Printable list of all the trauma SAQs

College Answer

Definition: "severe" (usually mild 32-35, moderate 28-32, and severe < 28C). Accidental implies spontaneous decrease in core temperature, usually in a cold environment (more common in elderly, neonates, unconscious, exhausted, hypothyroid etc).

Mortality is signficant. Signs are modified by associated injuries, medications, extremes of age, etc.

Temperature control lost (become poikilothermic, cooling to ambient temperature)

Cardiac : arrhythmias (eg. bradycardia. AF and VF) decreased mean blood pressure, contractility, cardiac output

Respiratory: decreased respiratory rate, respiratory acidosis 

CNS: variable effects on mentation and motor function; impaired judgement, disorientation, hyporeflexia

Haematology: coagulopatby, platelet dysfunction

Gastrointestinal: pancreatitis 

Renal: polyuria, dehydration, ARF

Discussion

The college specifies accidental hypothermia, which means the candidate could have included in their answer the entire spectrum of horrible environment-associated problems. One does not quietly cool on a clean surface. One typically is halfway immersed in an icy lake, trapped under a dead moose, or subject to another similarly complex retrieval situation. However, the college answer bypasses the accidental nature of the hypothermia, and speaks mainly of the non-specific consequences of low body temperature.

This topic is explored in greater depth in another chapter. The table of contents from this hypothermia chapter is a good summary of the physiological consequences of hypothermia

Endocrine and metabolic consequences

• Decreased metabolism and oxygen consumption
• Decreased carbohydrate metabolism and hyperglycaemia
• Decreased drug metabolism and clearance
• Essentially unchanged electrolytes

Haematological consequences

• Increased hematocrit and blood viscosity
• Neutropenia and thrombocytopenia
• Coagulopathy and platelet dysfunction

Respiratory consequences

• Decreased respiratory rate and medullary sensitivity to CO₂
• Acid-base changes: alkalosis and hypocapnea
  • Rise of pH with falling body temperature
  • Fall of PCO₂ with falling body temperature
  • Increased oxygen solubility and O₂-haemoglobin affinity

Cardiovascular consequences

• Decreased cardiac output and bradycardia
• QT prolongation and the J wave
• Arrhythmias - classically AF and VF
• Resistance to defibrillation
• Vasoconstriction

Renal consequences

• "Cold diuresis" due to decreased vasopressin synthesis

Central nervous system effects

• Confusion and decreased level of consciousness
• Shivering
• Increased seizure threshold

Immunological consequences

• Decreased granulocyte and monocyte activity

References

The above-referenced chapter on hypothermia has extensive references.

In order to simplify revision, I have identified four articles which cover this topic with a wealth of detail.

Wong, K. C. "Physiology and pharmacology of hypothermia." Western Journal of Medicine 138.2 (1983): 227.

Polderman, Kees H. "Application of therapeutic hypothermia in the intensive care unit." Intensive care medicine 30.5 (2004): 757-769.

Polderman, Kees H. "Mechanisms of action, physiological effects, and complications of hypothermia." Critical care medicine 37.7 (2009): S186-S202.

Mallet, M. L. "Pathophysiology of accidental hypothermia." Qjm 95.12 (2002): 775-785.

College Answer

Upper respiratory tract bums can be life threatening  unless appropriately recognised and treated. Severity  of  inhalational   injury  has been  related   to  various  factors:   beat  of  inhaled   gases, composition of gases (presence of particles, steam  and toxic products), duration of exposure, and pre·injury state.
Most of the upper .respiratory  tract  injury is due to  the thermal insult (augmented  by duration of exposure).

Initial  symptoms   may   relate  to  associated   injuries  (facial  burns),  early  oedema   (intra-oral, pharyngeal, supraglottic/glottic/subglottic) with respiratory distress secondary  to airway obstruction and increased  work of breathing (tachypnoea,  indrawing of soft tissues, tracheal tug), and patient · may be coughing or spitting carbonaceous material (signs are those of upper airway burn).

Management  includes  that of  associated  systemic  effects  such  as  bums  to  body  (hypovolaemic shock etc), and inhalation of toxins (carbon monoxide, cyanide etc.). Management  of  the  airway includes  appropriate  positioning  of  patient  (eg.  sitting  up), close monitoring, and early definitive management of airway patency. Oedema worsens over the first few hours (persists for days) and may rapidly cause airway obstruction  in untreated patients. Elective intubation should  be considered  early. A safe technique  which took into account the potential for full stomach and difficult intubation was expected to be detailed.

Discussion

Smoke inhalation is dealt with more broadly in Question 13 from the second paper of 2006. The lower respiratory complications of smoke inhalation are treated in greater detail in the answr toQuestion 26 from the first paper of 2012.

Apart from organising them by mechanism, symptoms and management, upper respiratory tract complications of smoke inhalation can be categorised by pathophysiology or anatomically, to make for a systematic answer.

Presented in this fashion, it could even be turned into a table.

Everyone likes tables.

Or, one can organise them by anatomical location:

A good summary of airway burns can be found in the 2012 article

References

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.

Gaissert, Henning A., Robert H. Lofgren, and Hermes C. Grillo. "Upper airway compromise after inhalation injury. Complex strictures of the larynx and trachea and their management." Annals of surgery 218.5 (1993): 672.

Bishop, Sophie, and Simon Maguire. "Anaesthesia and intensive care for major burns." Continuing Education in Anaesthesia, Critical Care & Pain 12.3 (2012): 118-122.

College Answer

Discussion on the effects of the ICS should include:

•    renal effects – capillary compression, decreased GFR/UO, ATN,

•    bowel – decreased SMA/coeliac flow, decreased pHi, bowel ischaemia

•    hepatic – decreased portal blood flow, lactate clearance

•    cardiac –decreased venous return/cardiac output, elevated PAOP/CVP/afterload

•    respiratory –increased PIP, shunt, Paw,

•    cerebral – increased ICP, decreased CPP

Description of a simple, sterile and practical technique for measurement of intra-vesical pressure was expected.

Pitfalls include:

•    using the wrong zero point

•    allowing a leak in the system to produce a falsely low reading

•    chronic cystitis, radiation cystitis producing a small contracted bladder with low compliance which gives a falsely high reading

•    pelvic haematoma producing a tight pelvic compartment with falsely elevated IAP.

Discussion

The majority of this question is answered by the discussion of Question 8 from the first paper of 2013. A slightly less formal discussion of abdominal compartment syndrome takes place in Question 21 from the second paper of 2006: "Outline the causes, consequences and the management of abdominal  compartment syndrome. "

The "pitfalls" section is not addressed anywhere else.

Briefly, the following are reasons as to why one's intrabdominal measurements may be wrong:

• Failure of technique
  • Improper setup of the measuring set
  • Improperly calibrated transducer
  • Inappropriate zero point
  • Leaking transducer system
• Confounding factors
  • Increased pelvic pressure
  • High detrusor tone
  • Detrusor fibrosis
  • Incompletely paralysed patient

References

College Answer

Organized approach is essential.   ATLS/EMST approach should be used.   Most emergency departments that receive trauma do so with facilities that support a trauma team concept.  Initial management should be undertaken as part of the trauma team, with roles usually well delineated.

Initial management requires simultaneous primary survey, resuscitation and assessment of history, followed by a secondary survey then definitive care.

Primary survey involves assessment of adequacy of airway, breathing and circulation (with interventions  at  each  point  whenever  identified),  followed  by  assessment  of  neurological  state (pupils, level of consciousness, localising signs) and adequate exposure to assess major injuries. Indications for endotracheal intubation should be clearly described (GCS < 9, hypoxia/respiratory distress  etc.).   Initial ventilatory  management  should be detailed  (respiratory  rate, tidal volume, blood gas goals etc).  Fluid administration and goals of resuscitation should be discussed. Relevant history should be obtained from ambulance  officers, family, witnesses  etc.   In particular details about the mechanism of injury and patient’s previous medical condition, medications and allergies etc.

Secondary survey involves a detailed head to toe examination to assess extent of injuries (including flanks, back and rectal examination), as well as a detailed neurological assessment.

Definitive  care  involves  planning  for  surgery,  other  specialist  involvement   and  transfer  as appropriate.

Discussion

A systematic approach to this answer would follow the normal ATLS pattern of the primary survey.

A) - Urgent assessment of the airway, and of the need for immediate intubation (with in-line spinal stabilisation). A very high spinal cord injury may have resulted in respiratory arrest.

The decreased level of consciousness suggests that intubation is required.

B) - Evaluation of respiratory function and chest injuries. This patient can potentially have a tension or non-tension pneumothorax or haemothorax, and this diagnosis needs to be made early in the primary survey. High FiO₂ should be administered. One should look for paradoxical respiration pattern due to flail chest, or diaphragmatic breathing due to high spinal cord injury.

C)

Features of hypovolemia (eg. cool peripheries, pallor) should be sought. Blood should be sampled for crossmatch, and uncrossmatched blood should be transfused if the patient is demonstrating features of anaemia. Large-bore IV access should be established.

Blood products should be preferentially used for resuscitation, with a 1:1:1 ratio of PRBCs, FFP and platelets. The MAP target for fluid resuscitation should be a MAP >50mmHg.

D) The level of consciousness should be assessed. Features of spinal cord injury should be pursued on examination. Pupils should be examined to assess for signs of herneation.

E) The patient needs to be rewarmed (presuming they are hypothermic) and a blood warmer should be connected to maintain normothermia in spite of massive resuscitation

After the completion of the primary survery, the following investigations must urgently take place:

• CXR
• Pelvic XR
• FAST US of the abdomen chest and praecordium can rapidly differentiate between the abovementioned causes of shock.
• CT trauma series, if available

This pathway of investigation should be abandoned and urgent damage control surgery should take place if any of the above assessment methods make it abundantly clear that a catastrophic shock state due to abdominal or thoracic haemorrhage is developing.

Definitive transfer arrangements must be made if definitive care cannot be offered at the current facility.

References

ATLS student course manual, 8th edition (Chapter 5) - American College of Surgeons Committee on Trauma

College Answer

Urgent early investigations include urea and electrolytes, full blood examination and blood group and cross match (done when initial venous access is obtained).   It is reasonable to also perform arterial blood gas analysis and a coagulation profile at this time.

During the resuscitation phase before the secondary survey, it is reasonable to get a lateral cervical spine, supine chest X-ray, and pelvis X-ray, as long as this can be done without moving the patient to  a  separate  area.    Some  specific  abdominal  assessment  should  be  made  as  the  patient  is unconscious (DPL, FAST or CT scan), earlier if haemodynamically unstable.  A urinary catheter (unless contraindicated) should be inserted at this time to monitor urine output, and an ECG should be obtained (± echocardiography or CVP monitoring if unsure of cardiovascular status).

More specific X-rays of suspected or high risk areas (eg. full cervical spine series, chest CT and head CT, limb and thoracic and lumbar spine X-rays) should be done when patient is haemodynamically stable and ideally before transfer to ICU or theatre (unless required urgently). Definitive exclusion of thoracic aortic injury (trans-oesophageal  echocardiography  or CT angiography) should be performed if clinically indicated when haemodynamically stable.

Repeat assessment of blood gases, Hb and coagulation may be needed early.

Intra-cranial pressure monitoring may be required depending on clinical status or CT appearance (in this 65 year old man). This is not usually urgent, but may facilitate titration of modalities to control ICP and CPP. It may be inserted in ICU or pre-operatively if prolonged time in the operating theatre is anticipated.

Discussion

This is a question about the initial blood workup and primary/secondary survey investigations.

Thus:

Bloods:

• FBC
• EUC
• CMP
• LFT
• Coags
• Crossmatch

Imaging

• Chest Xray
• FAST including pericardium
• Pelvic Xray
• Long bone Xrays
• CT trauma series including aortogram

Monitoring

• ECG
• Urine output
• Arterial invasive blood pressure
• ICP monitoring may be indicated if the intracranial pressure cannot be monitored clinically

References

ATLS student course manual, 8th edition (Chapter 5) - American College of Surgeons Committee on Trauma

College Answer

This patient has major trauma with head, limb and chest injuries, and should be managed in a centre that is experienced in trauma care.   If this hospital is not able to provide sufficient services then early communication with a receiving hospital is essential, and plans made for expedient transfer.

Specific neurosurgery may be necessary if intracranial haemorrhage is detected and should be performed within the first few hours.  Thoracic surgery is rarely required (eg. dependent on amount of bleeding from intercostal tubes), but surgery will be required for long bone fractures.  Compound fractures should be dealt with early (hours), as should injuries with vascular compromise.  Other operations are less urgent and the role of early fixation of fractures is controversial.  In the absence of significant  respiratory  compromise  it is probably reasonable  to progress to early fixation.   If instead there is concern about respiratory status then external fixation rather than internal fixation may be preferable on the first day, followed by more specific management a few days later.

Discussion

This question would benefit from a systematic response.

Thus:

• Definitive airway/ventilation management
  • The patient may remain intubated.
  • If this patient has had a severe traumatic brain injury, a tracheostomy may be required. If the C-spine is unstable this is best performed surgically, rather than percutaneously.
• Definitive hemostasis
  • This should be achieved by surgical repair of fractures, wounds, and organ damage. External fixation of long bone fractures is a valid alternative.
    • Early repair of contaminated wounds or compound fractures
    • Delayed closure of laparotomy wounds
    • Vac-dressing for abdominal defects
• Definitive neurological/neurosurgical management
  • Neurosurgical intervention
  • Standard neuroprotective measures
  • Referral to brain injury rehabilitation

References

ATLS student course manual, 8th edition (Chapter 5) - American College of Surgeons Committee on Trauma

College Answer

It may be very difficult to obtain adequate analgesia in patients with significant chest injuries. The various options available may be limited by associated injuries, in particular the presence of a closed head injury, an uncleared cervical or thoraco-lumbar spine, a coagulopathy or renal injury. The options available may also be limited by the area in which the patient will be managed, though these patients should be managed in at least a high dependency unit. Patient sensitivities or allergies, and past illnesses (eg. bleeding ulcer) may also restrict choices.
The options available which should be discussed are multiple and include combinations of:
•    simple parenteral opioids (infusion, boluses, PCA), with the use of adjuvant agents
(tramadol, NSAIDs, paracetamol, codeine)
•    regional techniques (including epidural analgesia with local anaesthetics and/or opioids, interpleural local anaesthetics or intercostal blocks).

Discussion

Pain management in chest injuries is touched upon in the answer to Question 26 from the first paper of 2010, "Outline the relative advantages and disadvantages of thoracic epidural analgesia compared to systemic opioid analgesia via a PCA (Patient Controlled Analgesia)"

To simplify revision, that comparison table is reproduced below.

Additionally, an excellent resource on acute pain management in chest injury is available from theJournal of Trauma, Injury, Infection and Critical Care.

Additional issues can be brought up.

Regional analgesic techniques are gaining in popularity:

• Paravertebral block
• Intercostal nerve block

Opiate-sparing analgesic agents can be used:

• paracetamol
• NSAIDs
• clonidine
• dexmedetomidine

Agents to manage a neuropathic component of the pain can be used:

• Gabapentin
• Pregabalin
• Amitryptilline

Non-pharmacological methods may be employed:

• PEEP to splint the rib fractures
• Early removal of chest drains

References

Karmakar, Manoj K., and Anthony M-H. Ho. "Acute pain management of patients with multiple fractured ribs." Journal of Trauma-Injury, Infection, and Critical Care 54.3 (2003): 615-625.

College Answer

a) Describe your initial management.

Initial management of trauma should be according to standard protocol.  Initial primary survey and resuscitation would address adequacy of airway (patency, need for ETT) and breathing (eg. excluding tension pneumothorax and major haemothorax). At the review of “circulation” phase, the presence of shock with obvious abdominal signs means urgent surgery is required (with simultaneous insertion of 2 wide bore IVs if not already present, removal of blood for Hb/platelets, crossmatch and clotting profile, rapid infusion of 2 litres of fluid [blood if significant previous non- blood resuscitation].  In the time until surgery is organised, it may be possible to perform a supine CXR, pelvic X-ray and/or a FAST (ultrasound) examination.   He must be treated with spinal precautions (including for intubation) as it must be assumed that there is an unstable cervical spine, with possible thoraco-lumbar spine injuries.  Attempts should be made to maintain his temperature stable (eg. >35-36°C).  Full secondary survey and specific investigations must be deferred until the haemodynamic state is adequately dealt with.

