Viva 4

A 54-year-old previously healthy male was admitted to ICU after 45% total body surface area burns.

He was pulled out of his garden shed, unconscious, by the fire brigade and was intubated at the scene of the incident by ambulance personnel.

He was admitted to ICU within one hour of injury.

Please describe methods of assessment of cutaneous burns injuries with regards to the depth of injury and body surface area estimates.

Devgan et al (2006) describes several ways of measuring the depth of a burn. In short, burns are classified according to depth: epidermal, superficial partial-thickness, deep partial-thickness, and full-thickness. These ccategories are usualluy determined at the bedside.

Clinical methods:

  • Wound appearance
  • Capillary blanching and refill
  • Capillary staining
  • Burn wound sensibility to light touch and pinprick


  • Thermography is a measurement of wound temperature. Temperature is taken as an indicator of wound depth; this is based on the expectation that deeper burns will have less persuion on their surface, and will therefore be colder. This technique has the major disadvantage of being significantly dependent on ambient temperature. If the evaporative heat loss from the wound has been significant (eg. if you dutifully washed it with cold water as you're supposed to) the wound will be colder and therefore will appear deeper to the thermographer. One might concieve of a situation where this leads to an unnecessary escharotomy.
  • Fluorescent dye infusion: like thermography, this is a method of assessing near-surface perfusion of a burns wound. The theory is that a poorly perfused full-thickness burn will have less dyne circulating in it, and therefore will not fluoresce under UV light. Though this method sounds really cool, it is unfortunately limited by poor light penetration under eschar, dye escape out of leak capillaries and the renal clearance mechanisms of fluoresceine.
  • Laser fluorescence videography is alos a dye-based method, but this time using a laser to make the dye show up. It has the advantage of being able to dynamically demonstrate tissue perfusion, but has all the disadvantages mentioned above (dye clearance, eschar etc). This modality has evloved to include fancy perfusion measurements such as laser Doppler. 

Problems with these methods:

  • Burns wound conversion: superficial burns tend to evolve into deeper burns over time, motivated by mechanisms which are thus far poorly understood. Assessment of burn depth is therefore a dynamic process.
  • Clinical assessment is inaccurate for intermediate burns: people are more easily able to spot superfical burns and full-thickness burns. Everything in the middle ends up a bit muddled. Heimbach et al (1984) found that clinical depth estimates are accurate only about two-thirds of the time.
  • Clinicians vary in their assessments; experience is required to make a valid assessment (i.e. the more burns you have seen, the better you are at assessing burns - which makes sense)

Gold standard:

  • Punch biopsy with histology: this is really the only way you can be truly sure how deep the wound is, but it is rarely practical to do this (and -as mentioned above- this is going to change as the burn wound undergoes conversion). Punch biopsy reveale protein coagulation, microvascular occlusion and tissue devitalisation; it is the method against which all other methods are compared.

As for body surface area estimates, the following methods are described:

Palmar surface method

  • Surface area of a patient's palm (including fingers) = 0.8% of total body surface area.
  • Palmar surface are can be used to estimate relatively small burns (< 15% ) or very large burns (> 85%).
  • For medium sized burns, it is inaccurate.

Wallace rule of nines

  • A good method estimating medium to large burns in adults.
  • The body is divided into areas of 9%, and the total burn area can be calculated.
    • 9% for each arm
    • 18% for each leg
    • 18% for the front of the torso
    • 18% for the back of the torso
    • 9% for the head
    • 1% for the perineum
  • It is not accurate in children.

Lund and Browder chart

  • the Lund-Browder Chart is the most accurate method.
  • It compensates for the variation in body shape with age and therefore can give an accurate assessment of burns area in children.
Describe the steps you would take in assessing this patient, and what you would look for
  1. Look for signs of  Airway burns
  2. Features of carbon monoxide or cyanide poisoning
  3. Hypotension, hypovolemia, adequacy of fluid resuscitation;
    Also, problems gaining vascular access (not through the burn, unless you have no choice).
    Other important burn patterns:
    1. Presence of circumferential burns
    2. Presence of corneal, perineal or genital burns 
  4. Decreased level of consciousness, head injury; analgesia
    - this guy is unconscious for some reason: was he drunk, did he get a head injury, etc?
  5. Electrolyte disturbance: hyponatremia and hyperkalemia
  6. Exposure and assessment of total burned areas
  7. Urine output (the most important parameter to guide fluid resuscitation)
  8. Haematocrit: haemoconcentration is a sign of volume depletion
  9. Temperature: the patient may either still be hot from the fire (in which case, put them out) or - more likely - they will be hypothermic from their loss of thermoregulation (in which case, expose them to radiant heat to maintain normothermia).

