’ (initially described in menstruating women using tampons and subsequently shown to be associated with other conditions including surgery, wounds, viral illness, skin infections, etc. [28,29]) can be high, especially if there is delay in recognition and subsequent management of the disease [30]. The center for disease control (CDC) [31] devised a strict set of criteria to define cases of toxic shock syndrome with a high degree of specificity as tabulated below: 1. Fever—temperature >38.9 8C, 102 8F 2. Rash—diffuse macular erythroderma 3. Desquamation—particularly of palms and soles, 1–2 weeks after onset of illness 4. Hypotension—systolic blood pressure <90 mmHg for adults or <5th percentile by age for children <16 yr of age or orthostatic syncope 5. Involvement of three or more of the following organ systems: Gastro-intestinal—vomiting or diarrhea at onset of illness Muscular—severe myalgia or creatin phosphokinase level twice upper limit of normal for laboratory Mucus membrane—vaginal, oropharyngeal, or conjunctival hyperemia Renal—blood urea nitrogen or creatinine level > twice upper limit of normal for laboratory or >5 white blood cells per high power field in absence of urinary tract infection
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Hepatic—total bilirubin, serum glutamic oxaloacetic transaminase or serum glutamic pyruvic transaminase > twice upper limit of normal for laboratory Hematological—platelets <100,000/mm3 Central nervous system—disorientation or alteration in consciousness without focal neurological signs when fever and hypotension are absent 6. Negative results on the following: Blood, throat or cerebrospinal cultures Serological tests for Rocky Mountain Spotted Fever, leptospirosis or measles
This case definition identifies patients with toxic shock syndrome based mainly on clinical grounds and is very useful when retrospectively analyzing suspected cases. It is widely accepted and utilized definition although it lacks sensitivity that may lead to cases of toxic shock syndrome not being diagnosed, especially in early stages. However, once toxic shock syndrome is suspected, its subsequent management should be aggressive and performed in a high dependency setting or intensive therapy unit. Circulatory support may necessitate the infusion of vast amounts of fluids, inotropes and the correction of cardiac dysfunction. Ventilatory support is often needed and biochemical and hematological abnormalities must be corrected. Appropriate antimicrobial therapy to stop further staphylococcal colonization and toxin production is advocated, however, this does not neutralize the toxins already produced. A synthetic peptide that can block the ability of the toxins to activate T-cells and thus suppress their effects even when the process of toxic shock syndrome has begun, gives hope for the future management [32]. However, to date, there is no test or set of criteria in widespread use that can reliably, with a high degree of specificity and sensitivity, diagnose toxic shock syndrome promptly and the management is guided by strong clinical suspicion.
5. Pulmonary complications Pulmonary complications occur in 15–20% of hospitalized burn victims and have been reported to account for as much as 70% of all deaths after thermal injury [33]. Chronic obstructive pulmonary dysfunctions, which may develop secondary to a single episode of smoke inhalation are reactive airway dysfunction syndrome, bronchiolitis obliterans, chronic bronchitis, and bronchiectasis [34]. Products of kerosene combustion like SO2, CO2, aldehydes and aromatic compounds are known pulmonary irritants. In the presence of water they form corrosive acids and bases that cause extensive mucosal injury leading to tracheo-bronchitis and chemical pneumonia [35]. Long-term pathological consequences can be mucosal gland hyperplasia, basement membrane thickening, smooth muscle hypertrophy, saccular bronchiectasis and bronchiolitis obliterans [36]. These changes can lead to increased small airway reactivity and asthma like syndrome resulting from chronic nonspecific inflammatory response, altered neural tone of bronchial smooth muscles, decreased
threshold of subepithelial irritant receptor and increased permeability of the pulmonary epithelium [34]. Diagnosis of smoke inhalation is largely clinical [37], although, currently bronchoscopy and xenon scans can contribute significantly. It has also been shown that presence of carbonaceous sputum correlates very well with abnormal scans [38]. Kinsella et al. [36], assessed the severity of smoke inhalation on the basis of clinical examination, history and presence of carboxyhemoglobin levels. The impact of inhalation injury on pneumonia is clinically important [39]. Onset of pneumonia can either be early, generally within 7 days of the burn injury, or later in the burn course when it usually accompanies generalized systemic sepsis. Diagnosis includes clinical features such as hyperthermia, cough, chest pain, wheezing, etc. or, in incubated patient, progressive respiratory deterioration with a change in the character of sputum (purulent), with changes on the chest radiograph showing a new or progressive infiltrate, consolidation, cavitation, or pleural effusion. Sputum culture is also helpful in diagnosis.