Discussion

This question is identical to Question 12 from the second paper of 2005.

References

College Answer

At this stage stability must be confirmed in other areas as well as haemodynamic.  Blood pressure goals should consider spinal perfusion pressure if spinal injury is suspected, and steroids should be considered in the first 8 hours.

Now is the time to ensure that oxygenation and ventilation are stable; coagulation should be assessed and corrected if abnormal; and temperature should be in target range.  Secondary survey should be completed, including detailed neurologic examination (eg. in an attempt to exclude spinal injury).   Spinal precautions should be continued for the interim.   The primary x-rays should be obtained (CXR, pelvic x-ray, lateral cervical spine) but now additional x-rays should be obtained as indicated (repeat CXR, spinal series ± CTs eg. of cervical spine, chest, abdomen).   Long bone injuries should be sought and excluded (or treated).  Other specialists should be asked to review patient as indicated (eg. cardiothoracic, spinal).  Antibiotics and tetanus prophylaxis should be prescribed if indicated.  Anti-ulcer prophylaxis should be instituted, and as should pharmacological prophylaxis for DVTs when contraindications subside.  Enteral feeding should be started as soon as practical.

Discussion

This question about post-splenectomy ICU management  is identical to Question 13 from the second paper of 2005.

References

College Answer

The additional complicating factor of pregnancy expands the differential diagnosis, and requires additional investigation and monitoring, and complicates the performance of many interventions. Standard ACLS/EMST management of the initial presentation should be performed.   

Primary survey: [airway {and cervical spine}, breathing, circulation, disability and exposure] with high flow oxygen and standard monitoring. Standard resuscitation and initial Xrays should be performed with a lead apron covering the abdomen whenever possible.

Secondary survey: Abdominal examination is even less reliable than usual, and concern about foetal well-being and the possibility of abruption should be considered.  Uterine rupture is rare without previous uterine surgery.  Early consultation should occur with an obstetrician, and Cardio-Toco-Graphic monitoring should be implemented. Focused Abdominal Sonography in Trauma is still reliable, and abdominal CT scan is not contraindicated, and may help in the diagnosis of abruption.

Discussion

This question forms a part of the "manage this pregnant trauma patient" spectrum of fellowship questions. For a general reference, one is directed to Question 3 from the first paper of 2007 (Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.). Question 6 from the first paper of 2000 also touches on the ways in which physiological changes in pregancy affect the scenario of trauma. Specific features of the cardiorespiratory changes in pregnancy can also be found on the page dedicated to this topic

In brief, one should recall the following issues:

• The airway is more difficult to control.
• There is an increased risk of aspiration
• The respiratory function is impaired by decreased FRC;
  • One needs to insert thei chest drains higher, so as to avoid the pushed-up diaphragms
• When setting up the ventilator, one needs to keep in mind that the PaCO₂ is supposed to be 30mmHg in late pregnancy.
• The total blood volume has expanded, the cardiac output is high, and thus signs of shock will develop late.
• Vena cava compression means the patient needs to be positioned at a 30° tilt
• Pelvic binders are inappropriate
• Pelvic fractures may threaten the near-term foetus
• Placental abruption may result in massive haemorrhage and needs to be excluded early in the primary survey
  • foetal heart rate monitoring is essential
• Retroperitoneal haemorrhage from dilated pelvic veins can be difficult to assess without ultrasound (but FAST is still effective)
• A vaginal examination needs to be performed, looking for amniotic fluid (a pH of 7.0-7.5 will confirm this - the normal vaginal pH is much lower than this)
• Rhesus-negative mothers need to receive IV immunoglobulin at least within 48 hours of the trauma
• Transfusion needs to be Rh compatible
• Antibiotic choices are limited; tetracyclines and fluoroquinolones are to be avoided
• The pregnant trauma patient is in an even more hypercoagulable state than the normal trauma patient, and thus requires special attention to DVT prophylaxis

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Soar, Jasmeet, et al. "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution." Resuscitation 81.10 (2010): 1400-1433.

Mattox, Kenneth L., and Laura Goetzl. "Trauma in pregnancy." Critical care medicine 33.10 (2005): S385-S389.

DROST, THOMAS F., et al. "Major trauma in pregnant women: maternal/fetal outcome." Journal of Trauma-Injury, Infection, and Critical Care 30.5 (1990): 574-578.

College Answer

Consider:   Immediate:   blood   for   group   (consider   Rhesus   isoimmunisation),  cross   match, electrolytes, full blood examination and coagulation profile.   Xrays of chest and cervical spine (&/or pelvis), delaying other Xrays until stable.
Early: abdominal ultrasound (FAST, uterus and foetal heart rate), CTG
Once stable: abdominal CT, thoracic and lumbar spine films (if can’t clear clinically in view of distractors). DPL probably not of additional help, unless other investigations unavailable.

Discussion

This question is about immediate bloods, and the investigations which form part of the secondary survey. How are these different in a pregnant patient? A generic approach to the pregnant trauma patient is discussed in Question 3 from the first paper of 2007.

The usual barrage of blood tests remains unchanged.

FBC, EUC, CMP LFT coags and crossmatch get sent away just as they would in any trauma patient, but the savvy candidate will mention the need for Rh blood grouping to prevent Rh isoimmunisation (where the mother is Rh negative and the foetus is Rh positive). An administration of anti-Rh IVIG can mop up any Rh-positive foetal erythrocytes which might have haemorrhaged into the maternal circulation, preventing the mother from developing her own anti-Rh antibodies (and thus preventing the haemolytic disease of the newborn).

An abdominal ultrasound (FAST) is still performed, with additional focus on the uterus; uterine rupture or placental abruption need to be detected early.

Foetal welfare can be monitored by CTG, and the O&G specialist should be invited to perfrom their own focused ultrasound to investigate the pregnancy.

Though radiation exposure is undesirable, it is tolerated (particularly in late term pregnancy) because organogenesis has already taken place, and because the risk from ionising radiation exposure is minute in comparison to the risk of missed injuries and haemorrhage.

References

Kuczkowski, K. M. "Trauma during pregnancy: a situation pregnant with danger." Acta Anaesthesiol Belg 56.1 (2005): 13-18. 

Oxford, Corrina M., and Jonathan Ludmir. "Trauma in pregnancy." Clinical obstetrics and gynecology 52.4 (2009): 611-629.

Goodwin, Hillary, James F. Holmes, and David H. Wisner. "Abdominal ultrasound examination in pregnant blunt trauma patients." Journal of Trauma-Injury, Infection, and Critical Care 50.4 (2001): 689-694.

College Answer

Practice management guidelines exist for the management of haemorrhage in pelvic fracture. The general principles are included below.

Angiography is not always required but may be life saving. It requires specialist radiology expertise (not necessarily widely available), requires transport to and needs to be performed in an area that may not be adequately set up for the complex monitoring and resuscitation that may be required in an unstable patient. Definitive selective embolisation may be able to be achieved to control arterial bleeding where other strategies (e.g. pelvic stabilisation or laparotomy) have failed.

Some form of surgical management is probably required in all cases, as at least some form of immobilisation (usually external fixation) will be required for unstable pelvic fractures. Laparotomy is indicated for the associated traditional signs of intra-abdominal bleeding or intestinal perforation. Apart from definitive stabilisation, other definitive surgical management is not usually helpful apart from general packing (without exploration) for venous haemorrhage, and rarely ligation of internal iliac arteries for uncontrollable arterial haemorrhage. Some aspects of surgical management may be able to be performed outside the operating room; otherwise transport is required (but to an area set up for ongoing monitoring and stabilisation).

Discussion

Since 2004, technology has moved on, and so the opinion has shifted in favour of early angioembolisation. Even in 2003 this study supported the use of earlier angio for anybody with evidence of arterial bleeding. Furthermore, there is good evidence for a angiographic "mop-up" of bleeding which has not resolved after external surgical fixation.

This question would benefit from a 2 × 2 table of advantages and disadvantages.

References

Miller, Preston R., et al. "External fixation or arteriogram in bleeding pelvic fracture: initial therapy guided by markers of arterial hemorrhage." Journal of Trauma-Injury, Infection, and Critical Care 54.3 (2003): 437-443.

Flint Jr, LEWIS M., et al. "Definitive control of bleeding from severe pelvic fractures." Annals of surgery 189.6 (1979): 709.

Cullinane, Daniel C., et al. "Eastern Association for the Surgery of Trauma practice management guidelines for hemorrhage in pelvic fracture—update and systematic review." Journal of Trauma and Acute Care Surgery 71.6 (2011): 1850-1868.

Metsemakers, W-J., et al. "Transcatheter embolotherapy after external surgical stabilization is a valuable treatment algorithm for patients with persistent haemorrhage from unstable pelvic fractures: outcomes of a single centre experience." Injury 44.7 (2013): 964-968.

Rossaint, Rolf, et al. "Management of bleeding following major trauma: an updated European guideline." Crit care 14.2 (2010): R52.

College Answer

Initial management of trauma should be according to standard protocol.
Initial primary survey and resuscitation should address adequacy of airway (patency, need for ETT)
and breathing (eg. excluding tension pneumothorax and major haemo-thorax).
At the review of “circulation” phase, the presence of shock with obvious abdominal signs means urgent surgery is required, with simultaneous insertion of 2 wide bore IVs if not already present, removal of blood for Hb/platelets, cross-match and clotting profile, rapid infusion of 2 litres of fluid [blood if significant previous non-blood resuscitation].
In the time until surgery is organised, it may be possible to perform a supine CXR, pelvic X-ray and/or a FAST (ultrasound) examination/DPL/abdominal CT if able to be kept haemo-dynamically stable. Consideration of angiography if stability maintained and expertise available.
He must be treated with spinal precautions (including for intubation) as it must be assumed that there is an unstable cervical spine, with possible thoraco-lumbar spine injuries.

Attempts should be made to maintain his temperature stable (eg. > 35-36°C). Full secondary survey and specific investigations must be deferred until the haemo-dynamic state is adequately dealt with. 

Discussion

This patient has four major issues:

• Potential high spinal injury
• Lower left chest injuries
• Features of shock, which may be haemorrhagic or spinal
• A painful distending abdomen, which may be due to solid organ trauma.

A systematic approach to this answer would follow the normal ATLS pattern of the primary survey.

A) - Urgent assessment of the airway, and of the need for immediate intubation (with in-line spinal stabilisation). A very high spinal cord injury may have resulted in respiratory arrest.

B) - Evaluation of respiratory function and chest injuries. This patient can potentially have a tension or non-tension pneumothorax or haemothorax on the left side, and this diagnosis needs to be made early in the primary survey. High FiO₂ should be administered. One should look for paradoxical respiration pattern due to flail chest, or diaphragmatic breathing due to high spinal cord injury.

C)

The major differentials for this shock state include the following:

• Left haemothorax
• Abdominal haematoma due to splenic injury
• Cardiac tamponade
• High spinal cord section

Features of hypovolemia (eg. cool peripheries, pallor) should be sought. In any case, volume replacement is indicated in each of the abovementioned differentials. Blood should be sampled for crossmatch, and uncrossmatched blood should be transfused if the patient is demonstrating features of anaemia. Large-bore IV access should be established.

Blood products should be preferentially used for resuscitation, with a 1:1:1 ratio of PRBCs, FFP and platelets. The MAP target for fluid resuscitation should be a MAP >50mmHg.

D) The level of consciousness should be assessed. Features of spinal cord injury should be pursued on examination

E) The patient needs to be rewarmed (presuming they are hypothermic) and a blood warmer should be connected to maintain normothermia in spite of massive resuscitation

After the completion of the primary survery, the following investigations must urgently take place:

• CXR
• Pelvic XR
• FAST US of the abdomen chest and praecordium can rapidly differentiate between the abovementioned causes of shock.
• CT trauma series, if available

This pathway of investigation should be abandoned and urgent damage control surgery should take place if any of the above assessment methods make it abundantly clear that a catastrophic intraabdominal source of bleeding is responsible for the shock state.

References

ATLS student course manual, 8th edition (Chapter 5) - American College of Surgeons Committee on Trauma

College Answer

At this stage stability must be confirmed in other areas as well as haemo-dynamic. Blood pressure goals should consider spinal perfusion pressure if spinal injury is suspected (may be unable to achieve target “normal” MAP in presence of high spinal injury), steroids should be considered in the first 8 hours following injury (“NASCIS II”).

Now is the time to ensure that oxygenation and ventilation are stable; coagulation should be assessed and corrected if abnormal; and temperature should be in target range.

Secondary survey should be completed, including detailed neurologic examination (eg. in an attempt to exclude spinal injury). Spinal precautions should be continued for the interim. The primary X rays should be obtained (CXR, pelvic X-ray, lateral cervical spine) but now additional
X-rays should be obtained as indicated (repeat CXR, spinal series ± CTs eg. of head, cervical spine, chest, abdomen). Long bone injuries should be sought and excluded (or treated).

Other specialists should be asked to review patient as indicated (eg. cardiothoracic, spinal). Antibiotics and tetanus prophylaxis should be prescribed if indicated.
Anti-ulcer prophylaxis should be instituted, and as should pharmacological prophylaxis for DVTs when contraindications subside. Enteral feeding should be started as soon as practical, and glycaemic control should be implemented.

Discussion

This question is about the management of a trauma patient who returns from theare following damage control surgery. It seems some definitive management (splenectomy) has already taken place.

The college mention the use of corticosteroids in spinal cord injury; this is not something we do any more. In fact, there is no strong evidence behind any of the pharmacologial measures. However, the idea of "spinal perfusion pressure" is interesting. The current guidelines are not so bold as to suggest a MAP of 85, but they do recommend the systolic not be allowed to drop below 90, which is slightly contrary to the doctrine of permissive hypotension in damage control resuscitation.

Anyway, the college baits us with the words "little is known of his other injuries".

A secondary survey must take place, including the following:

• Coags, troponin, CK, EUC FBC and LFTs
• ECG
• Repeat CXR
• Xrays of the long bones
• CT trauma series, including fine slice through the C spine

A systematic, boring response to the question of supportive management would resemble the following:

A) - Airway control and adequate secretion clearance with suctioning, given the increased risk of pneumonia

B) - Adequate ventilation and oxygenation, with sufficient PEEP to splint the rib fractures and prevent left-sided atelectasis

C) - Haemodynamic control, with less conservative MAP targets - maintaining a MAP >65 mmHg, and SBP >90mmHg.

D) - Attention to spinal precautions, and deescalation of hard collar as soon as the spine is cleared. Adequate analgesia.

E) - Control of electrlytes, paying attention to the calcium

F) Adequate fluid resuscitation, aiming for a high normal urine output given the tendency of these patients to dveelop ATN due to haemoglobinuria and rhabdomyolysis

G) Reassessment of the abdomen to exclude ongoing bleeding.

Insertion of an NG tube if permitted by facial injuries, and commencement of enteral feeding, with the aim to supply a daily minimum of 2g protein per kg of body mass.

Ulcer prophylaxis with PPI may not be necessary of the enteral nutrition is well tolerated.

Glucose control should be established with insulin as needed.

H) Corection of anaemia and dilutional coagulopathy;

Attention to thromboprophylaxis, given that trauma (and especially spinal trauma) patients have the highest likelihood of developing DVTs.

I) No indication for antibiotics at this stage. An ADT should be given IM if it was omitted in ED.

References

Hurlbert, R. John. "Strategies of medical intervention in the management of acute spinal cord injury." Spine 31.11S (2006): S16-S21.

AANS Guidelines for the management of acute cervical spine and spinal cord injuries.

"Blood pressure management after acute spinal cord injury." Neurosurgery. 2002 Mar;50(3 Suppl):S58-62.

College Answer

Many candidates provided long lists of regional techniques, but did address the issues of when to use and when not to use a technique. Consider asking “why don’t we perform more epidurals in our patients?”.