Specific things theyneed to mention:

  • airway burns
  • carbon monoxide/cyanide
  • maintaining their temperature 
  • access issues (eg. use of an IO)
  • circumferential burns
The patient is unconscious, ventilated with 100% FiOusing a mandatory mode. Vital signs and VBG result are as follows:

SpO2 100% 

BP 85/45

HR 135 (sinus)

Temp 34.9° C

carbon monoxide toxicity

Please interpret these data.


  • There is acidaemia
  • The CO2 is unhelpful
  • There is a metabolic acidosis
  • There is virtually no compensation (the expected CO2 is around 24 mmHg)
  • The anion gap is raised (27.6 if you include potassium in your calculation). The ABG machine somehow came up with an AG of 23.5, which demonstrates that all you sheep should learn to think for yourselves
  • The delta ratio is around 1.3 (assuming the albumin is 40)
  • Oxygenation is difficult to asses, this being a venous gas.
  • Having said that, the carboxyhaemoglobin is through the roof (FCOHb is 28.1%)
  • The Hb value is 171, which is a pretty high haematocrit - suggesting that there is significant haemoconcentration taking place. 

In summary, this is a mixed metabolic and respiratory acidosis, mainly due to a high lactate. The patient gives the impression of being under-resuscitated. On top of that, there is significant carbon monoxide toxicity.

What are the possible causes of this raised lactate?

Smart money would be on:

  • Shock, hypovolaemia, haemorrhage
  • Hepatic hypoperfusion (due to haemorrhage, trauma (eg. blast)
  • Carbon monoxide toxicity (tissue hypoxia)
  • Cyanide toxicity

Less likely:

  • Drug-induced (eg. if the patient has overdosed on something like metformin)
  • Seizure (due to hypoxia, head injury or drugs)
  • Sepsis
What is the relationship of carboxyhaemoglobin concentration to symptoms? At what level would you expect to become symptomatic? 
  • If you are a one-pack-a-day smoker, your carboxyhemoglobin is about 6%, but could be as high as 10%.
  • At around 15%, one becomes dizzy and ataxic; a nasty headache  develops
  • At 25% consciousness may be lost.
  • Survival is unlikely at concentrations of 50% or more.
How long does carboxyhaemoglobinaemia last after the end of inhalational exposure?
  • Normally the halflife is said to be six hours.
  • In the presence of a large concentration of oxygen the halflife can be as brief as 30 minutes, because oxygen competes for the same haemoglobin molecules.
The patient remains hypotensive. How would you calculate the fluid requirements?

Any reasonable approach would be satisfactory. The Parkland formula is still the most widely quoted resuscitation protocol for burns.  The original Parkland formula was introduced by Baxter and Shires in 1968. 

  • The "modified" Parkland formula is quoted below:
  • First 24 hrs:
    • Hartmanns (or Ringer's Lactate)
    • 4 ml per kg per percent BSA (counting full-thickness burns only)
    • First half of this volume is given over the first 8 hours
    • No colloid in the first 24 hours
  • Next 24 hours
    • No more crystalloid
    • Albumin infusion:
      (no specific albumin concentration is being targeted)
    • Maintain a urinary output of 0.5–1 ml/hour
What would be your choice of fluid for this resuscitation?

Most of theresuscitation formulae suggest Ringer's lactate, which is very similar (but not identical) to Hartmanns solution found in Australia. In brief, Ringer's has the same ingredients by in a slightly lower concentration: the osmolality of Ringers is 273 mOsm/kg, whereas Hartmanns is 279 mOsm/kg. Generally speaking, the authors all recommend against saline, given the adverse effects of hyperchloremic acidosis. A retrospective case control study by Walker et al (2001) were able to demonstrate a significant difference in acid-base balance, strongly favouring the balanced solutions.

