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In general, burns questions from the fellowship exam tend to have a strong "airway" flavour to them. Physiological consequences of burns as a broad topic has not been asked about. For instance, Question 26 from the first paper of 2012 is concerned mainly with the effects on the respiratory system. This question is well answered by the Burns, Oxygenation and Ventilation page from the LITFL CCC; as an exam-oriented summary this resource leaves little to be desired. The chapter stretching below trends more towards rant than summary, and is offered as an extended footnote to the CCC page and the college model answer to Question 26.
Additional attention to thermal injury is found in burns-related chapters within the "Trauma, Burns and Drowning" revision topic area:
Question 30 from the second paper of 2009, Question 28 from the second paper of 2010 and Question 11 from the first paper of 2013 were all essentially identical investigations of the candidate's ability to recall the features of airway burns, This topic is discussed at length in a dedicated chapter on airway burns.
A BMJ article from the "ABC of burns" series contains Table 1, "Warning signs of airway burns", which I reproduce below:
Question 18 from the second paper of 2012 presents the candiates with a pair of burned-looking legs, and asks what the complications of such burns might be. Compartment syndrome is on the top of the list.
This is one of those areas of burns management which has become the subject of numerous books and PhD theses. Instead of linking to those, I will instead offer a link to some pragmatic guidelines from www.vicburns.org.au. Another excellent resource is this 2004 review article by Norman and Judkins.
Major mechanisms of pain in the setting of burns:
Key features of a successful approach:
It is extremely rare for a common house fire to burn somebody's brain, given that its defence has been a priority from an evolutionary standpoint. Not so for electical burns, however. The path taken by electricity is often going to involve the brain and spine (as these are highly vascular, and vascularity is what largely determines conductivity). The immediate result is usually coma; similarly to the effects of defibrillation on the myocardium, all the voltage-gated channels open in the wake of a large current, and the consequence is a simultaneous depolarisation of all involved neurons. This manifests as a seizure, and a post-ictal stupour usually ensues.
A review of 90 consecutive electrical burns cases (Grube et al, 1990) has revealed that even severe electrical injury to the CNS is likely to be well tolerated in the long term. I quote Baiba Grube directly:
Like most trauma-exposed people, the burns patients tend to develop various new psychological problems, and their pre-existing issues are amplified (Van Loey et al, 2003)
The average severe burns patient is covered in numerous dressings, and they are getting soaked with exuduate. In the 1950s, Moore at al collected these exudate-encrusted dressings and analysed them to estimate the electrolyte losses of burns patients. In short, exudate fluid largely resembles plasma, and the proportion of lost electrolytes resembles the loss of blood volume, and its diluting replenishment by pure water.
Hyperkalemia associated with giving sux to burns patients is a well documented phenomenon, and ebveybody ends up having to memorise it as one of the contraindications for giving sux, no matter which primary exam they sat. It has been known about for some time (Schaner et al, 1969). The problem seems to have more to do with prolonged immobility than with the burn itself (Van Loey et al, 2003)
If you think about it, there are a hundred reasons for the kidneys to go off in this setting, and none of them are specific to the actual thermal injury. The following is a short list of reasons as to why a shocked patient might develop renal failure. According to Chrysopoulo et al (1999) the incidence of this may be around 5% (in a retrospective case series).
On a more exotic note, one might find their burns patient having a raise urea due to excess protein catabolism.
One need not dwell on this issue overlong; it is clear that the skin is one's main heat exchange surface, and with the loss of a large area of skin one also loses one;s ability to control the exchange of body heat with the external environment. Moreover, there is a constant loss of warm fluid in the form of exudate, which is exchanged with dressings. Secretions deliver water to the surface of the wounds and into dressings, or the dressings themselves may be soaked with saline - either way, the water evaporates, robbing the patient by convective loss. In the acute setting, it is important to remember that the burns patient is likely to receive up to 25% of their body weight in resuscitation fluid which might all be at room temperature.
In short, hypothermia is to be expected.
This is a chronic inflammatory state which persists for months. It starts around the fifth day after the burn. Herndon et al (2004) describe these abnormalities in an excellent article from the Lancet. The following are its characteristic features:
This endocrine abnormality is partly due to the release of cortisol and partly due to the catecholamine excess which is associated with recovery from severe burns. But wait, you might say: can't you β-block those, and make it all go away? You'd be right. Indeed, Herndon et al (2001) have published a randomised controlled trial (25 children, half randomised to receive propanolol) which demonstrated precisely that. The β-blocked children were substantially less protein-wasted after two weeks of propanolol - their fat-free body mass did not decrease at all, whereas the untreated children lost 9% of theirs.
Lawrence et al (1993) found patients with "massive" burn injury developed haemolysis. None of the patients in this paper survived long than three days. I cannot get hold of this paper in full text, but it seems the "massive" burns were truly massive - one of the patients didn't last more than 45 minutes. One might surmise that the haemolysis is the direct action of extreme heat on a large proportion of the bloodstream. In olden days, haemolysis in burns was seen more frequently because the patients frequently received poorly matched blood products (Topley ey al, 1963)
This arises in haemolysis. The automated cell counter becomes "confused" by multiple red cell fragments and incorrectly recognizes them as platelets, hence the pseudo.