Advantages of regional anaesthetic techniques include

•    reduced narcotic use to achieve analgesia– less respiratory depression, especially in chest injury or high risk of respiratory failure (elderly, COPD, etc)

•    less ileus (reduce risk of aspiration, tolerance of enteral feeds, etc)

•    less interference with mental status (harder to attribute obtundation to drugs or injury)

•    reduces use of non narcotics, eg NSAIDS (renal impairment, platelet function); tramadol (confusion in elderly); paracetamol – all just adjuncts anyway and less efficacious than regional in severe pain; ketamine – hypertension, tachycardia, dissociative effects, etc)

Disadvantages (general)

•    often redundant in sedated, ventilated patient

•    not proven in critically-ill to be any better in terms of outcome in critically ill patients – thus not a lot of strong evidence to support use in critically ill over above alternatives

•    problems with local anaesthetic toxicity fairly uncommon with newer agents given by infusion (eg ropivacaine via epidural) – but some other regional blocks (eg brachial plexus catheters, pleural catheters, etc can get to higher dosages and greater risk of toxicity)

•    may still need narcotic adjuncts

•    technical expertise required

•    difficulty covering multiple sources of pain

•    sympathetic blockade, problems with coagulopathy, need for patient positioning, anatomical landmarks may be difficult

•    catheters over longer term => risk of infection. Also confused patients more likely to dislodge them

•    monitoring of blockade in uncooperative patient may be impossible

•    removal with DVT prophylaxis may be an issue

Disadvantages (local)

•    related to sites of placement – eg vascular injection, pneumothorax, other neuro injury, etc, etc. Also neuro blockade in presence of “uncleared” neurological injury and following plastic surgery for nerve injury.

Discussion

It is difficult to lump epidural and other regional techniques together.

So, I un-lumped them, for largely cosmetic reasons. 

References

Wu, Christopher L., et al. "Thoracic epidural analgesia versus intravenous patient-controlled analgesia for the treatment of rib fracture pain after motor vehicle crash." Journal of Trauma-Injury, Infection, and Critical Care 47.3 (1999): 564-567.

MACKERSIE, ROBERT C., et al. "Prospective evaluation of epidural and intravenous administration of fentanyl for pain control and restoration of ventilatory function following multiple rib fractures." Journal of Trauma-Injury, Infection, and Critical Care 31.4 (1991): 443-451.

Kieninger, Alicia N., et al. "Epidural versus intravenous pain control in elderly patients with rib fractures." The American journal of surgery 189.3 (2005): 327-330.

Moon, M. Ryan, et al. "Prospective, randomized comparison of epidural versus parenteral opioid analgesia in thoracic trauma." Annals of surgery 229.5 (1999): 684.

Jarvis, Amy M., et al. "Comparison of epidural versus parenteral analgesia for traumatic rib fractures: a meta-analysis." OPUS 12 (2009): 50-57.

Scherer, R., et al. "Complications related to thoracic epidural analgesia: a prospective study in 1071 surgical patients." Acta anaesthesiologica scandinavica 37.4 (1993): 370-374.

Kapral, Stephan, et al. "The effects of thoracic epidural anesthesia on intraoperative visceral perfusion and metabolism." Anesthesia & Analgesia 88.2 (1999): 402-406.

College Answer

Key Features

a)  CO/CN toxicity – Lactic acidosis, high SvO2, mental confusion, hypotension
b)  Upper airway obstruction from airway oedema – soot in the pharynx, singed hair, stridor, hoarseness, oropharyngeal erythema, oedema and blistering
c)  Chemical burns to the lungs which result in mucosal damage, bronchitis, mucous plugging and pulmonary oedema – Bronchospasm, bronchorrhoea, raised a-a gradient

Discussion

Smoke inhalation injuries are discussed in greater detail in the answer to Question 26 from the first paper of 2012.  One can divide this issue into mechanisms of thermal and inhalational injury, pathophysiological changes, damage at varying anatomical levels, and probably all of the above are reasonable approaches.

Presented in this fashion, it could even be turned into a table.

Everyone likes tables.

Or, one can organise them by anatomical location:

A good summary of airway burns can be found in this 2012 article

References

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.

Gaissert, Henning A., Robert H. Lofgren, and Hermes C. Grillo. "Upper airway compromise after inhalation injury. Complex strictures of the larynx and trachea and their management." Annals of surgery 218.5 (1993): 672.

Bishop, Sophie, and Simon Maguire. "Anaesthesia and intensive care for major burns." Continuing Education in Anaesthesia, Critical Care & Pain 12.3 (2012): 118-122.

College Answer

Causes:

Abdominal trauma
Massive retroperitoneal hematomas

Major burns following fluid resuscitation

Massive intra-abdominal hemorhage

Major Consequences:
a)  Decrease in Qt because of a decrease in venous return

b)  Decreased renal perfusion

c)  Impaired thoracic compliance

d)  Bowel ischemia

Management
a)  Monitoring intra-abdominal pressure

b)  Abdominal decompression

c)  Adequate decompression of GI tract

d)  Avoiding excess fluid resuscitation

Discussion

A slightly more formal-looking exploration of abdominal compartment syndrome can be found in Question 8 from the first paper of 2013. Brief notes on the pathophysiology of abdominal compartment pressure and its measurement are available, with references for the time-rich exam candidate.

Causes of abdominal compartment syndrome:

Primary ACS: increased compartment pressure due to abdominal pathology

• Massive ascites, eg. portal vein thrombosis
• Retroperitoneal hematoma
• Abdominal trauma with crush injury

Secondary ACS: increased compartment pressure due to fluid resuscitation

• Abdominal infection eg peritonitis
• Pancreatitis
• Major trunk burns with massive fluid resusicitation (thus, restriction of abdominal expansion)

Consequences of abdominal compartment syndrome:

• Hypotension due to decreased preload
• Renal failure due to decreased renal blood flow (venous and arterial)
• Lactic acidosis due to impared hepatic blood flow
• Gastric erosions and ulceration due to impaired gastric blood flow
• Intestinal ischaemia due to impaired intestinal blood flow
• Poor gut transit, ileus, and decreased tolerance of NG feeds
• Decreased FRC and therfore increased atelectasis, worsening gas exchange, decreased compliance of the respiratory system, leading to hypoxia and hypercapnea
• Raised intracranial pressure

Management of abdominal compartment syndrome:

• Prevention:
  • Avoid overvigorous fluid resusictation
  • Patients at risk of ACS should perhaps remain open-abdomen after largescale abdominal surgery
  • monitor the compartment pressure
• Management
  • Staged closure of abdominal defect
  • Vasopressors to maintain MAP within a certain range (some aim for an abdominal perfsion pressure of >60mmHg)
  • Titrate PEEP to optimise V-Q matching, to maintain normoxia and normocapnea
  • If compartment pressure remains elevated, neuromuscular blockade can be considered
  • If pressure remains high in spire of NMJ blockade, may consider opening the abdomen (if it is closed)

References

Cheatham, Michael Lee. "Abdominal compartment syndrome." Current opinion in critical care 15.2 (2009): 154-162.

Maerz, Linda, and Lewis J. Kaplan. "Abdominal compartment syndrome."Critical care medicine 36.4 (2008): S212-S215.

Saggi, Bob H., et al. "Abdominal compartment syndrome." Journal of Trauma-Injury, Infection, and Critical Care 45.3 (1998): 597-609.

Cheatham, Michael L., et al. "Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension." Journal of Trauma-Injury, Infection, and Critical Care 49.4 (2000): 621-627.

College Answer

Symptoms ie   dyspnoea, confusion,

Signs               Respiratory, CNS, cutaneous,

Causes            Long Bone #s, smaller bones, sickle cell, compression liposuction etc

Treatment:      Supportive ie O2, CPAP, Ventilation.

Discussion

For a ten mark question, the college answer - though technically hitting all the correct notes- appears a little austere.

A more generously expanded answer could be constructed using the various published review literature on the subject. It would resemble something like the following:

Symptoms of fat embolism

• Confusion is usually the earliest symptom
• Dyspnoea
• Tachypnoea
• Haemoptysis
• Usually, with a latent period (say, some days after the manipulation of a fracture).

Signs of fat embolism

• • Respiratory features: moist crepitations over all lung fields, hypoxia, cyanosis
  • Characteristic petechial rash, usually over the anterior axillary fold and at the root of the neck, as well as on the buccal mucosa and the conjunctiva. This distribution can be explained by fat droplets accumulating in the aortic arch prior to embolisation to nondependent skin via the subclavian and carotid vessels.

• • Fever
  • Tachycarda
  • Retinal haemorrhages
  • Visible fat droplets on ophthalmoscopy
  • Jaundice
  • Renal impairment
  • Anaesthetists often note a sudden drop in end-tidal CO₂ concentration during a stable steady state.

Laboratory features

• • Thrombocytopenia
  • Anaemia (sudden decrease)
  • High ESR
  • Fat macroglobulinaemia

Causes of fat embolism

• • Long bone fractures
  • Liposuction
  • Bone marrow harvest
  • Lymphography
  • Acute pancreatitis
  • Necrosis of a fatty liver
  • Acute sickle cell crisis (with marrow necrosis)

Management of fat embolism

• Boring, non-specific treatment:
  • O₂ supplementation
  • Positive pressure ventilation
  • Correction of coagulopathy
  • Replacement of platelets
  • Correction of the source problem (i.e. reduction of fractures)

Weird management strategies have been advanced, such as heparin (which supposedly encourage lipase activity and discourages the formation of pletelt aggregates). Alcohol intoxication seems to be somehow protective against fat embolism.

References

Mellor, A., and N. Soni. "Fat embolism." Anaesthesia 56.2 (2001): 145-154.

Gurd, Alan R., and R. I. Wilson. "The fat embolism syndrome." Journal of Bone & Joint Surgery, British Volume 56.3 (1974): 408-416.

Myers, R., and J. J. Taljaard. "Blood alcohol and fat embolism syndrome." J Bone Joint Surg Am 59.7 (1977): 878-880.

Hofmann, S., G. Huemer, and M. Salzer. "Pathophysiology and management of the fat embolism syndrome." Anaesthesia 53.S2 (1998): 35-37.

College Answer

a High flow 02 to avoid maternal and fetal distress

b.  Reduced respiratory reserve

c.  Matemal compensation for blood loss is at ilie expense of uteroplacental flow

d.  Avoid aortocaval compression

e.  Transfusion should be Rh compatible

f   All Rh negative mothers to receive lg because of the immunological risk of minor fetomatemal hemorrhage

g.  Minimal exposure to radiation

h.  U/S may be preferable

i.    Retroperitoneal hemorrhage, placental abruption, fetal distress may occur

j.     Premature labour may be precipitated

k.  Need for regular cardiotocograph.

I.     ·Pelvic binders may be unsuitable

m. Physiological anemia of pregnancy

Discussion

The management of the pregnant poly-trauma patient is discussed elsewhere.

This is one of those questions which could fit equally well into the "pregnancy and obstetrics" category.

In summary:

• Airway issues
  • The airway is more difficult to control.
  • There is an increased risk of aspiration due to decreased gastric emptying and weakened lower oesophageal sphincter.
• Respiratory issues
  • The respiratory function is impaired by decreased FRC;
  • One needs to insert their chest drains higher, so as to avoid the pushed-up diaphragms
  • When setting up the ventilator, one needs to keep in mind that the PaCO₂ is supposed to be 30mmHg in late pregnancy.
• Circulatory issues
  • The total blood volume has expanded, the cardiac output is high, and thus signs of shock will develop late.
  • Vena cava compression means the patient needs to be positioned at a 30° tilt
• Neonatal and foetal welfare
  • Pelvic binders are inappropriate
  • Pelvic fractures may threaten the near-term foetus
  • Placental abruption may result in massive haemorrhage and needs to be excluded early in the primary survey
  • Foetal heart rate monitoring is essential
  • Early transfer to an O&G-equipped hospital is essential
  • Retroperitoneal haemorrhage from dilated pelvic veins can be difficult to assess without ultrasound
  • A vaginal examination needs to be performed, looking for amniotic fluid (a pH of 7.0-7.5 will confirm this - the normal vaginal pH is much lower than this)
• Transfusion and general haematology issues
  • Rhesus-negative mothers need to receive IV immunoglobulin at least within 48 hours of the trauma
  • Transfusion needs to be Rh compatible
  • The pregnant trauma patient is in an even more hypercoagulable state than the normal trauma patient, and thus requires special attention to DVT prophylaxis
• Drug choices
  • Antibiotic choices are limited; tetracyclines and fluoroquinolones are to be avoided
  • If urgent caesarian delivery is planned, intubation drugs wil affect the foetus; thus there is need for NICU involvement for ventilation

Issues to consider in investigations and the secondary survey

• The usual barrage of blood tests remains unchanged.
• FBC, EUC, CMP LFT coags and crossmatch get sent away just as they would in any trauma patient, but the savvy candidate will mention the need for Rh blood grouping to prevent Rh isoimmunisation (where the mother is Rh negative and the foetus is Rh positive). An administration of anti-Rh IVIG can mop up any Rh-positive foetal erythrocytes which might have haemorrhaged into the maternal circulation, preventing the mother from developing her own anti-Rh antibodies (and thus preventing the haemolytic disease of the newborn).
• An abdominal ultrasound (FAST) is still performed, with additional focus on the uterus; uterine rupture or placental abruption need to be detected early.
• Foetal welfare can be monitored by CTG, and the O&G specialist should be invited to perfrom their own focused ultrasound to investigate the pregnancy.
• Though radiation exposure is undesirable, it is tolerated (particularly in late term pregnancy) because organogenesis has already taken place, and because the risk from ionising radiation exposure is minute in comparison to the risk of missed injuries and haemorrhage.

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Soar, Jasmeet, et al. "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution." Resuscitation 81.10 (2010): 1400-1433.

Mattox, Kenneth L., and Laura Goetzl. "Trauma in pregnancy." Critical care medicine 33.10 (2005): S385-S389.

DROST, THOMAS F., et al. "Major trauma in pregnant women: maternal/fetal outcome." Journal of Trauma-Injury, Infection, and Critical Care 30.5 (1990): 574-578.

College Answer

Important considerations include:

a) Other injuries need to be ruled accounted for that may have implications – spinal injury, intra-abdo injury (though abdo pain from intra-abdo injury not likely to be totally masked by epidural local anaesthetic)

b) Coagulopathy is a contraindication

c) Epidural Local anaesthetic/opiate combination at thoracic level likely to be associated with hypotension/bradycardia needing volume and likely inotropic support –relatively contraindicated in a middle aged male on beta blockers.

Infusion vs bolus vs PCEA

d) Other epidural analgesics – opiate alone eg fentanyl, pethidine or epidural clonidine –

doses/frequency

Complications:

a)  Hypotension, bradycardia

b)  Masking of abdominal / evolving neurological signs

c)  Inadequate analgesia due to limited / patchy block

d)  Increased pain in unblocked areas – relative phenomenon esp with bony injury eg shoulder.

e)  Short duration of blockade – catheters usually removed after 3 days.

f)      Epidural haematoma / abscess

g)  Epidural drug side effects – pruritus, nausea, respiratory depression

h)  Hypotension on mobilisation

Discussion

Thoracic epidural anaesthesia is compared to a parenteral opiate PCA in Question 26 from the first paper of 2010.

Management considerations:

• More difficult to assess the patient; abdominal block tends to obscure changes in clinical condition
• Choice of drug needs to be considered
• The injuries will persist longer then the catheter (max. 5 days)
• Contraindicated in coagulopathy
• May be contraindicated in bony vertebral injury

Complications of thoracic epidural

• Hypotension will develop
• Bradycardia will develop
• Changes in sympathetic innervation of the abdominal viscera may increase abdominal visceral perfusion, thus increasing blood loss from damaged solid organs.
• Opiates will cause pruritis
• There may be respiratory depression and respiratory muscle paralysis with a high block
• There is a risk of infection (epidural abscess)
• There is a risk of epidural haematoma
• There is a risk of dural puncture or spinal cord damage
• The epidural may not work, or the block may be patchy

References

Wu, Christopher L., et al. "Thoracic epidural analgesia versus intravenous patient-controlled analgesia for the treatment of rib fracture pain after motor vehicle crash." Journal of Trauma-Injury, Infection, and Critical Care 47.3 (1999): 564-567.

MACKERSIE, ROBERT C., et al. "Prospective evaluation of epidural and intravenous administration of fentanyl for pain control and restoration of ventilatory function following multiple rib fractures." Journal of Trauma-Injury, Infection, and Critical Care 31.4 (1991): 443-451.

Kieninger, Alicia N., et al. "Epidural versus intravenous pain control in elderly patients with rib fractures." The American journal of surgery 189.3 (2005): 327-330.

Moon, M. Ryan, et al. "Prospective, randomized comparison of epidural versus parenteral opioid analgesia in thoracic trauma." Annals of surgery 229.5 (1999): 684.

Jarvis, Amy M., et al. "Comparison of epidural versus parenteral analgesia for traumatic rib fractures: a meta-analysis." OPUS 12 (2009): 50-57.