The ambulance officers who intubated the patient raised concerns about the possibility of airway burns. What are the clinical features which might confirm this suspicion?

Historical features associated with airway burns

  • Explosions
  • Fires in an enclosed space
  • Exposure to heated steam
  • Fires involving volatile solvents
  • Corrosive ingestion

Clinical features of airway burns

  • Stridor, hoarseness, or cough
  • Burns to face, lips, mouth, pharynx, or nasal mucosa
  • Soot in sputum, nose, or mouth ("carbonaceous material"
  • Singed vibrissae (the zoological term for innervated whisker hairs, misapplied to the coarse nasal hair which grows in human nostrils and has no role in tactile sensing)
  • Bronchocopic findings of tracheal erythema, oedema or or ulceration.
  • Dyspnoea, decreased level of consciousness, or confusion
  • Hypoxaemia (low pulse oximetry saturation or arterial oxygen tension) or increased carbon monoxide levels (>2%)
The patient's ABG demonstrates improving oxygenation and diminishing FCOHb levels. Hypotension persists in spite of generous fluid resuscitation. The lactate continue to increase  (up to 15.0 mmol/L). What possibilities does this raise?

The candidate may offer a series of sensible options, among which hepatic injury would need to be a prominent differential. 

However, the answer I really want to hear is "cyanide toxicity".

Diagnosis of cyanide toxicity rests on historical features which are strongly suggestive (eg. inhalation of smoke in a plastic-based fire) as well as severe lactic acidosis, and in the absence of carbon monoxide poisoning.

The history raises possibility of cyanide toxicity (apparently the patient has a history of volatile solvent abuse and large amounts of acrylic glue were found in the burning shed).
What are the other features of cyanide toxicity?
  • bradycardia
  • tachypnoea
  • severe metabolic acidosis - predominantly due to lactate
  • high central venous oxygen saturation (low OER)
  • acute renal failure
  • acute hepatic dysfunction
  • acute heart failure and pulmonary oedema
  • circulatory failure, shock
  • coma and seizures
What is the pathophysiology of cyanide toxicity?
  • The best discussion of this mechanism (brief enough for revision work) can be found in theChest case study about the unresponsive biochemistry professor in the bath tub (Mutlu et al, 2002)
  • Lactic acidosis develops due to the uncoupling of oxidative phosphorylation: cyanide interferes with the  electron transport chain by binding to the ferric Fe3+ ion of cytochrome oxidase. The mechanism of lactic acidosis due to cyanide toxicity is discussed elsewhere.
  • Neurotoxicity occurs at modest doses; initially there is CNS stimulation (dizziness, confusion, restlessness, and anxiety) which is followed by stupor, opisthotonus, convulsions, fixed dilated pupils and unresponsive coma. This is due to the cyanide-stimulated release of excitatory neurotrasmitters, such as NMDA and glutamate.
  • Oxidative damage to lipid bilayers due to free radical generation tends to break the blood-brain barrier and causes a vasodilated SIRS-like state of cardiovascular collapse (but this tends to happen only with very large doses)
  • The development of pulmonary oedema, pulmonary vasoconstriction and coronary artery spasm are blamed on "biogenic amines", vasoactive substances which are supposedly liberated from cyanide-affected endothelia. There is not a lot to back this up in the literature.
The serum cyanide level comes back as 50 µmol/L. What management would you recommend?

Just FYI, this is what the blood levels mean:

  • 8-20 µmol/L = mild symptoms
  • 20-38 µmol/L = tachycardia, vasodilation
  • 38-95 µmol/L = decreased level of consciousness
  • 95 µmol/L and above = almost uniformly fatal