In an audit of Finnish burns patients, Kallinen et al (2012) identified DIC in 10% of severe burns patients. This seems to be a manifestation of severe SIRS in most cases. In the most severe of burns, DIC may be caused by the appearance of burned cellular debris in the circulation (Lippi et al, 2010)
Not just entire book chapters, but entire books have been written on this topic. Probably the most succinct resource on it would have to be the UpToDate article. To the penniless public, I will also recommend the free online 2006 article by Deirdre Church, from Clinical Microbiology Reviews - it is ridiculously detailed. The CICM examiners ultimately decided that this was a good topic of discussion for Question 7 from the second paper of 2022, which asked about the risk factors, local signs, systemic features and diagnostic challenges of identifying infection in patients with thermal injuries.
From UpToDate:
Local signs:
Systemic features:
The ABA has a somewhat contested set of criteria, on which the above is based.
The BMJ had published a series of 12 articles, titled "the ABC of burns".
These are a valuable resource. Some are linked to below:
Jeschke MG, Chinkes DL, Finnerty CC, et al. "Pathophysiologic response to severe burn injury". Ann Surg. 2008;248:387–401
Enkhbaatar, Perenlei, and Daniel L. Traber. "Pathophysiology of acute lung injury in combined burn and smoke inhalation injury." Clinical Science 107.2 (2004): 137-144.
Whitener, D. R., et al. "Pulmonary function measurements in patients with thermal injury and smoke inhalation." The American review of respiratory disease 122.5 (1980): 731-739.
Crapo, Robert O. "Smoke-inhalation injuries." JAMA 246.15 (1981): 1694-1696.
Williams, Felicia N., et al. "Changes in cardiac physiology after severe burn injury." Journal of burn care & research: official publication of the American Burn Association 32.2 (2011): 269.
Wilmore, Douglas W., et al. "Catecholamines: mediator of the hypermetabolic response to thermal injury." Annals of surgery 180.4 (1974): 653.
Asch, MORRIS J., et al. "Systemic and pulmonary hemodynamic changes accompanying thermal injury." Annals of surgery 178.2 (1973): 218.
Crum, Ralph L., et al. "Cardiovascular and neurohumoral responses following burn injury." Archives of Surgery 125.8 (1990): 1065-1069.
GRUBE, BAIBA J., et al. "Neurologic consequences of electrical burns." Journal of Trauma and Acute Care Surgery 30.3 (1990): 254-258.
Van Loey, Nancy EE, and Maarten JM Van Son. "Psychopathology and psychological problems in patients with burn scars." American journal of clinical dermatology 4.4 (2003): 245-272.
Patterson, David R., et al. "Psychological effects of severe burn injuries." Psychological Bulletin 113.2 (1993): 362.
Van Loey, Nancy EE, and Maarten JM Van Son. "Psychopathology and psychological problems in patients with burn scars." American journal of clinical dermatology 4.4 (2003): 245-272.
Chrysopoulo, Minas T., et al. "Acute renal dysfunction in severely burned adults." Journal of Trauma and Acute Care Surgery 46.1 (1999): 141-144.
Herndon, David N., and Ronald G. Tompkins. "Support of the metabolic response to burn injury." The Lancet 363.9424 (2004): 1895-1902.
Moore, Francis D., et al. "The role of exudate losses in the protein and electrolyte imbalance of burned patients." Annals of surgery 132.1 (1950): 1.
Latenser, Barbara A. "Critical care of the burn patient: the first 48 hours." Critical care medicine 37.10 (2009): 2819-2826.
Hauhouot-Attoungbre, M. L., et al. "[Disturbances of electrolytes in severe thermal burns]." Annales de biologie clinique. Vol. 63. No. 4. 2004.
SCHANER, PAUL J., et al. "Succinylcholine-Induced Hyperkalemia In Burned Patients-1." Anesthesia & Analgesia 48.5 (1969): 764-770.
Martyn, J. A. Jeevendra, and Martina Richtsfeld. "Succinylcholine-induced Hyperkalemia in Acquired Pathologic States Etiologic Factors and Molecular Mechanisms." The Journal of the American Society of Anesthesiologists 104.1 (2006): 158-169.
LAWRENCE, CHRISTINE, and BULENT ATAC. "Hematologic changes in massive burn injury." Critical care medicine 20.9 (1992): 1284-1288.
Kallinen, Outi, et al. "Multiple organ failure as a cause of death in patients with severe burns." Journal of Burn Care & Research 33.2 (2012): 206-211.
Lippi, Giuseppe, Luigi Ippolito, and Gianfranco Cervellin. "Disseminated intravascular coagulation in burn injury." Seminars in thrombosis and hemostasis. Vol. 36. No. 4. 2010.
Topley, E., et al. "The relation of the isoagglutinins in pooled plasma to the haemolytic anaemia of burns." Journal of clinical pathology 16.1 (1963): 79-86.
Wolfe, John HN, et al. "Anergy, immunosuppressive serum, and impaired lymphocyte blastogenesis in burn patients." Archives of Surgery 117.10 (1982): 1266-1271.
Herndon, David N., et al. "Reversal of catabolism by beta-blockade after severe burns." New England Journal of Medicine 345.17 (2001): 1223-1229.
Schultz, Laura, et al. "Identification of predictors of early infection in acute burn patients." Burns 39.7 (2013): 1355-1366.
Lago, Kathryn, et al. "Difficult to treat infections in the burn patient." Surgical infections 22.1 (2021): 95-102.
American Burn Association Consensus Conference on Burn Sepsis and Infection Group, et al. "American Burn Association consensus conference to define sepsis and infection in burns." Journal of burn care & research 28.6 (2007): 776-790.