Scherer, R., et al. "Complications related to thoracic epidural analgesia: a prospective study in 1071 surgical patients." Acta anaesthesiologica scandinavica 37.4 (1993): 370-374.

Kapral, Stephan, et al. "The effects of thoracic epidural anesthesia on intraoperative visceral perfusion and metabolism." Anesthesia & Analgesia 88.2 (1999): 402-406.

College Answer

a) List 5 clinical signs commonly associated  with base of skull fractures.

1)  CSF rhinorrhoea
2)  CSF otorrhoea
3)  Battle’s sign
4)  Raccoon eyes
5)  Haemotympanum
6)  Cranial nerve palsies.

b) List 3 life threatening complications of base of skull fractures

Panhypopituitarism
Basal meningitis
Carotid artery trauma or pseudoaneurysms
Cavernous sinus thrombosis

c) Briefly outline the role of prophylactic antibiotics in the management of base of skull fractures.

BOS # predispose patients to meningitis because of possible direct contact of bacteria in paranasal sinuses, nasopharynx or middle ear with CNS. Also CSF leak is associated with a greater risk of contacting meningitis. Few RCTs exist and the primary end point was a reduction in meningitis.

1) No role for prophylactic antibiotic therapy whether there is CSF leak or not.
2) Do not reduce the risk of meningitis.

Discussion

Features of base of skull fracture are better covered in Question 14.3 from the second paper of 2010.

Base of skull fracture is also asked about in Question 30.1 from the second paper of 2011.

In brief, the features are:

• CSF otorrhoea
• Haemotympanum
• Racoon eyes (adults call it "bilateral periorbital haematoma")
• CSF rhinorrhoea
• Cranial nerve abnormalities:
  • CNI damage (loss of olfaction)
  • CN II entrapment (visual field defects or blindness)
  • CN VII palsy (facial paralysis)
  • CN VIII palsy (deafness)
• Blephaerohaematoma (i.e. of the eyelid)
• Pneumoencephalus (more of a radiological finding)
• Bloody otorrhoea
• CSF otorrhoea

Complications of a base of skull fracture include the following:

• Meningitis/encephalitis
• Carotid artery dissection
• Cavernous sinus thrombosis
• Pneumocephalus due to positive pressure ventilation
• Accidental cannulation of the cranial cavity with the nasogastric tube
• Carotido-cavernous fistula
• CSF fistula

As for the antibiotics; a 1998 meta-analysis had concluded that "antibiotic prophylaxis after basilar skull fractures does not appear to decrease the risk of meningitis." This conclusion was supported bya 2011 Cochrane review.

References

Pretto, Flores L., C. S. De Almeida, and L. A. Casulari. "Positive predictive values of selected clinical signs associated with skull base fractures." Journal of neurosurgical sciences 44.2 (2000): 77-82.

Tubbs, R. Shane, et al. "William Henry Battle and Battle's sign: mastoid ecchymosis as an indicator of basilar skull fracture: Historical vignette." Journal of neurosurgery 112.1 (2010): 186-188.

Katzen, J. Timothy, et al. "Craniofacial and skull base trauma." Journal of Trauma and Acute Care Surgery 54.5 (2003): 1026-1034.

Samii, Madjid, and Marcos Tatagiba. "Skull base trauma: diagnosis and management." Neurological research 24.2 (2002): 147-156.

Villalobos, Tibisay, et al. "Antibiotic prophylaxis after basilar skull fractures: a meta-analysis." Clinical infectious diseases 27.2 (1998): 364-365.

Ratilal, Bernardo O., et al. "Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures." Cochrane Database Syst Rev 8 (2011).

College Answer

Key feature. Damage Control Surgery involves a 4 phase approach to major emergency abdominal injuries:

•    recognition of at risk patient
•    Limited, focused surgery for control of haemorrhage and address contamination with temporary abdominal closure,

•    restoration of near normal physiology – cardiovascular resuscitation, rewarming (usually active) if hypothermic, correction of coagulopathy (blood products and aFVII) and acidosis.  – with optimization of ventilation and
•    re laparotomy at 24 – 36 hours with removal of packs, definitive surgery and formal abdominal closure, where possible.

Important complications

New onset or uncontrolled surgical bleeding
Abdominal compartment syndrome (ACS),
inability to wake and wean (open abdomen / planned return to theatre)
missed injuries in the multiply injured patient (need for full examination on admission)

Discussion

An excellent article on this is available from 2004 (Critical Care Clinics). The topic of damage control surgery is also discussed briefly in the answer to Question 20 from the first paper of 2011. To simplify revision, that answer is replicated below:

Definition:

• Rapid termination of an operation after control of life-threatening bleeding and contamination followed by correction of physiologic abnormalities and definitive management.

Rationale:

• Hypothermia, acidosis, and coagulopathy render attempts at definitive surgical repair less likely to succeed.
• The surgical control of immediately lifethreatening injuries and the establishment of haemostasis must be achieved early, but definitive management can be delayed in most cases.
• Definitive management can take place safely once the physiological abnormalities are corrected.

Key principles:

• Control of haemorrhage
• Control of contamination
• Use of temporary shunts to bypass ligated vascular injuries
• Delay of abdominal closure, or temporary wound closure

Complications upon returning to the ICU:

Remember that the patient was not being definitively managed in theatre; if you are lucky they are bleeding slightly less than they were before they went to theatre, but in general the resuscitation is only half-complete. Not only that, but they were probably rushed through the ED, and a secondary survey (or trauma CT) may not have been performed.

Thus, one can anticipate the following:

• Old, uncontrolled traumatic bleeding
• New, uncontrolled surgical bleeding
• Uncontrolled coagulopathy, hypothermia and acidosis
• An open abdomen (thus, high sedation and analgesia requirements)
• Abdominal compartment syndrome (if they decided to close it)
• Missed injuries

References

Morrison, C. Anne, et al. "Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in trauma patients with hemorrhagic shock: preliminary results of a randomized controlled trial." Journal of Trauma and Acute Care Surgery 70.3 (2011): 652-663.

Kaafarani, H. M. A., and G. C. Velmahos. "Damage Control Resuscitation In Trauma." Scandinavian Journal of Surgery (2014): 1457496914524388.

Jaunoo, S. S., and D. P. Harji. "Damage control surgery." International Journal of Surgery 7.2 (2009): 110-113.

Schreiber, Martin A. "Damage control surgery." Critical care clinics 20.1 (2004): 101-118.

College Answer

a) Complications
•          Arrhythmia (severe hypothermia)
•          Pneumonia
•          Aspiration pneumonitis (water, sand, vomit)
•          Acute lung injury/ARDS
•          Hypoxic encephalopathy
•          Multiple organ dysfunction
•          Trauma brain injury or other traumatic injuries (particularly at surf beaches or jetties)
•          Electrolyte abnormality

b) Risk factors for severe neurological injury
•          At scene
o Immersion > 10 minutes
o Delay in CPR commencement
•          In the Emergency Department
o Asystole on arrival in ED
o CPR > 25 minutes
o Fixed dilated pupils and GCS< 5
o Fixed dilated pupils and pH < 7.0
•          In the ICU
o No spontaneous movements and abnormal brainstem function at 24 hours
o Abnormal CT scan within 36 hours of submersion

Discussion

The complications from drowning are best expressed as a structured list.

Briefly:

A) - Aspiration of contaminated water or salt water

B) - Pulmonary oedema, atelectasis, poor gas exchange. High risk of pneumonia.

- Possibly, also ARDS due to surfactant loss (seawater submersion)

C) - Hypotension, circulatory collapse, arrhythmia

D) - Hypoxic brain injury

E) - Transient electrolyte disturbance due to even prolonged submersion. Hypothermia

F) - Hypovolemia due to hydrostatic effects of immersion. Renal failure due to global hypoxia.

It would appear the college generally just wanted the candidates to regurgitate the contents of Box 80.1 (page 820) from the "Submersion" chapter by Cyrus Edibam and Tim Bowles. 

Paraphrased, the box contains the following risk factors for death or severe neurological injury:

Factors at the site of submersion:

• Immersion for more than 5 minutes
• Delay in CPR of more than 10 minutes

Factors on presentation to the ED

• Fixed dilated pupils
• GCS of 3

Factors after admission to the ICU:

• GCS less than 6
• Arterial pH less than 7.00 upon arrival to ICU
• No spontaneous purposeful movement and the abnormal brainstem function after 48 hours
• Abnormal CT within 36 hours

The risk factors for poor neurological outcome which appear in the college answer suggest that they consider pre-hospital arrest may have occurred in this patient, in which case all the various cardiac arrest associated risk factors also apply.

The the above box, one may also add the following:

• Warm water drowning
• Submersion time > 10 minutes (a good independent predictor of neurological outcome)

Generally, the risk factors for poor neurological recovery after cardiac arrest can be extracted from the massive table which is featured in the answer to Question 4 from the second paper of 2013, "Describe the clinical signs and investigations available to predict poor neurological outcome in comatose survivors of cardiac arrest." 

References

The ARC ALS2 manual (2011) has a section on drowning (pp. 127). This was my main source of information.

Pearn, John. "The management of near drowning." British medical journal (Clinical research ed.) 291.6507 (1985): 1447.

Giammona, Samuel T., and Jerome H. Modell. "Drowning by total immersion: effects on pulmonary surfactant of distilled water, isotonic saline, and sea water." American Journal of Diseases of Children 114.6 (1967): 612-616.

Modell, Jerome H., et al. "Physiologic effects of near drowning with chlorinated fresh water, distilled water and isotonic saline." Anesthesiology 27.1 (1966): 33-41.

Young, Richard SK, Edwin L. Zalneraitis, and Elizabeth C. Dooling. "Neurological outcome in cold water drowning." Jama 244.11 (1980): 1233-1235.

Suominen, Pertti, et al. "Impact of age, submersion time and water temperature on outcome in near-drowning." Resuscitation 52.3 (2002): 247-254.

College Answer

Diaphragm rupture; 
a) Frequently no direct symptoms or signs referable

b) Shoulder pain
c) Left >> right, usually associated with other injuries

d) Intrathoracic bowel
e) Obscured diaphragm shadow on CXR
f)_If delayed presentation – post prandial epigastric or thoracic pain

g) Rarely gastric herniation or volvulus

Rectal examination:
a.   Absent anal tone  - cord lesion (unless relaxants administered)
b.  Palpable sphincter rupture
c.   Displaced (high riding) prostate – ruptured urethra
d.  High tenderness in anterior quadrants – ruptured viscus e.   Pelvic haematoma – pelvic fracture
f.   Palpable bony disruption – sacro-coccygeal / pelvic fracture

g.   Visible external lacerations / bleeding.

Discussion

Traumatic diaphragmatic rupture is usually pretty obscure.

Radiological findings are usually all the findings you get. The CXR is usually diagnostic.

However, one can occasionally unearth some of the following (non-specific) clinical features:

• Hypoxia
• Decreased air entry on the affected side
• Decreased chest excursion on the affected side
• Dull percussion note
• Bowel sounds in the chest
• Ileus and bowel obstruction due to volvulus
• Shoulder pain
• Stool or bile in the chest drain

As for the rectal examination; one looks for

• Sphincter tone (cord injury)
• Gross blood (GI tract injury)
• Swelling (pelvic haematoma)
• "High riding" prostate - urethral injury
• Mobile coccyx- sacral or coccygeal fracture
• Obvious external anal damage
• Disrupted rectal wall integrity

According to a recent review, the PR changed management in 1.2% of observed cases.

LITFL have some choice words about this investigation.

References

García-Navarro, Ana, et al. "[Traumatic diaphragmatic rupture]." Cirugia espanola 77.2 (2005): 105-107.

Morley, J. E. "Traumatic diaphragmatic rupture." Hospital 30.80 (1974): 1.

Willsher, Peter C., and Richard J. Cade. "Traumatic diaphragmatic rupture."Australian and New Zealand Journal of Surgery 61.3 (1991): 207-210.

Simpson, J., et al. "Traumatic diaphragmatic rupture: associated injuries and outcome." Annals of the Royal College of Surgeons of England 82.2 (2000): 97.

Porter, John M., and Caesar M. Ursic. "Digital rectal examination for trauma: does every patient need one?." The American surgeon 67.5 (2001): 438-441.

College Answer

You are asked to review a 64 year old man who has been brought to the emergency department having been burned in a house fire.  There is no coherent history available from the patient  and you observe that he is drowsy and confused, and, has a persistent cough.   His heart rate is 120 bpm, blood pressure 88/52 mmHg, respiratory rate 28 and oxygen saturations are 94 % on high flow oxygen via a non re-breather mask.

30.1     List the initial priorities in management.

1)  Resuscitation including primary and secondary survey
2)  Assessment and management of potential airway burn injury – mention consideration of early intubation, not cutting ET tubes and avoiding nasal tubes.
3)  Obtain large bore iv access and administration of fluid bolus (20mls/kg) for probable hypovolaemic shock- mention that groins are usually spared in burns and are a good site for clean skin vas cath access.
4)  Look for signs of traumatic injury and assess extent of body surface area and depth of burn
5)  Awareness of risk of hypothermia
6)  Seek collateral history for past medical history and medication history and history of acute events

30.2     What features on history and examination would suggest a significant airway injury?

1.  Burns occurring in a closed space
2.  Cough, stridor, hoarseness of voice
3.  Burns to face, lips, mouth, pharynx or nasal mucosa
4.  Soot in sputum, nose or mouth
5.  Hypoxaemia or dyspnoea
6.  Carboxyhaemoglobin levels > 2%
7.  Acute confusional state or depressed level of consciousness

30.3     Give a differential diagnosis for his conscious level.

1.  Traumatic brain injury
2.  Carbon monoxide / CN - poisoning
3.  Alcohol intoxication/drug overdose
4.  Other pathology precipitating loss of consciousness eg stroke, intracranial haemorrhage, seizure-related, hypoglycaemia

Discussion

This question is identical to Question 11 from the first paper of 2013, and closely resembles Question 28 from the second paper of 2010 (except in 2010 the 64 year old male mutated into a three year old child).

References

College Answer

1. Raccon eyes
2. Battle’s sign
3. CSf rhinorrhoea
4. CSF otorrhoea
5. Hemotympanum
6. Lower cranial nerve palsies

Discussion

This question is very similar to Question 14.3 from the second paper of 2010 and Question 30.1 from the second paper of 2011.

References

College Answer

a)  Outline how burns are classified.

Burns are classified by depth of injury.

Superficial (formerly first degree):
•    Epidermis only

Partial Thickness (formerly second degree): 
•      Superficial

• Epidermis and upper layer of dermis

•      Deep

• Extend to deeper layer of dermis

Full Thickness (formerly third degree) 
•     All layers of dermis and may involve underlying tissue

b)  List three methods for estimating the total body surface area affected by a burn injury.

•    Lund-Browder Chart
•    The Rule of Nines
•    The Rule of Palm

c)  Other than the burn type and extent, list the other important features of the physical examination that should be noted as part of the initial clinical assessment  of the patient described above.

•    Basic   resuscitation   status:   Airway   patency,   Breathing,   Circulatory   status, Conscious level
•    Adequacy of resuscitation to date: heart rate, blood pressure, urine output
•    Evidence of associated trauma
•    Evidence of airway burn and inhalational injury: stridor, burns around nose and mouth, carbonaceous sputum
•    Presence of facial and/or corneal burns, perineal burns
•    Presence     of     circumferential    burns,     evidence    of     extremity    compartment syndrome, ventilator inadequacy
•    Evidence of rhabdomyolysis
•    Evidence of inhalation of toxic gases eg CO
•     Temperature
•    Adequacy of analgesia
•    Potential problems with vascular access
•    Evidence of drug / alcohol ingestion and/or co-morbid conditions eg epilepsy

Discussion

a)  Outline how burns are classified.

Little can be added to the college answer, as it is a fairly straightforward question. The table below comes from the Clinical Practice Guidelines of the Royal Children's Hospital in Melbourne.

b)  List three methods for estimating the total body surface area affected by a burn injury.

The college gives the following three methods:

• The Wallace Rule of Nines
  • The body is divided into areas each valued as 9%.
  • Not accurate in children
• The Rule of Palm
  • The palm is considered to be 1% of the body surface area.
  • Good for estimating very small, or very large burns.
• Lund-Browder Chart
  • Most accurate method; compensates for the change in body surface proportions in children

c)  Other than the burn type and extent, list the other important features of the physical examination that should be noted as part of the initial clinical assessment  of the patient described above.

