Prophylactic antibiotics should be used in acute burn injury: FALSE.
Skin integrity is part of the body’s defense against infection. Loss of that integrity secondary to burn injury is one of the reasons this patient population is at risk of infection. The injury also disrupts both the humoral and cell-mediated immune system. The immune suppression is immediate and prolonged, and the patient has an increased susceptibility to local and systemic infections.
Despite this, the practice guidelines of the International Society for Burn Injury do not recommend the use of prophylactic antibiotics at the time of injury. Barajas-Nava et al, the authors of the 2010 Cochrane review, concluded that the available evidence is limited and in general does not demonstrate that antibiotic prophylaxis reduces the risk of burn wound infection, invasive infections, or mortality associated with infection.
Furthermore, use of prophylactic antibiotics may lead to systemic sepsis with multidrug resistant organisms through selective pressure, making therapeutic treatment very difficult. Infection prophylaxis should be aimed at the wound, with good cleaning of the burn as well as the adjacent normal skin, and use of dressings that have an antimicrobial action. General principles of barrier nursing, hand hygiene, good invasive line care and nutritional support should also be part of the bundle of care.
Use Half Dextrose Darrow’s for fluid resuscitation in burn injury: FALSE.
Half-strength Darrow's solution has been used extensively for childhood dehydration throughout the world. However, the major disadvantage is the low sodium concentration (see Table 1). Dextrose solutions should not be used in shock for the fluid resuscitation of children because large volumes of glucose-containing intravenous solutions do not effectively expand the intravascular compartment and may result in hyperglycemia and a secondary osmotic diuresis as well as hyponatraemia.
The reason for intravenous fluid resuscitation in acute burn injury is to prevent burn shock, which is a unique combination of hypovolaemic, distributive and cardiogenic shock. Hypovoalemia results from loss into the extravascular space due to increased capillary permeability (and results in the typical oedema post 24 hours of injury), as well as loss via exudate of the wound since the skin integrity is lost. Distributive shock is part of the systemic inflammatory response leading to vasodilation secondary to the massive release of inflammatory mediators. Lastly decreased contractility of the myocardium is the cardiogenic component.
The goal of fluid resuscitation in shock is to restore tissue perfusion and organ dysfunction. Isotonic crystalloids, balanced crystalloids or colloids can be used to restore plasma volume effectively and every solution has advantages and disadvantages, however no guideline promotes the use of Half Dextrose Darrow’s for fluid resuscitation in burn injury and it is detrimental to use this as the resuscitation fluid in acute burn injury.
Pain is just part of the process in burns and there is nothing I can do: FALSE.
The pain that follows a burn injury is due to the stimulation of skin nociceptors that respond to heat, mechanical distortion and other stimuli including chemical stimuli which may be exogenous or endogenous (eg inflammatory mediators). Nerve endings that are entirely destroyed will not transmit pain, but those that remain undamaged and exposed will generate pain throughout the time and course of treatment. The initial pain of injury is followed by the emergence of both primary and secondary hyperalgesia. Primary hyperalgesia is a result of inflammatory mediators which sensitises the active nociceptors at the site of injury.
This causes the wound and immediately adjacent skin to become sensitive to any mechanical stimuli. Secondary hyperalgesia is the continuous or repeated peripheral stimulation of nociceptive afferent fibres leading to increased sensitivity in surrounding unburned areas. This is mediated by the spinal cord and exacerbated by the mechanical stimulation that occurs as a result of frequent dressings changes and surgeries.
Lastly, damaged and regenerating nerve tissues can give rise to complex neuropathic pain syndromes. There may be hyperalgesia, which is an increased response to a painful stimulus and allodynia which is a painful response to a normally innocuous stimulus. This may be a significant problem beginning early in the post-injury period and may persist for many years after the initial injury.