6. Cardiac complications The early impact on the heart of severely burnt patients (total body surface area >50%), includes myocardial suppression resulting in a decreased cardiac output, increased cardiac workload, myocardial ischemia and cardiac decompensation during large fluid shifts and wound sepsis [40]. The decreased cardiac output can be attributed to: (1) increased sympathetic activity and concomitant inadequate sympathetic-adrenal medullary response associated with a major burn; (2) hypovolemia and venous pooling resulting in myocardial ischemia; (3) myocardial damage by toxic substances such as myocardial depressant substance [41] called tumor necrosis factor-alpha (TNF-alpha) released partially from myocytes stimulated by endotoxin or thermal injury [42,43]. The diverse effects of TNF-alpha on cardiac function include reversible biventricular dilation, decreased ejection fraction, decreased response to fluid resuscitation and catecholamine stimulation, myocarditis, cardiac failure and dilated cardiomyopathy especially during septic shock. The effects of TNF-alpha are enhanced by serum interleukin-1 beta (IL-1 beta) [44]. Acute cardiac infection occurs in approximately 2% of such patients. Pathogens enter the vasculature by way of the burn wound via thrombophlebitis related to central lines or from the lungs and subsequent systemic dissemination results in cardiac involvement. The myocardium is the principle site involved leading to a high mortality rate [45,46], especially combined with burn induced immunosuppression and acute myocardial dysfunction seen with the effect of burn or infection induced TNF-alpha and IL-1 beta [44]. Recovery from this complication is rare and those who survive such an ordeal typically need to undergo a series of wound debridement procedures, skin grafting,
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and reconstructive surgical procedures that make for a long period of hospitalization [47]. A deficiency in special nutritional elements such as selenium and taurine may also result in dilated cardiomyopathy. Repeated wound debridement, blood loss and chronic anemia requiring a large volume of blood transfusion, with blood hemolysis and hemosiderin deposits occurring within the general circulation and myocardium may finally elicit secondary irreversible pathological changes to the heart. Under such circumstances, electrolyte imbalance may also arise that may lead to dilated cardiomyopathy. Other causes may include a prolonged clinical course, myocardial lesions, or a previous history of congestive heart failure [48].
7. Electrolyte imbalance Patients with major burns are particularly prone to hypernatremia. When the initial fluid resuscitation is carried out with hypertonic saline, hypernatremia may develop early on the first or second day due to an increase in the sodium load but may manifest later on the fourth or fifth day, when water loss exceeds sodium excretion [49]. The burn surface, particularly with higher total body surface area involvement, itself provides a vast area for free water loss leading to dehydration and subsequent hypernatremia. Furthermore, the burn patients who suffered a combination of inhalation injury and cutaneous burns have been reported to have a higher fluid requirement with the increment amounting to 35–44% in excess of that predicted by Parkland formula [50]. Burn patients are perpetually in a catabolic state and therefore, require hyper-caloric feeds to shift them to an anabolic phase. They may also need frequent administration of blood, plasma, albumin, sodium bicarbonate to counter acidosis, total parental nutrition solutions, and antibiotics; all of which can increase the sodium load. Pyrexia in the septic patient also causes increased free water losses, both cutaneous and respiratory. Urea diuresis from protein loading and breakdown of proteins from burn catabolism liberating osmotically active particles add further to free water losses. Low levels of antidiuretic hormone have been suggested to contribute to the development of hypernatremia [51]. Burn patients may present with a high output despite impaired renal tubular function and diminished concentration ability, thus promoting free water losses via kidney contributing to the development of hypernatremia [52]. Dudley et al. [53] reported a case of fatal hypernatremia related to a mannitol induced osmotic diuresis used in the management of hemoglobinuria in extensive burns. Burns as well as septicemia tend to induce stress hyperglycemia leading to solute diuresis that promote hypernatremia [54]. Hypernatremia has also been shown to depress the normal fat metabolism thereby preventing the formation of osmotically free water that is normally released during fat metabolism, consequently leading to a breakdown of proteins with release
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of an excess of osmoles causing this hyperosmolar state to be self-perpetuating and resistant to therapy [55]. It has been reported that the presence of severe septicemia simultaneously overwhelms all homeostatic mechanisms that help to maintain normal serum sodium levels promoting hypernatremia, which may impromptu, appear in a burn patient signaling the presence of septicemia [56].
8. Multiple organ failure Multiorgan failure, reported to be responsible for 67% of burn deaths, is felt to be caused by several possible engines including infection [57], tissue injury [58], bacterial translocation from the gut [59], and inadequate oxygen delivery [60]. These mechanisms are of particular significance in burnt patients, with their frequent wound-related bacteremias, high oxygen delivery needs and their possible enhanced gut permeability, perhaps explaining the frequent occurrence multiorgan failure as the proximate cause of death.
9. Total parenteral nutrition Total parenteral nutrition can also contribute to organ dysfunction. Total parenteral nutrition-associated alterations in hepatic function with intrahepatic cholestasis and fatty infiltration are common and so are glucose intolerance, and ventilatory impairment. Animal studies demonstrate that total parenteral nutrition is associated with a loss of gut barrier function and increased rates of bacterial translocation [61]. Prophylactic control of gastric pH to prevent stress ulceration may lead to gastric overgrowth with Gramnegative organisms and is likely to increase the rate of nosocomial pneumonia [62]. Gastric colonization with common ICU pathogens is frequent and is significantly correlated with the development of invasive infection at multiple sites, including the lungs, the urinary tract and the blood [63,64].
10. Conclusion In an increasingly litigious society, where public demands for accountability within the health-care system are becoming the norm, it is important to be aware of the medicolegal aspects of trauma in general. There being a large list of complications following burn, some of them having even a fatal outcome, allegations of negligence may not be unusual. What a medical man is required to do, is to maintain the standard of care, and the standard of care which, the law requires, is not assurance of good outcomes but such a degree of care as a normally skillful member of the profession may reasonably be expected to exercise in the actual circumstances of the case in
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question. The law permits taking chances of some measure of risks in public interest so that various kinds of activities should go on. The purpose to be served, if sufficiently important, justifies the assumption of an abnormal risk. A balance has, therefore, to be drawn between the importance and usefulness of an act and the risk created thereby. The kind of risk involved, in turn, determines the precautions to be taken.
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