The assessment of a burns patient is covered in greater detail by the BMJ series.

• ABCs
• Evidence of poor oxygen carriage or utilisation(carbon monoxide or cyanide toxicity)
• Evidence of associated trauma
• Evidence of airway burns
• Presence of circumferential burns
• Presence of corneal, perineal or genital burns
• Vascular access
• Hypothermia
• Flid balance (and vigorous resuscitation)
• Analgesia, and whether it is adequate
• Features of intoxication
• Features of non-accidental injury

References

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

PRUITT Jr, BASIL A., DARYL R. ERICKSON, and ALAN MORRIS. "Progressive pulmonary insufficiency and other pulmonary complications of thermal injury."Journal of Trauma and Acute Care Surgery 15.5 (1975): 269-379.

Hettiaratchy, Shehan, and Remo Papini. "Initial management of a major burn: II—assessment and resuscitation." Bmj 329.7457 (2004): 101-103.

Hettiaratchy, Shehan, and Peter Dziewulski. "Pathophysiology and types of burns." Bmj 328.7453 (2004): 1427-1429.

Ansermino, Mark, and Carolyn Hemsley. "Intensive care management and control of infection." Bmj 329.7459 (2004): 220-223

College Answer

Discussion

The college table is well organised, and little can be added to it, other than some literature references. In summary, a couple of biggish meta-analysis papers from 2009 both discovered the following key features:

• There was no mortality difference
• There was no ICU length of stay difference
• There was no hospital length of stay difference
• Epidural was associated with more hypotension
• PCA was associated with more pneumonia
• Pain control was better with epidural.

Thus:

References

Wu, Christopher L., et al. "Thoracic epidural analgesia versus intravenous patient-controlled analgesia for the treatment of rib fracture pain after motor vehicle crash." Journal of Trauma-Injury, Infection, and Critical Care 47.3 (1999): 564-567.

MACKERSIE, ROBERT C., et al. "Prospective evaluation of epidural and intravenous administration of fentanyl for pain control and restoration of ventilatory function following multiple rib fractures." Journal of Trauma-Injury, Infection, and Critical Care 31.4 (1991): 443-451.

Kieninger, Alicia N., et al. "Epidural versus intravenous pain control in elderly patients with rib fractures." The American journal of surgery 189.3 (2005): 327-330.

Moon, M. Ryan, et al. "Prospective, randomized comparison of epidural versus parenteral opioid analgesia in thoracic trauma." Annals of surgery 229.5 (1999): 684.

Jarvis, Amy M., et al. "Comparison of epidural versus parenteral analgesia for traumatic rib fractures: a meta-analysis." OPUS 12 (2009): 50-57.

College Answer

A clinical photograph of Battle’s sign was supplied.

b) What does it indicate? 
Base of skull fracture

c)  What associated signs support the diagnosis mentioned in Question 14.3 b?

•    CSF otorrhoea
•    Haemotympanum
•    Racoon eyes
•    CSF rhinorrhoea
•    Cranial nerve abnormalities

Discussion

This image was misappropriated from the ACI website ( NSW Agency for Clinical Innovation).

Battle's sign (named after Dr William Henry Battle, rather than any association with warfare) apparently has a 100% positive predictive value for base of skull fracture.

Features associated with a base of skull fracture include several features which the college did not mention. I have tagged them on to the end of their list, for completeness:

• CSF otorrhoea
• Haemotympanum
• Racoon eyes (adults call it "bilateral periorbital haematoma")
• CSF rhinorrhoea
• Cranial nerve abnormalities:
  • CNI damage (loss of olfaction)
  • CN II entrapment (visual field defects or blindness)
  • CN VII palsy (facial paralysis)
  • CN VIII palsy (deafness)
• Blephaerohaematoma (i.e. of the eyelid)
• Pneumoencephalus (more of a radiological finding)
• Bloody otorrhoea
• CSF otorrhoea

References

Pretto, Flores L., C. S. De Almeida, and L. A. Casulari. "Positive predictive values of selected clinical signs associated with skull base fractures." Journal of neurosurgical sciences 44.2 (2000): 77-82.

Tubbs, R. Shane, et al. "William Henry Battle and Battle's sign: mastoid ecchymosis as an indicator of basilar skull fracture: Historical vignette." Journal of neurosurgery 112.1 (2010): 186-188.

Katzen, J. Timothy, et al. "Craniofacial and skull base trauma." Journal of Trauma and Acute Care Surgery 54.5 (2003): 1026-1034.

Samii, Madjid, and Marcos Tatagiba. "Skull base trauma: diagnosis and management." Neurological research 24.2 (2002): 147-156.

College Answer

a.   Briefly outline the initial priorities in management.

•    Resuscitation including primary and secondary survey
•    Assessment and management of potential airway burn injury – mention consideration of early intubation,
•    Obtain large bore iv access and administration of fluid bolus (20mls/kg) for probable hypovolaemic shock- mention that groins are usually spared in burns and are a good site for clean skin vas cath access.
•    Look for signs of traumatic injury and assess extent of body surface area and depth of burn
•    Awareness of risk of hypothermia
•    Seek collateral history for past medical history and medication history and history of acute events

b.  List the features from the history and your examination of this child which would suggest a significant airway injury.

•    Burns occurring in a closed space
•    Cough, stridor, hoarseness of voice
•    Burns to face, lips, mouth, pharynx or nasal mucosa
•    Soot in sputum, nose or mouth
•    Hypoxaemia or
•    Dyspnoea
•    Carboxyhaemoglobin  levels > 2%
•    Acute confusional state or depressed level of consciousness

c.   List 4 likely causes for his altered conscious state.

•    Traumatic brain injury
•    Carbon monoxide / CN – poisoning
•    Hypoxic insult
•    Other     pathology     precipitating     loss     of     consciousness     eg     seizure-related, hypoglycaemia, drug ingestion

Discussion

This question - though posing as a question about a paediatric patient - closely resembles Question 11 from the first paper of 2013, where the candidates were asked exactly the same series of questions about a slightly singed 64 year old male.

References

College Answer

 “Damage  control  resuscitation”  as applied to the management  of the major trauma patient integrates permissive  hypotension,  haemostatic  resuscitation and damage control surgery.

Outline  the  key  principles  of  each  of  these  three  strategies,  including  the rationale.

a.   Permissive hypotension

1. Keep SBP low enough to avoid exsanguination but high enough to maintain perfusion.

2. Relates to disruption of an unstable clot by higher pressures and worsening of bleeding.

b.  Haemostatic resuscitation

i.       Correct hypothermia

1.    Decreases platelet responsiveness.
2.    Increases platelet sequestration in liver and spleen
3.    Reduces Factor function eg Factors XI and XII
4.    Alters fibrinolysis

ii.       Correct acidosis

1.    pH strongly effects activity of Factors V, VIIa and X.
2.    Acidosis inhibits thrombin generation
3.    Cardiovascular  effects of acidosis (pH <7.2) – decreased  contractility  and CO,  vasodilatation  and  hypotension,  bradycardia  and  increased dysrhythmias.

iii.       Treat coagulopathy early and aggressively

1.    Many coagulopathic  changes  occur early after trauma,  therefore  need to correct early.
2.   Use much higher FFP to PRBC ratios (1:1/2:3) than previously used. Is associated with improved survival.
3.    Higher platelet to PRBC transfusion ratios also becoming more popular but evidence is less clear.
4.    Cryoprecipitate  provides an additional option for Factor replacement  for a lower volume of fluid.
5.    rFVIIa has been used in trauma, but off label and anecdotally.

iv.       The use of blood  products  instead  of isotonic  crystalloid  fluid aiming  for limited volume replacement

1.    Large   volume   crystalloids   can   lead   to   dilutional   coagulopathy   and exacerbate bleeding.
2.    Crystalloids  have  no  O2  carrying  capacity  and  do  little  to  correct  the anaerobic metabolism and O2 debt associated with shock.
3.    Need less volume of blood product  therefore  likely to be less tissue and organ (eg lung, small intestine mucosa) oedema and failure (eg pulmonary oedema, abdominal compartment syndrome)
4.   Hypertonic saline is another option (proven restored microvascular flow, decreased tissue oedema, attenuated inflammatory response).

c.   Damage control surgery

1.    Management     of    the     metabolic    derangement     of    ongoing    bleeding supersedes the need for definitive surgery
2.    Abbreviated operations that control haemorrhage and contain spillage from the alimentary and urogenital tracts.
3.    Rapid   transfer   to  ICU   for   correction   of   acidosis,   coagulopathy   and hypothermia
4.    Definitive operation is deferred.
5.    These operations tend to have a high complication rate
6.    Survival is given preference over morbidity.

Discussion

Permissive hypotension

Definition:

• Allowing a subnormal MAP in a trauma patient;
• " The strategic decision to delay the initiation of fluid resuscitation and limit the volume of resuscitation fluids/blood products administered to the bleeding trauma patient by targeting a lower than normal blood pressure, usually a systolic blood pressure of 80–90 mmHg or a mean arterial pressure (MAP) of 50 mmHg" - Kaafarani et al, 2014

Rationale:

• In penetrating trauma, a lower MAP may improve hemostasis.
• Improved hemostasis may result in smaller transfusions, decreased coagulopathy, and less transfusion-associated adverse events

Key principles:

• Goal is hemostasis, rather than the actual low blood pressure
• MAP of 50 appears to be associated with decreased transfusion requirements but not increased adverse events

Haemostatic resuscitation

Definition:

• Rapid correction of hemostasis-impairing factors, such as hypothermia hypocalcemia and acidosis
• Resuscitation with a balanced combination of blood products, which in combination resemble the composition of whole blood, aiming to avoid dilutional coagulopathy.

Rationale:

• Unbalanced transfusion strategies lead to depletion of coagulation factors and exacerbation of dilutional coagulopathy.

Key principles:

• Early and aggressive transfusion of blood products aiming for a ratio of PRBCs, FFP, and platelets that approximates 1:1:1
• Use of hemostatic agents such as tranexamic acid (strongly supported by evidence)

Damage control surgery

An excellent article on this is available from 2004 (Critical Care Clinics)

Definition:

• Rapid termination of an operation after control of life-threatening bleeding and contamination followed by correction of physiologic abnormalities and definitive management.

Rationale:

• Hypothermia, acidosis, and coagulopathy render attempts at definitive surgical repair less likely to succeed.
• The surgical control of immediately lifethreatening injuries and the establishment of haemostasis must be achieved early, but definitive management can be delayed in most cases.
• Definitive management can take place safely once the physiological abnormalities are corrected.

Key principles:

• Control of haemorrhage
• Control of contamination
• Use of temporary shunts to bypass ligated vascular injuries
• Delay of abdominal closure, or temporary wound closure

References

Morrison, C. Anne, et al. "Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in trauma patients with hemorrhagic shock: preliminary results of a randomized controlled trial." Journal of Trauma and Acute Care Surgery 70.3 (2011): 652-663.

Kaafarani, H. M. A., and G. C. Velmahos. "Damage Control Resuscitation In Trauma." Scandinavian Journal of Surgery (2014): 1457496914524388.

Jaunoo, S. S., and D. P. Harji. "Damage control surgery." International Journal of Surgery 7.2 (2009): 110-113.

Schreiber, Martin A. "Damage control surgery." Critical care clinics 20.1 (2004): 101-118.

College Answer

a) List the likely causes of this man's shock state.

• Hypovolaemia
  • Ongoing blood loss related to trauma including missed injuries
  • Ongoing blood loss related to the emergency splenectomy
  • Under-resuscitation prior to ICU admission
• Cardiogenic causes
  • Cardiac contusion
  • Myocardial ischaemia with pre-existing heart disease
  • Primary arrhythmia unlikely cause as rate only 140
• Obstructive causes
  • Cardiac tamponade
  • Tension pneumothorax
  • Fat embolism syndrome (less likely with compound tibial fracture)
  • PE (less likely in acute stage)
• Distributive shock states (sepsis, spinal) and anaphylaxis unlikely with cold peripheries

b) List the clinical features that would help distinguish between these likely causes

• Hypovolaemia (ongoing bleeding / under-resuscitation)
  • Jugular venous pressure not visible
  • Positive response to passive leg raise
• Cardiac tamponade
  • Evidence of pulsus paradoxus upon auscultation in determining blood pressure
  • Raised jugular venous pressure upon inspiration (Kussmaul's sign)
  • Muffled heart sounds
• Cardiac contusion
  • Evidence of heart failure (raised jugular venous pressure, fine inspiratory crackles) 25
• Tension pneumothorax
  • Surgical emphysema
  • Tracheal deviation away from side of pneumothorax
  • Quiet breath sounds on side of side of pneumothorax

c) What echocardiographic features are associated with the causes you have described?

• Hypovolaemia
  • Reduced left ventricle end diastolic area
  • LV end systolic cavity obliteration
  • Reduced inferior vena cava diameter with pulse variation
• Cardiac tamponade
  • Right atrial systolic collapse and right ventricular diastolic collapse
  • Increased pericardial fluid
  • Swinging heart
  • Dilated IVC
• Cardiac contusion
  • Regional wall motion abnormalities
• Tension pneumothorax
  • Reduced left ventricle end diastolic area
  • Distended superior vena cavae

Discussion

This is a question about the different causes of shock in trauma, and their relevant features, with a focus on the early use of ultrasound.

Questions a) and b) clearly favour the candidate who has recently done the EMST and is familiar with the ATLS manual, which is the best source for this sort of thing. I made my own summaries when I did that course.

Because questions a) and b) are rather straightforward, I will focus more on the echocardiographic investigation of shock in trauma.

A certain James Lai (FRCA, FANZCA) has published a brilliant set of slides for public delectation, which does this topic justice.

A 2011 study has also demonstrated that fluid assessment can be carried out quickly and effectively using IVC diameter and IVC respiratory variation, although in this study a surgical intensivist or an ultrasonographer (rather than an ED registrar) were performing the study. To address this concern, the same group later demonstrated that even a shaved ape could be trained to perform a limited goal-directed TTE.

Interestingly, there are also many studies of transoesophageal echo in trauma. One is tempted to salute the bravery of the man who would jam a TOE probe down into a trauma patient. However, it certainly seems to be helpful. A study comparing transthoracic and trasoesophageal assessment has demonstrated that TOE is significantly more accurate, and that TTE in severe chest trauma usually gives unsatisfactory images.

References

Ferrada, Paula, et al. "Transthoracic focused rapid echocardiographic examination: real-time evaluation of fluid status in critically ill trauma patients."Journal of Trauma and Acute Care Surgery 70.1 (2011): 56-64.

Ferrada, Paula, et al. "Limited transthoracic echocardiogram: so easy any trauma attending can do it." Journal of Trauma and Acute Care Surgery 71.5 (2011): 1327-1332.

Chirillo, Fabio, et al. "Usefulness of transthoracic and transoesophageal echocardiography in recognition and management of cardiovascular injuries after blunt chest trauma." Heart 75.3 (1996): 301-306.

College Answer

a) What clinical sign is illustrated here?

Racoon or Panda eyes

b) What does this indicate?

Frontal base of skull fracture

c) List 2 other clincal signs which may be present which might support your answer in b?

Haemotympanum

CSF rhinorrohea or otorrhoea.

Discussion

I shall not waste too much time on this; only to point out that these signs have a very high positive predictive value for the presence of fractures and intracranial lesions.

Features of base of skull fracture are better covered in Question 14.3 from the second paper of 2010.

References

Herbella, Fernando AM, et al. "‘Raccoon Eyes’(periorbital haematoma) as a sign of skull base fracture." Injury 32.10 (2001): 745-747.

Pretto, Flores L., C. S. De Almeida, and L. A. Casulari. "Positive predictive values of selected clinical signs associated with skull base fractures." Journal of neurosurgical sciences 44.2 (2000): 77-82.

College Answer

a)  What clinical sign is illustrated in this picture?

Conjunctival petechiae

b)  What is the likely cause of the respiratory failure?

Fat embolism syndrome

Discussion

This question depicts a well known clinical sign and does not require a massive amount of cognitive effort.

Fat embolism syndrome has well-described features, and most people will connect trauma, breathing difficulty and conjunctival petechii. Fat rises, and the petechii appear on whatever the uppermost bodypart happens to be.

References

Gurd, Alan R., and R. I. Wilson. "The fat embolism syndrome." Journal of Bone & Joint Surgery, British Volume 56.3 (1974): 408-416.