While pain is certainly part of the patients clinical journey, it is the role of the clinician to alleviate that pain. The pain should be addressed in four components. Procedural pain of short to medium duration and usually high intensity during or after dressing changes, and physiotherapy of affected joints. Ketamine is a safe, versatile and effective drug if given in the correct dose, to address this procedural pain. Tachyphylaxis must be taken into account with increasing doses required to achieve the same effect.
Background or resting pain is dull in nature but of long duration when the patient is between procedures, and breakthrough pain is of short duration associated with rest pain where the regular dosing or analgesia prescribed is inadequate. Multimodal analgesia, in the correct dose and correct frequency must be prescribed.
Requirements are dynamic and increase post-surgery and decrease as healing occurs. Paracetamol and opioids are the mainstay of treatment, with anti-inflammatories being very effective if no contra-indications like kidney injury or stress ulceration are present. Lastly the long term chronic neuropathic pain needs to addressed.
Gabapentin is the drug of choice with additional agents such as amitriptyline and sodium valproate, not forgetting that other issues like depression and anxiety also need to be addressed. Analgesia protocols for both background pain and procedural pain are shared in Tables 2 and 3.
Diarrhoea in a child with burns is gastroenteritis: FALSE.
Sepsis in a burn patient can be challenging to diagnose because of the concomitant inflammatory response and the hypermetabolic response in larger surface area burns. Pyrexia greater than 38.5 degrees, tachycardia or tachypneoa higher than normal for that patient or gastrointestinal dysfunction for example diarrheoa, vomiting or abdominal distension are common signs of sepsis in burns. It is important to recognise that gastrointestinal dysfunction is likely to be sepsis as opposed to gastroenteritis. This distinction is critical because the management is vastly different.
True gastroenteritis is treated with oral or intravenous rehydration only. If this management is instituted when the problem is in fact systemic burn sepsis, the patient’s condition will deteriorate to multi organ failure and death because the sepsis remains untreated, and no antibiotics are administered.
Systemic burn sepsis can lead to vasodilation secondary to the inflammatory response associated with sepsis. The low-pressure system of the splanchnic circulation is vulnerable to the subtle drop in vascular resistance, and this leads to ileus which may manifest as diarrheoa, abdominal distension or vomiting. The gastrointestinal dysfunction must be recognised as potential sepsis, and a septic screen done, looking for supporting evidence of sepsis as well as the source. Antibiotics should be administered, which will cover nosocomial organisms unless the patient has been an outpatient, and intravenous fluids with a balanced crystalloid like ringer’s lactate initiated. Half dextrose Darrow’s is still not an appropriate resuscitation fluid in this case.
Once the skin grafts have taken and the wounds are healed, the patient can be discharged: FALSE.
While acute burn management is intensive in the acute phase until healing, care needs to be ongoing as part of rehabilitation and scar management even after healing. Long term problems include post burn scarring, itch, and neuropathic pain as well as psychosocial issues. Patients should be followed up at about four to six weeks post complete healing to start scar management.
Post-burn scar problems include hypertrophy, vascularity or hypo/hyperpigmentation with the most extreme pathology being contracture.
Scar management includes scar massage with aqueous cream in a particular fashion three times daily, pressure garments tailor made for the patient by an occupational therapist and maybe the use of silicone sheets and Hypafix® and or splinting over problem areas.
The follow up frequency will depend on the severity of the scar pathology and continue for a period of two years until the scar is mature. Surgical intervention may be necessary to improve functional and cosmetic deficiencies.
Lastly, in the case of a chronic burn wound where healing has taken place over a prolonged period, with either delayed grafting or no grafting performed and healing of deep burns by secondary intention, there is a risk of developing a Marjolin’s ulcer. This is the development of a squamous cell carcinoma within the burn scar and should be suspected in any new wound presenting in a burn scar or previously healed burn wound months or years later. Biopsy is required to make the diagnosis and then referral for surgical management.
Table 1: Darrow's solution recommendation to address dehydration in paediatric burn patients
Table 2: Analgesia protocols for background pain
Table 3: Analgesia protocols for procedural pain