  • Decontamination may to be effective (however most cyanides are rapidly absorbed).
    • Cyanide has a short half-life (~ 2 hours), but in massive overdose the decontamination of plasma by dialysis may be feasible and has contributed to the survival of at least one historical victim (Wesson et al, 1985).
  • Hydroxycobalamin
    • Hydoxycobalamin binds cyanide and forms cyanocobalamin
    • This is the antidote of choice
    • Advantages include a lack of toxicity for non-poisoned victims (thus, it may be given empirically)
    • The onset of action is rapid
    • It may be given in the pre-hospital setting and requires no monitoring.
    • The side efects are relatively minor; perhaps the most striking is the tendency for the body fluids to turn a vivid red-orange color.
    • dicobalt edetate may be an alternative cobalt-based binder, but hydroxycobalamin is more widely available, and much less toxic. LITFL mentions that dicobalt edetate causes "seizures, chest pain and dyspnoea, head and neck swelling, hypotension, urticaria and vomiting"
  • Sodium thiosulfate
    • Sulfur donors in general act by offering a sulfur ion to the endogenous rhodanese enzyme which converts cyanide to thiocyanate
    • Like hydroxycobalamin, this is a reasonably safe option - there are few side effects.
  • Induction of methaemoglobinaemia
    • Methaemoglobin binds free cyanide and forms cyanmethaemoglobin.
    • Various drugs are available for this. Sodium nitrite and amyl nitrite are the most frequently quoted. Methylene blue is also available, but is not without its side-effects.
    • Hall and Rumack, writing in the mid-1980s, recommended a sniff of a freshly cracked amyl nitrite inhaler as the first-line rescue therapy, presumably because back in those days everybody had a few of those in their back pocket at all times.

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station. 


The BMJ had published a series of 12 articles, titled "the ABC of burns".
These are a valuable resource. Some are linked to below:


Devgan, Lara, et al. "Modalities for the assessment of burn wound depth."Journal of burns and wounds  (2006) 5: e2.

Heimbach, David M., et al. "Burn Depth Estimation-Man or Machine.Journal of Trauma and Acute Care Surgery 24.5 (1984): 373-378.

Johnson, R. Michael, and Reg Richard. "Partial-thickness burns: identification and management." Advances in skin & wound care 16.4 (2003): 178-187.

Buehler JH, Berns AS, Webster JR, Addington WW, Cugell DW: Lactic acidosis from carboxyhemoglobinemia after smoke inhalation. Ann Intern Med 82:803–805, 1975.

Rioux JP, Myers RA (1988). "Methylene chloride poisoning: a paradigmatic review". J Emerg Med 6 (3): 227–238

Kubic VL, Anders MW, Engel RR, Barlow CH, Caughey WS. Metabolism of dihalomethanes to carbon monoxide. I. In vivo studies. Drug Metab Dispos. 1974 Jan-Feb;2(1):53–57.

Zikria, B. A., et al. "Smoke and carbon monoxide poisoning in fire victims." The Journal of Trauma and Acute Care Surgery 12.8 (1972): 641-645.

Mitra, Biswadev, et al. "Fluid resuscitation in major burns.ANZ journal of Surgery 76.1‐2 (2006): 35-38.

Haberal, Mehmet, A. Ebru Sakallioglu Abali, and Hamdi Karakayali. "Fluid management in major burn injuries." Indian journal of plastic surgery: official publication of the Association of Plastic Surgeons of India 43.Suppl (2010): S29.

Fodor, Lucian, et al. "Controversies in fluid resuscitation for burn management: Literature review and our experience." Injury 37.5 (2006): 374-379.

Lund, Tjostolv, et al. "Upper airway sequelae in burn patients requiring endotracheal intubation or tracheostomy." Annals of surgery 201.3 (1985): 374.

Bartlett, Robert H., et al. "Acute management of the upper airway in facial burns and smoke inhalation." Archives of Surgery 111.7 (1976): 744-749.

Hall, Alan H., and Barry H. Rumack. "Clinical toxicology of cyanide." Annals of Emergency Medicine 15.9 (1986): 1067-1074.

Beasley, D. M. G., and W. I. Glass. "Cyanide poisoning: pathophysiology and treatment recommendations." Occupational medicine 48.7 (1998): 427-431.

Mutlu, Gökhan M., et al. "An unresponsive biochemistry professor in the bathtub." CHEST Journal 122.3 (2002): 1073-1076.

Cummings, T. F. "The treatment of cyanide poisoning." Occupational Medicine 54.2 (2004): 82-85.

Wesson, D. E., et al. "Treatment of acute cyanide intoxication with hemodialysis." American journal of nephrology 5.2 (1985): 121-126.