Tachakra, S. S. "Distribution of skin petechiae in fat embolism rash." The Lancet 307.7954 (1976): 284-285.

College Answer

Life-threatening situation and management involves a multi-disciplinary approach following EMST guidelines.

• Obtain large-bore IV access (2 x 14G IV cannulae in ACFs) and send blood for cross-match and appropriate investigation

• Resuscitation fluids – crystalloid / colloid / blood (group specific or cross-matched dependent on urgency) administered to resuscitation end-points (MAP 60-70) in ratio of packed cells to FFP and platelets 1:1

• Avoid excessive movement of the pelvis and stabilize with sheet or commercial external pelvic stabilizer device

• CXR and secondary survey to look for other sources of bleeding

• Investigate for associated intra-abdominal or intra-pelvic injuries with FAST scan and/or CT scan if patient has stabilized with resuscitation

• Urgent consultation with interventional radiologist for angiography and embolization if other sources of bleeding excluded and if interventional radiology service available

• Urgent consultation with orthopaedic surgeon for external fixation

• Urgent consultation with general surgeon if intra-abdominal blood or evidence of intestinal perforation

• Aortic balloon occlusion also described as temporizing measure for patients in extremis from pelvic bleeding

• Analgesia

• Antibiotics if suspected / proven disruption of bowel or urinary tract

Discussion

This question would benefit from a systematic approach.

Supportive management:

A) Assessment of the airway and of the need for immediate intubation, while maintaining C-spine precautions

B) Ventilation with high FiO₂; investigation of possible aspiration with CXR and ABG.

C) Establishment of IV access and correction of hypovolemia;

urgent collection of a sample for a crossmatch of blood and urgent administration of available uncrossmatched blood.

Assess for retroperitoneal and pelvic bleeding with FAST +/- CT

D) Investigate causes of fall related to intracranial events, eg. ICH,

intoxication, seizure, etc.

E)Correct hypothermia, hypocalcemia and acidosis

Specific management:

Ensure haemostasis; the following options are available

• Blood product replacement to ensure normal coagulation function
• Pelvic binder
• Tranexamic acid and/or Factor VIIa
• Direct external compression of the aorta
• Intra-aortic balloon occlusion
• Reduction of acetabular fracture by lower limb traction
• Angioembolisation by interventional radiologist
• Surgical exploration / external fixation

What say the literature? This 2007 article essentially echoes the suggestions made by the college. 

References

ATLS student course manual, 8th edition (Chapter 5) - American College of Surgeons Committee on Trauma

Geeraerts, Thomas, et al. "Clinical review: initial management of blunt pelvic trauma patients with haemodynamic instability." Critical Care 11.1 (2007): 204.

Heetveld, Martin J., et al. "Hemodynamically unstable pelvic fractures: recent care and new guidelines." World journal of surgery 28.9 (2004): 904-909.

Martinelli, Thomas, et al. "Intra-aortic balloon occlusion to salvage patients with life-threatening hemorrhagic shocks from pelvic fractures." Journal of Trauma and Acute Care Surgery 68.4 (2010): 942-948.

Douma, Matthew, Katherine E. Smith, and Peter G. Brindley. "Temporization of Penetrating Abdominal-Pelvic Trauma With Manual External Aortic Compression: A Novel Case Report." Annals of emergency medicine (2013).

College Answer

Can affect 4 anatomic areas of the respiratory tract:

•  Supraglottal, tracheobronchial, and pulmonary parenchymal, and chest/abdominal wall.

Derangements include:

1.  Supraglottal

Loss of airway patency due to mucosal oedema

Loss of airway reflexes due to coma (e.g. blast Traumatic brain injury, intoxications such as carbon monoxide,)

2.  Tracheobronchial

Bronchospasm resulting from inhaled irritants

Mucosal oedema and endobronchial sloughing causing small airway occlusion, leading to intrapulmonary shunting.

3.  Pulmonary Parenchymal

Pulmonary (alveolar) oedema and collapse leading to decreased compliance, and further intrapulmonary shunting.

Loss of tracheobronchial epithelium and airway ciliary clearance contributing to tracheobronchitis and pneumonia.

Barotrauma, ARDS, pleural effusions, Ventilator associated pneumonia, TRALI and tracheobronchitis may all result from Intensive Care resuscitation, and treatments of the above.

4.  Mechanical

Circumferential full thickness burns of the chest and abdomen may cause reduced static compliance resulting in restrictive ventilator defect, made worse by large volumes of oedema with fluid resuscitation and capillary leak.

5.  Other

Toxic inhalation of carbon monoxide (CO) resulting in a left shift of the ODC and oxygen transport capacity (Carboxy Hb) and decreased cellular oxidative processes.

Other toxic gases NH3, HCL – pulmonary oedema,mucosal irritation and ALI CN- poisoning, cellular hypoxia

Increased metabolic requirements may overwhelm a respiratory system already impaired by all the above.

Discussion

This question asks, "what are the influences of smoke inhalation on respiratory function and gas exchange?" The college has decided to divide their answer anatomically. An equally valid systematic approach could see the candidate divide this issue into ventilation, diffusion, shunting and oxygen transport.

Ventilation

• Decreased respiratory effort due to a decreased level of consciousness
• Poor lung expansion resulting in a restrictive ventilatory defect, due to the presence of circumferential torso burns (or even non-circumferential)
• Poor air entry due to upper/lower airway burns; an obstructive pattern of ventilation
• Decreased lung compliance due to pulmonary thermal injury, ensuing pulmonary oedema and ARDS
  • Pulmonary oedema could also be due to the vigorous fluid resuscitation
  • ARDS could also be due to the SIRS which results from widespread burns.

Diffusion

• Decreased gas exchange due to increased pulmonary interstitial and alveolar fluid, due to pulmonary thermal injury

Shunting

• Increased shunt fraction due to collapse of oedematous lungs
• Increased shunt fraction due to airway swelling, obstruction and subsequent atelectasis
• Increased sputum retention and increased risk of pneumonia due to epithelial damage and impaired mucociliary escalator function.

Oxygen transport

• Decreased oxygen delivery to tissues, due to:
  • Metabolic/respiratory acidosis and consequent right shift of oxygen-haemoglobin dissociation curve
  • Carbon monoxide poisoning
• Decreased oxygen utilisation due to cyanode poisoning

References

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.

College Answer

In addition to management by a trauma team following EMST principles, this case requires additional early obstetric, neonatal and anaesthetic input. The operating theatre needs to be alerted to the possibility of the need for emergency Caesarian section. In an elderly primigravida this is likely to be a ‘precious’ pregnancy.

Other specific management issues include:

High flow oxygen to avoid maternal and fetal distress. Reduced respiratory reserve with decreased FRC. Potential for relative difficulty in intubation

Maternal compensation for blood loss is at the expense of utero-placental blood flow. Left lateral tilt to avoid aorto-caval compression.

Transfusion should be Rhesus compatible and immunoglobulin should be given if she is Rhesus negative because of the immunological effects of minor feto-maternal haemorrhage. 
Physiological anaemia of pregnancy

Minimise exposure to radiation – ultra-sound alternatives may be preferable. (DPL contra-indicated).

Retroperitoneal haemorrhage, placental abruption or fetal distress may occur and premature labour may be precipitated.

If pelvic fractures present, pelvic binders may not be suitable. Regular fetal monitoring is required. 
Bereavement issues in the event of an adverse fetal outcome

Discussion

This question forms a part of the "manage this pregnant trauma patient" spectrum of fellowship questions. For a general reference, one is directed to Question 3 from the first paper of 2007 (Outline the special considerations involved in the care of a pregnant patient involved in multi-trauma.). Specific features of severe multi-trauma in pregnancy can also be found on the page dedicated to this topic. 

In summary:

• Airway issues
  • The airway is more difficult to control.
  • There is an increased risk of aspiration due to decreased gastric emptying and weakened lower oesophageal sphincter.
• Respiratory issues
  • The respiratory function is impaired by decreased FRC;
  • One needs to insert their chest drains higher, so as to avoid the pushed-up diaphragms
  • When setting up the ventilator, one needs to keep in mind that the PaCO₂ is supposed to be 30mmHg in late pregnancy.
• Circulatory issues
  • The total blood volume has expanded, the cardiac output is high, and thus signs of shock will develop late.
  • Vena cava compression means the patient needs to be positioned at a 30° tilt
• Neonatal and foetal welfare
  • Pelvic binders are inappropriate
  • Pelvic fractures may threaten the near-term foetus
  • Placental abruption may result in massive haemorrhage and needs to be excluded early in the primary survey
  • Foetal heart rate monitoring is essential
  • Early transfer to an O&G-equipped hospital is essential
  • Retroperitoneal haemorrhage from dilated pelvic veins can be difficult to assess without ultrasound
  • A vaginal examination needs to be performed, looking for amniotic fluid (a pH of 7.0-7.5 will confirm this - the normal vaginal pH is much lower than this)
• Transfusion and general haematology issues
  • Rhesus-negative mothers need to receive IV immunoglobulin at least within 48 hours of the trauma
  • Transfusion needs to be Rh compatible
  • The pregnant trauma patient is in an even more hypercoagulable state than the normal trauma patient, and thus requires special attention to DVT prophylaxis
• Drug choices
  • Antibiotic choices are limited; tetracyclines and fluoroquinolones are to be avoided
  • If urgent caesarian delivery is planned, intubation drugs wil affect the foetus; thus there is need for NICU involvement for ventilation

Issues to consider in investigations and the secondary survey

• The usual barrage of blood tests remains unchanged.
• FBC, EUC, CMP LFT coags and crossmatch get sent away just as they would in any trauma patient, but the savvy candidate will mention the need for Rh blood grouping to prevent Rh isoimmunisation (where the mother is Rh negative and the foetus is Rh positive). An administration of anti-Rh IVIG can mop up any Rh-positive foetal erythrocytes which might have haemorrhaged into the maternal circulation, preventing the mother from developing her own anti-Rh antibodies (and thus preventing the haemolytic disease of the newborn).
• An abdominal ultrasound (FAST) is still performed, with additional focus on the uterus; uterine rupture or placental abruption need to be detected early.
• Foetal welfare can be monitored by CTG, and the O&G specialist should be invited to perfrom their own focused ultrasound to investigate the pregnancy.
• Though radiation exposure is undesirable, it is tolerated (particularly in late term pregnancy) because organogenesis has already taken place, and because the risk from ionising radiation exposure is minute in comparison to the risk of missed injuries and haemorrhage.

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Soar, Jasmeet, et al. "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution." Resuscitation 81.10 (2010): 1400-1433.

Mattox, Kenneth L., and Laura Goetzl. "Trauma in pregnancy." Critical care medicine 33.10 (2005): S385-S389.

DROST, THOMAS F., et al. "Major trauma in pregnant women: maternal/fetal outcome." Journal of Trauma-Injury, Infection, and Critical Care 30.5 (1990): 574-578.

College Answer

a)

• There is an extensive burn injury of the left lower leg consisting of areas of:
  • 1st degree burn - erythematous areas of skin without blistering
  • 2nd degree superficial partial thickness and likely deep partial thickness with blistering
  • 3rd Degree - Full thickness - white and mottled area although 4th degree cannot be excluded.

b)

• 4 possible complications:
  • Infection
  • Ischaemia
  • Scarring
  • Contracture
  • Pain
  • Amputation
  • DVT

c)

Important clinical features

• Other areas of burn – extent and type
• Basic resuscitation status, adequacy of resuscitation status to date and vital signs including urine output 
• Associated trauma
• Evidence of airway burn or inhalational injury
• Evidence of inhalation of toxic gases
• Evidence of facial, corneal or perineal burns
• Circumferential burns or evidence of compartment syndrome
• Temperature
• Analgesia requirements
• Vascular access issues 
• Co-existing conditions such as epilepsy or drug intoxication

Discussion

It is incredibly difficult to find an image of a burned left lower leg on Google which features the precise injuries which were described by the college answer. The best I could do is the above image of a couple of burned legs, retrieved without any permission whatsoever from an EMSWorld article on burns care. The picture itself is credited to Dr James H. Holmes IV, Burn Center Director Wake Forest University Baptist Health. The caption describes it as "Thermal burn injury involving anterior of both legs, uninjured areas include where shorts, socks and shoes provided partial protection. This is a 15% TBSA burn. Each leg, including the foot, is 18%. For this burn, the anterior surface of each leg, minus the area of the foot and the upper leg shielded by clothing, is approximately 15%. The patient is pictured following debridement upon admission at a burn center".

The possible complications of such a burn? One struggles to add anything to the already complete list provided by the college.

• Compartment syndrome and limb ischaemia
• Rhabdomyolysis
• Escharotomy
• Amputation
• Infection
• Scarring
• Peripheral nerve compression
• Contracture
• Pain
• DVT
• Loss of function

What are other important features on the initial clinical assessment of this patient?

This answer should follow some sort of system.

A) - Airway burns

B) - Carbon monoxide or cyanide poisoning

C) - Hypotension, hypovolemia, adequacy of fluid resuscitation;

- problems gaining vascular access

D) - Decreased level of consciousness, head injury; analgesia

E) - Electrolyte disturbance

- Exposure and assessment of total burned areas

F) - Urine output

References

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

PRUITT Jr, BASIL A., DARYL R. ERICKSON, and ALAN MORRIS. "Progressive pulmonary insufficiency and other pulmonary complications of thermal injury."Journal of Trauma and Acute Care Surgery 15.5 (1975): 269-379.

Hettiaratchy, Shehan, and Remo Papini. "Initial management of a major burn: II—assessment and resuscitation." Bmj 329.7457 (2004): 101-103.

Hettiaratchy, Shehan, and Peter Dziewulski. "Pathophysiology and types of burns." Bmj 328.7453 (2004): 1427-1429.

Ansermino, Mark, and Carolyn Hemsley. "Intensive care management and control of infection." Bmj 329.7459 (2004): 220-223.

College Answer

Assess for signs of life and if absent commence CPR, check underlying rhythm and treat appropriately following APLS guidelines

Airway and breathing Administer 100% oxygen

Intubation for airway protection and suction with ETT cuffed size 7 (ILCOR guidelines – cuffed ETT’s acceptable in children) (age/4 +4) (half size bigger and smaller available) with C spine precautions

Ventilate with appropriate settings (Vt 6-8ml/kg, RR 15-20, PEEP > 5cm H2O) SpO2 and ETCO2 monitoring, ABG and CXR 
May get some discussion re management of ARDS

Circulation

Assess pulse rate and volume, blood pressure and capillary return, Doppler may be helpful if hypothermic 
Secure IV access

If inadequate circulation fluid bolus of 20 ml/kg 0.9% Saline – avoid hypotonic intravenous fluids

Consider inotrope support early Blood glucose, FBE, U & E

Cerebral support 
Avoid any further episodes of hypoxia and hypercarbia

Optimise circulation

Temperature

Actively rewarm to core temperature of 34oC Passively rewarm over 34oC

If post cardiac arrest – maintain hypothermia 32.5 – 33.5oC for > 24 hours

Other

Primary and secondary survey for associated trauma

Look for precipitating cause (hypoglycaemia, epilepsy, drug/alcohol ingestion, marine envenomation) 
Antibiotics not indicated routinely

Collateral history – immersion time, resuscitation at scene, medical history Admit to ICU with appropriate paediatric expertise

Counsel family regarding likely outcomes

Discussion

This question would benefit from a systematic answer. The college answer is already quite systematic; there is little that can be added to it without this turning into an unmanageably long discussion.

First step: assess for signs of life/confirm cardiac arrest.

If cardiac arrest is confirmed, follow the pediatric ALS algorithm.

Next step: Primary survey;

Important pre-hospital issues

• Unskilled rescuers should avoid drowning themselves.
• Do not start CPR while still in the water (one should not need to say this)
• CPR should not be of the compression-only variety (you really need the breaths)
• Avoid all active attempts to "force" the water out by placing the person face-down or any sort of abdominal thrusting, as this will only lead to the aspiration of stomach contents.
• Do not stop the resuscitation of the hypothermic drowning victim (the ICU doctors might want to publish another case report of miraculous ECMO-aided survival).

Emergency management issues

1. Assessment of the airway and of the need for immediate intubation.
   Drowning is associated with a high risk of aspiration (and not just of lake water).
2. Ventilation with high FiO₂
   High PEEP, 12-15
   Investigation of possible aspiration with CXR and ABG
3. Establishment of IV access and correction of hypovolemia;
   drowning victims may become hypovolemic following prolonged immersion due to the hydrostatic effects of water (particularly salt water)
4. Investigate causes of drowning related to intracranial events, eg. ICH, or trauma resulting from a fall into submerged obstacles
5. Assessment of temperature, and rewarming (the immersed patient is invariably hypothermic, as it is rare to drown in a body of water with an ambient temperature higher than human core body temperature).

ICU management issues

1. Assessment of the airway device effectiveness (i.e. is it in the right main bronchus?)
   Bronchoscopy and suction as indicated by copious aspirated material.
2. Lung protective ventilation; open lung strategy
   No benefit in corticosteroids
3. Assess the effectiveness of volume resuscitation; give more.
4. Sedation as required: no specific recommendations can be made.
   If the patient has had a cardiac arrest, therapeutic hypothermia might be worthwhile.
5. Electrolytes are unlikely to be deranged by this stage.
6. Renal function is unlikely to be impaired
7. There is no reason to omit normal nasogastric feeds
8. Monitor Hb, and satisfy yourself that there is no haemolysis.
9. There is no need for antibiotics.

References

The ARC ALS2 manual (2011) has a section on drowning (pp. 127). This was my main source of information.

Pearn, John. "The management of near drowning." British medical journal (Clinical research ed.) 291.6507 (1985): 1447.

College Answer

1. Definitions
   • IAH is defined as a sustained IAP ≥12 mmHg
   • ACS is defined as a sustained IAP >20 mmHg (with or without APP <60 mmHg) that is associated with new organ dysfunction OR as IAH-induced new organ dysfunction without a strict IAP threshold.

(iii) IPP = MAP – IAP

1. Measuring IAP
   • Patient is supine and no active abdominal muscle contractions
   • Clamp the urinary catheter, after ensuring it is freely flowing and not obstructed.
   • 25 ml of sterile saline is instilled into the bladder via a port in the urinary catheter catheter and the catheter filled with fluid
   • A pressure transducer is connected to the urinary catheter, between the clamp and the bladder
   • Allow 30-60 seconds after instillation of the saline so as to allow for bladder detrusor muscle relaxation
   • Zero transducer at the mid-axillary line and at the level of the iliac crest
   • Measure pressure at end-expiration
2. Physiological mechanisms

Cardiac 
Decreased cardiac output –

• Reduced venous return - due to intrabdominal venous compression and raised intrathoracic pressure.
• Increased systemic afterload – due to increased compression of intrabdominal arterial vessels, and PVR due to raised intrathoracic pressure.
• Decreased Right Ventricular output from raised intrathoracic pressure, raised PVR Increased CVP and LVEDP - Reduced compliance - due to elevation of diaphragm displacing the heart and increased afterload (see above).

Hypotension – decreased cardiac output.

Respiratory

• Deteriorating O2 A-a gradients due to increased – raised diaphragm and atelectasis, increased intrapulmonary shunt / V/Q mismatch
• Hypercapnia – decreased chest wall and lung compliance.
• Increased airway pressure – altered respiratory compliance.

Discussion

A slightly less formal discussion of abdominal compartment syndrome takes place in Question 21from the second paper of 2006: "Outline the causes, consequences and the management of abdominal  compartment syndrome. "Brief notes on the pathophysiology of abdominal compartment pressure and its measurement are available, with references for the time-rich exam candidate.

First, the definitions. These are derived from a 2011 consensus statement, from which much of the below information is derived.

Specifically, the definitions were copied verbatim from Table 1, "Consensus definitions list"; one might notice that they are identical to the college answer.

Intra-abdominal Hypertension (IAH)

A sustained or repeated pathological elevation in IAP ≥ 12 mmHg

Abdominal Compartment Syndrome (ACS)

A sustained IAP> 20 mmHg (with or without an APP < 60 mmHg) that is associated with new organ dysfunction/failure

Abdominal Perfusion Pressure (APP)

APP = MAP − IAP.

Measurement of intra-abdominal pressure

• Empty the bladder
• Clamp IDC
• Attach noncompressible tubing and transducer
• Inject 20ml of fluid into the bladder
• Wait for the detrusor to relax (60 seconds)
• Zero the transducer to atmosphere, at mid-axillary line and at the level of the iliac crest
• Measure the pressure at end-expiration
• The measurement is valid under the following conditions:
  • Patient is supine
  • Muscle contraction is eliminated (eg. NMJ blockers)

List the adverse cardiorespiratory effects of an increase in IAP in a mechanically ventilated patient and outline the physiological mechanisms that account for these effects.

The college demands we focus on the cardiorespiratory consequences.

Thus:

• Decreased respiratory compliance, increased peak airway pressures- due to the pressure of the abdominal contents on the diaphragm
  • Atelectasis
  • Risk of pneumonia
  • Increased intrathoracic pressure due to the compensatory reliance on higher PEEP
• Decreased preload, thus hypotension
• Increased afterload, thus increased LV workload

References

Oh's Intensive Care manual: Chapter   45   (pp. 520) Abdominal  surgical  catastrophes by Stephen  J  Streat

Malbrain, Manu LNG, et al. "Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions." Intensive care medicine 32.11 (2006): 1722-1732.

Cheatham, Michael L., et al. "Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension." Journal of Trauma-Injury, Infection, and Critical Care 49.4 (2000): 621-627.

Bailey, Jeffrey, and Marc J. Shapiro. "Abdominal compartment syndrome."Critical Care 4.1 (2000): 23.

Cheatham, Michael Lee. "Abdominal compartment syndrome." Current opinion in critical care 15.2 (2009): 154-162.

Maerz, Linda, and Lewis J. Kaplan. "Abdominal compartment syndrome."Critical care medicine 36.4 (2008): S212-S215.

Saggi, Bob H., et al. "Abdominal compartment syndrome." Journal of Trauma-Injury, Infection, and Critical Care 45.3 (1998): 597-609.

College Answer

• a)
  • Resuscitation including primary and secondary survey
  • Assessment and management of potential airway burn (including early intubation, not cutting ETT, avoiding nasal tube)
  • Obtain large bore IV access and administration of fluid bolus (20 ml/kg) for probable hypovolaemic shock (mention groins are usually spared in burns and are a good site for clean skin vascath access
  • Look for signs of traumatic injury and assess extent of body surface area and depth of burn
  • Risk of hypothermia
  • Seek collateral history for past medical history, medication history and history of acute events

• b)
  • Burns occurring in a closed space
  • Cough, stridor, hoarseness of voice
  • Burns to face, lips, mouth, pharynx or nasal mucosa
  • Soot in sputum, nose or mouth
  • Hypoxaemia or dyspnea
  • Carboxyhaemoglobin levels >2%
  • Acute confusional state or depressed conscious level

• (c)
  • Traumatic brain injury
  • CO / Cyanide poisoning
  • Alcohol intoxication / drug overdose
  • Other pathology eg CVA, intracranial haemorrhage, seizure-related, hypoglycaemia

Discussion

A structured answer to (a) would resemble the following:

A) Assessment of the airway and of the need for immediate intubation

B) Ventilation with high FiO₂; investigation of possible carbon monoxide poisoning with ABG, and investigation for pulmonary thermal injury with CXR.

C) Establishment of secure vascular access, and the administration of crystalloid to replace intravascular volume.

• Some mention of the estimation of burns area should probably be made; the Wallace rule of nines is a good method for adults.
• Fluid resuscitation should be vigorous, given that the greatest amount of fluid loss in burns patients in over the first 24 hours.
• The Parkland formula may be used to estimate fluid resuscitation requirements, even though it frequently underestimates the fluid requirements

The college wanted a specific mention of the groins as regions which are frequently spared in house fires. I presume this excludes those fires which started in the groin.

D) Adequate analgesia and sedation

Features suggestive of airway burns:

A BMJ article from the "ABC of burns" series contains Table 1, "Warning signs of airway burns", which I reproduce below:

• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low pulse oximetry saturation or arterial oxygen tension) or increased carbon monoxide levels (>2%)

This table, with minimal modification, seems to form the basis of the college answer.

Other differentials for a decreased level of consciousness in a burned trauma patient include the following:

Burn and trauma-associated:

• Traumatic brain injury
• Carbon monoxide poisoning and thus hypoxia
• Cyanide poisoning and thus hypoxia
• Intoxication

Generic differentials:

• Stroke
• Intracranial infection
• Hypoglycaemia
• Post-ictal state
• Cerebral vasculitis
• Hypothyroidism/hypoadrenalism

Many others could be generated. Maybe this guy was assaulted, and then left for dead in a shed which was set ablaze as a forensic countermeasure.

References

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

PRUITT Jr, BASIL A., DARYL R. ERICKSON, and ALAN MORRIS. "Progressive pulmonary insufficiency and other pulmonary complications of thermal injury."Journal of Trauma and Acute Care Surgery 15.5 (1975): 269-379.

Hettiaratchy, Shehan, and Remo Papini. "Initial management of a major burn: II—assessment and resuscitation." Bmj 329.7457 (2004): 101-103.

Cartotto, Robert C., et al. "How well does the Parkland formula estimate actual fluid resuscitation volumes?." Journal of Burn Care & Research 23.4 (2002): 258-265.

Ansermino, Mark, and Carolyn Hemsley. "Intensive care management and control of infection." Bmj 329.7459 (2004): 220-223.

Michielsen, Dirk PJ, and Cynthia Lafaire. "Management of genital burns: a review." International journal of urology 17.9 (2010): 755-758.

College Answer

a)

• Ruptured liver
• Free intraperitoneal fluid (blood) +++

b)

• Advantages: non-invasive; ability to exclude retroperitoneal injuries; ability to grade solid organ injury; shows were where the intra-abdominal blood is coming from; may reveal associated pelvic and spinal injuries; ability to detect clinically unsuspected injuries
• Limitations: radiation dose; the need to give intravenous contrast; relatively poor sensitivity for hollow viscus, mesenteric, retroperitoneal, and diaphragmatic injuries; difficulty getting an unstable patient to the CT scanner.

c)

Competing interests of life-threatening haemorrhage and need for anticoagulation (MVR) and in this instance haemorrhage is greater risk

Cease warfarin therapy and give:

Vitamin K 5 – 10 mg IV (recommended in Australian guidelines but controversial as may cause resistance when warfarin needs re-starting. Balance of risks and lower dose may be preferable)

AND

Prothrombin complex concentrate (Prothrombinex-VF) 50 IU/kg AND

Fresh frozen plasma 150 – 300 ml OR If PCC not available

FFP 15 ml/kg 
Tranexamic acid as soon as possible

Other blood products (packed cells, platelets, cryoprecipitate) as indicated Titrate therapy against measurement of coagulopathy (APTT, PT, fibrinogen, platelets)

TEG if available 
Prevent / correct hypothermia, acidosis, hypocalcaemia

Discussion

The image above is not from the original exam paper, but rather stolen shamelessly fromRadiopedia.org. It represents a large laceration in the right lobe of the liver, with a perihepatic hematoma.

Now, as for the advantages and disadvantages of CT in blunt abdominal trauma;

a good recent article discusses these points as well as offering tables of injury severity grading.

• Advantages of CT:
  • Rapid
  • Non-invasive
  • Readily available
  • Allows assessment of clinically undetectable injuries
  • Good sensitivity for solid organ damage
  • Contrast extravasation can suggest the source of bleeding
• Disadvantages of CT:
  • Radiation exposure
  • Contrast exposure
  • Exposure of the patient to the risk of transfer
  • Poor sensitivity for hollow organ damage

As for the corection of coagulopathy; the answer should at least include the competition between the need for anticoagulation and the need for haemostasis. If one bleeds to death, one's circulation will cease and with blood stagnating in the left atrium those valve leaflets will get clot on them anyway, so perhaps the haemostasis is a priority.

The discussion of haemostasis in this patient can be divided into two subtopics: what to do about the warfarin, and what generic strategies are there to achieve medical haemostasis in a trauma patient.

Reversal of warfarin anticoagulation

A generic discussion of warfarin reversal guidelines takes place in another chapter, and Question 15.1 from the second paper of 2011 deals with the reversal of warfarin in a patient with a suprathereapeutic INR.

In brief, this is a warfarinised patient with clinically significant bleeding, and thus it does not matter what his INR is. The most recent guidelines suggest the following multi-agent strategy:

• 5-10mg of Vitamin K
• prothrombinex 50.0 units/kg
• FFP 150–300mL.

Medical haemostasis in major trauma

The use of tranexamic acid in trauma is also well-established, and one would administer 1g of this substance immediately.

The college points out that TEG would be the ideal means of assessing the coagulation system (and fibrinolysis), but this is still being debated.  If TEG is not available (and it is infrequently available) then PT APTT and fibrinogen levels would guide one's resuscitation.

There is widespread disagreement as to what proportion to give; typically one is guided by the volume of blood transfused and by the changes in coagulation parameters.

Ultimately, one might arrive at a situation where Factor VIIa is pulled out, in spite of this being an off-license use of this product. This controversy is better discussed in Question 12 from the first paper of 2007, where the college invites us to "white short notes" about it.

References

Fang, Jen-Feng, et al. "Usefulness of multidetector computed tomography for the initial assessment of blunt abdominal trauma patients." World journal of surgery 30.2 (2006): 176-182.

Soto, Jorge A., and Stephan W. Anderson. "Multidetector CT of blunt abdominal trauma." Radiology 265.3 (2012): 678-693.

Ross I Baker, Paul B Coughlin, Hatem H Salem, Alex S Gallus, Paul L Harper and Erica M WoodWarfarin reversal: consensus guidelines, on behalf of the Australasian Society of Thrombosis and Haemostasis Med J Aust 2004; 181 (9): 492-497.

There is also this local policy document.

College Answer

a)
 Lower injury severity scores overall.
 More severe extremity injuries.
 More thoracic injury.
 Less brain injury – controversial.
 Longer extraction time may make for higher risk for crush injury.

b)
Airway
 Increased risk of partial airway obstruction when lying flat.
 Possibility of difficult intubation and difficult bag mask ventilation (cervical collar, neutral position, pre-existing signs of airway obstruction, possible sleep apnoea syndrome).

Breathing
 Increased difficulty inserting chest drains.
 Possible obesity hypoventilation syndrome.
 Increased risk of atelectasis.

Circulation
 Need for appropriately sized BP cuff.
 IV access more difficult so consider early inter-osseous access.

Other
 Caution with analgesia.
 Clinical signs, e.g. pneumothorax, difficult to detect by palpation and auscultation.
 Log rolling requires additional assistants.

c)
 Bedside investigation avoids transfer to CT scanner.
 Technically challenging with difficulty achieving adequate beam penetration and image quality.
 FAST is less sensitive than in non-obese.
 False positive pericardial collections are more common in the obese.

Discussion

Change in the pattern of injuries associated with morbid obesity

• Injury scores are lower in obese patients (Arbabi et al, 2003)
• Pattern of blunt trauma is different (Boulanger et al, 1992)
  • Injuries that are more likely:
    • pulmonary contusion
    • rib fractures
    • pelvic injuries
    • kneedislocations (Fuchs et al, 2014)
    • extremity fractures
    • proximal upper extremities seem to get it worst (Evans et al, 2011)
  • Injuries that are less likely:
    • head injuries
    • liver injuries
• "Obese people injured in vehicular crashes had a similar injury pattern with no difference in seating position, direction of impact, seat belt use, and ejection."

Influence of morbid obesity on the primary and secondary survey

1. - Difficult airway; difficult bag-mask ventilation more likely than actual difficult intubation.
   - Short handle may be required for direct laryngoscopy; most people would just resort to the videolaryngoscope.
   - When intubating, the FRC is small and the patient will become hypoxic rapidly, which means fewer attempts will be possible.
   - Increased risk of obstruction, even when awake
   - When obtunded, a virtual certainty of obstruction
    
2. - Poor chest wall compliance
   - Increased risk of atelectasis
   - Obesity hypoventilation syndrome
   - Difficult access for chest drains
   - Difficult windows for trauma TTE
   - Difficult auscultation and percussion, eg. for pneumothorax
   - Increased aspiration risk
    
3. - Difficulty measuring accurate blood pressure (need for appropriate size cuff)
   - Realistic possibility that no cuff will be appropriate and arterial access may be required
   - Difficult IV access- CVC as well as PIVC; the college answer recommends to go straight for the intraosseous needle
   - Intraosseous access is hardly fool-proof and can also be frustrated by obesity, considering especially the likelihood of there being bilateral knee prostheses
   - Possibility of pulmonary hypertension, cor pulmonale or CCF makes haemodynamic management more complex
    
4. - Likely, CO₂ retention and narcosis (influences doses of induction drugs)
   - Medullary sensitivity to CO₂ will be even more reduced by opiates
   - Some sort of syndromic condition may complicate neurological assessment (eg. Prader Willi syndrome)
    
5. - Log rolling will require additional assistants, or some sort of unusual equipment.

Influence of morbid obesity of FAST assessment

• Morbid obesity is one of the limitations of FAST
• Difficult insonation of the appropriate spaces; image quality is likely to be poor
• Pericardial fat can be misinterpreted as clotted blood
• Perinephric fat may be misinterpreted as intraperitoneal free fluid
• The advantage is, if you can't fit into the CT scanner this is all you've got.

References

Bochicchio, Grant V., et al. "Impact of obesity in the critically ill trauma patient: a prospective study." Journal of the American College of Surgeons 203.4 (2006): 533-538.

Diaz Jr, Jose J., et al. "Morbid obesity is not a risk factor for mortality in critically ill trauma patients." Journal of Trauma and Acute Care Surgery 66.1 (2009): 226-231.

Lambert, David M., Simon Marceau, and R. Armour Forse. "Intra-abdominal pressure in the morbidly obese." Obesity surgery 15.9 (2005): 1225-1232.

Boulanger, Bernard R., et al. "Body habitus as a predictor of injury pattern after blunt trauma." Journal of Trauma and Acute Care Surgery 33.2 (1992): 228-232.

Dhungel, Vinayak, et al. "Obesity delays functional recovery in trauma patients." journal of surgical research 193.1 (2015): 415-420.

Ciesla, David J., et al. "Obesity increases risk of organ failure after severe trauma." Journal of the American College of Surgeons 203.4 (2006): 539-545.

Arbabi, Saman, et al. "The cushion effect." Journal of Trauma and Acute Care Surgery 54.6 (2003): 1090-1093.

Evans, David C., et al. "Obesity in trauma patients: correlations of body mass index with outcomes, injury patterns, and complications." The American surgeon 77.8 (2011): 1003-1008.

Fuchs, I., et al. "Vascular Injury in Obese Patients after Ultra-Low-Velocity Trauma." J Anesth Clin Res 5.488 (2014): 2.

College Answer

Patients with "unstable" injuries may be at risk of secondary injury if passive or active movements are not limited.
Brain- Traumatic Brain Injury:
 Head up (venous drainage)
 May be at odds with spinal precautions
 Priority given to greatest identified injury
 Can nurse flat in bed, with entire bed angled head up
 Avoid venous obstruction if TBI (collar and jugular CVC)
C-Spine injury
 Collar (which type not esp evidence based- Philadelphia/Aspen/hard collar)
 Particular attention to head hold in movement including airway manipulation
 Lie flat (but can tilt bed if head elevation dictated by underlying TBI)
 Log roll acceptable but recommended to use 4 people
 Can side lie with wedge to minimise pressure injury
 Should aim to remove collar as early as possible, and many trauma hospitals institute a Radiological clearance protocol using CT or MRI.
 If injury is identified then collar should not be removed until definitive treatment is defined (fixation/hard collar/conservative mx)
 Prolonged collar placement may lead to pressure injuries
 C-spine collar may make airway access more difficult
Thoraco-lumbar spine injury
 Lie flat (no bending) or side lie with a wedge.
 Log roll (4 person).
 Radiologic clearance protocols used commonly.
Pelvic fractures
 Haemodynamic instability may be related to pelvic injury
 Mechanically unstable pelvic fractures may be worsened by rolling/side lie/ sitting
 Pelvic binders may be required if haemodynamically unstable
 Additional fixation once injury identified- or removed if not.

Long bone fractures
 No universal position restrictions
 In event of clinical suspicion long bones should be immobilised to prevent embolic and haemorrhagic complications and pain
Other points
Competing injuries- precautions should relate to the most serious identified injury - e.g. a cleared spine may mean a patient can be sat up, but not in the setting of a co-existing mechanically unstable pelvis.
Likewise:
 Management of ICP in TBI takes precedence over use of cervical collars.
 Chest injuries/hypoxia takes precedence over spinal precautions
 Intubation and securing the airway takes precedence over cervical collars/head holds
Urgency exists in identifying injuries at the earliest possible time (secondary and tertiary survey) in order to remove or increase position restrictions for the individual patient.
Emphasis should be on own practice, no single "right way" but sensible risk/benefit based approach including clinical and radiologic findings to guide practice.

Examiners' comments: Candidates who did not pass this question did not think broadly and gave a limited answer and did not adequately address the issue of competing injuries and risk v benefit.

Discussion

Positioning for head injury

• Ideally, head up 45 degrees. At least angle the bed.
• It seems to position the patient at least 30° head up decreases the ICP but does not decrease the CPP.
• At least in the pediatric population, the angle of the bed is directly related to intracranial pressure.
• Ideally, the C-spine collar should be removed. A good study of intracranial pressure with and without the rigid collar found that one can decrease the intracranial pressure of a TBI patient by about 4-5mmHg simply by removing the rigid collar and using something like sandbags to stabilise the neck.
• The risk of head-up positioning may be haemodynamic instability, particularly if the sympathetic nervous system is not working (eg. severe diabetes, Parkinson disease or spinal injury)

Positioning for C-spine injury

• Hard collar is required if an injury is confirmed or suspected.
• The patient must lie flat, and be log-rolled.
• Clearance of the C-spine should occur as soon as it is practical
• There are many problems with wearing a collar for a prolonged period (eg. pressure areas, increased ICP, and so forth)

Positioning for T/L spine injuries

• The patient must lie flat, and be log-rolled.
• No bending is permitted
• The risk of such flatness is an increased incidence of VAP

Positioning for severe chest injuries

• Sit them up at least 30° if the head permits
• Do not lie them with the flail segment down. That lung has probably had a contusion anyway. Lie them "good lung down" - oxygenation will improve.
• Gentle lateral rotation may be appropriate
• Low-air-loss technology: specialist beds which turn the patient by inflating and deflating air cushions; a turning arc of 40-90° is possible.
• These are soft beds, unsuited for unstable spinal or pelvic injuries

Positioning in pelvic fractures

• The unstable pelvis must be in a binder
• Overmuch manipulation will result in haemodynamic instability
• Predictably, the solution is to fix the pelvis; angioembolisation may not be possible because the bleeding is frequently venous.
• While unfixed, the patient must lie flat
• Nurse patient on a firm mattress to ensure consistent pelvic support
• Ensure appropriate fitting of specialist equipment (e.g. pelvic binder belt)
• Maintain flat, straight alignment of whole body at all times.
• Log-roll patients
• Use spinal boards and flat-surface hoist
• If the patient is expected to have an unfixed pelvis for a prolonged period (eg. if they have no private health insurance and were not the victim of a work-related injury), to ameliorate the effects of prolonged immobility one may use continuous lateral rotation therapy using RotoRest or similar specialist beds
• Low-air-loss pressure mattresses are contraindicated in spinal or pelvic instability.

Positioning in long bone fractures

• Traction is indicated for the reduction of long bone lower limb fractures which are awaiting repair.
• This is a significant limitation on positioning
• The patient in traction is also difficult to transport
• Traction must come down for transfer fom bed to bed

Positioning for the pregnant trauma patient

• Gravid uterus restricts the use of pelvic fixators and pelvic binders
• A tilt may be required to improve haemodynamics, but it may be counterproductive for long bone traction  or spinal immobilisation
• Supine flat position may be required for spinal immobilisation, which will decrease FRC and compromise respiratory function

Competing interest

• Airway vs. C-spine collar:
  • Airway wins; the collar can be removed and inline stablisation attempted for intubation
• Head injury vs. C-spine injury:
  • Head injury wins, even if the C-spine is unstable the ICP must be managed properly. Remove the collar and sandbag the neck. Paralyse and sedate the patient.
  • If they must remain flat, then angle the bed so the head is still up.

References

Christie, Robert James. "Therapeutic positioning of the multiply-injured trauma patient in ICU." British Journal of Nursing 17.10 (2008): 638-642.

College Answer

Secondary adrenal insufficiency secondary to pituitary injury. Treatment is with IV hydrocortisone.

Discussion

The image above was once a normal CT brain. You would not believe the difficulty of finding a CT with a sella turcica fracture via Google Images. Thus, a normal CT brain image was acquired, and a sella turcica fracture was photoshopped into it. Trainees should be aware that this is a poor second to an actual CT image, and that the college tend to use real CT images. The original was omitted from the publicly available paper, presumably because the college plans to reuse it.

Anyway: pituitary trauma.

It happens.

And it is not always associated with grossly obvious sella turcica trauma.

The question is a short one, and as such does not merit an indepth answer (see the college model).

If one were interested in more detail about secondary adrenal insufficiency due to pituitary trauma, one could read this 2005 article from Critical care medicine.

Adrenal insufficiency in general is explored in greater depth elsewhere.

References

Kusanagi, Hiroaki, Kazunari Kogure, and Akira Teramoto. "Pituitary insufficiency after penetrating injury to the sella turcica." Journal of Nippon Medical School 67.2 (2000): 130-133.

Feiz-Erfan, Iman, et al. "Incidence and pattern of direct blunt neurovascular injury associated with trauma to the skull base." (2007). J. Neurosurg. / Volume 107 / August, 2007

Kelly, Daniel F., et al. "Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report." Journal of neurosurgery 93.5 (2000): 743-752.

Tanriverdi, Fatih, et al. "High risk of hypopituitarism after traumatic brain injury: a prospective investigation of anterior pituitary function in the acute phase and 12 months after trauma." The Journal of Clinical Endocrinology & Metabolism91.6 (2006): 2105-2111.

Benvenga, Salvatore, et al. "Hypopituitarism secondary to head trauma." The Journal of Clinical Endocrinology & Metabolism 85.4 (2000): 1353-1361.

Cohan, Pejman, et al. "Acute secondary adrenal insufficiency after traumatic brain injury: A prospective study*." Critical care medicine 33.10 (2005): 2358-2366.

College Answer

a)

Type of fluid:
 Fluid resuscitation of patient with moderate to severe burns consists of an isotonic crystalloid
solution, such as Hartmann’s solution or plasmalyte. Large volumes of 0.9% NaCl may be
associated with hyperchloremic metabolic acidosis.
 The colloids (albumin) are more expensive, and do not improve survival, compared to
crystalloids.
 The use of hypertonic saline does not provide better outcomes than isotonic saline.

Estimating fluid requirements:
 No formula provides a precise method for determining the burn victim's fluid requirements; the
formulas described provide only a starting point and guide to initial fluid resuscitation. Patient
age, severity of burns and co-morbidities can substantially alter the actual fluid requirements
of individual patients. Patient response to fluid therapy needs careful monitoring and
adjustment as clinically indicated
 Parkland (or Baxter or consensus) Formula (most widely used):
Fluid requirement (ml) = 4 x body weight x percentage of burns. (Only deep)
One half of the calculated fluid is given over the first eight hours and the remaining over the
next 16 hours.
The rate of infusion should be as constant as possible; sharp decrease in infusion rates can
cause vascular collapse and increase in edema.
 Modified Brooke Formula:
Fluid requirement (ml) over the initial 24 hours = 2 x body weight x percentage of burns.
This formula may reduce the total volume used in fluid resuscitation without causing harm.
 Following initial resuscitation, IV fluids are administered to meet baseline fluid needs and
maintain urine output.
 Care should be taken to avoid fluid overload, as associated with multiple co-morbidities.

b)
 Unidentified blood loss / inadequate fluid resuscitation
 Distributive shock with large fluid shifts
 Cyanide toxicity
 Compartment Syndrome, including abdominal compartment
 Cardiogenic Shock (severe myocardial suppression caused by burns)
 Carbon monoxide poisoning
 Ingestion of toxins (ethylene glycol, methanol, salicylates)

Additional Examiners’ Comments:
Candidates omitted discussion on rationale for choice of fluid

Discussion

A detailed dissection of fluid resuscitation for the burns patient  is performed in the Required Reading section. Physiologic consequences of burns is also covered there.

In brief:

Fluid resuscitation end point:

• urine output of 0.5-1.0 ml/kg/hr (Paratz et al, 2014)
• MAP >65mmoHg

Choice of fluids:

• Resuscitation should use a balanced solution to avoid hyperchloraemic acidosis (Walker et al, 2001)
• Most formulae recommend Ringer's Lactate; the locally available version is Hartmanns
• The disadvantage of crystalloid is the potential need for massive volume
• Historically, significantly more fluid is given to burns patients  then is predicted by any formula (Mitra et al, 2006). This is known as "fluid creep" and is associated with significant complications, of which the most serious is abdominal compartment syndrome.
• Colloid (eg. albumin) is also recommended by many of the formulae
• The advantage of colloid is that it may alleviate "fluid creep" and achieve haemodynamic goals more rapidly and with less volume
• There is no evidence that albumin improves survival or organ dysfunction (Melinyshyn et al, 2013)
• The theoretical advantage of hypertonic saline is earlier achievement of haemodynamic goals and the avoidance of burns-associated hypernatremia. However, hypertonic saline solutions were associated with a fourfold increase in the risk of renal failure and a twofold increase in the risk of death (Huang et al, 1995)

Resuscitation formulae

It is probably worth adding that this patient is at high risk of inhalational injury. He was unconscious, and sharing a small enclosed space with his fire. Naver et al (1985) demonstrated that patients with smoke inhalation injury and airway burns require a larger volume of fluid resuscitation. The total volume is increased up to 35% - 65%.

Causes of shock in the unconscious burns patient:

Let this be an exercise in generating differentials.

• Wrong BP measurement (eg. arterial line is not zeroed)
• Cardiogenic shock
  • Due to cytokine storm of severe burns
  • Due to carbon monoxide toxicity (i.e. severe tissue hypoxia)
  • Due to cyanide toxicity (i.e. mitochondrial failure)
  • Due to a myocardial infarction (due to increased myocardial oxygen consumption in context of burns, on top of pre-existing ischaemic heart disease)
• Abdominal compartment syndrome (over-resuscitation)
• Tension pneumothorax (explosion)
• Spinal injury neurogenic shock (unrecognised due to unconsciousness)
• Blood loss from some internal injury or due to DIC
• Under-resuscitated burns shock (i.e. fluid shifts)
• SIRS vasoplegia
• Anaphylaxis to some drug given in hospital

In more detail:

References

College Answer

References

Oh's Intensive Care manual: Chapter 64   (pp. 684) General  obstetric  emergencies by Winnie  TP  Wan  and  Tony  Gin

Soar, Jasmeet, et al. "European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution." Resuscitation 81.10 (2010): 1400-1433.

Mattox, Kenneth L., and Laura Goetzl. "Trauma in pregnancy." Critical care medicine 33.10 (2005): S385-S389.

DROST, THOMAS F., et al. "Major trauma in pregnant women: maternal/fetal outcome." Journal of Trauma-Injury, Infection, and Critical Care 30.5 (1990): 574-578.

College Answer

a)

Uncoupling of oxidative phosphorylation
Failure of enzyme systems
Membrane permeability
increased Na leak into cells
ADP depleted
Sweat gland damage from heat

b)

Prognosis depends on core temp, duration of hyperthermia and presence of comorbidities.

c)

Haemoconcentration (dehydration), haemolysis
Hypernatremia
LFT derangements (cholestatic, early sign),
Renal impairment,
DIC often delayed onset and a/w worse prognosis
CK rise (exertional type),
Lactate rise.
During treatment: CXR pulmonary oedema (centralise fluid, ALI), low PO4, Ca, glucose,

d)

ABC (Airway protection if GCS low etc. ) & control of seizures if present

Remove from offending environment,

Rapid cooling to 39 C (duration of hyperthermia major determinant of outcome): remove clothing, sponge cold water, ice, fans, cooling blankets, cold intravenous fluids gastic lavage with cold solutions, immersion (young and military), cold dialysis, etc. Monitor core temp closely

Volume and electrolyte resuscitation and close monitoring
ABG,
Eectrolytes. NB Risk of cerebral oedema
CVC
 

Additional comments:
In general there was a knowledge deficit relating to the pathophysiology of heat stroke. Some candidates failed to address cooling and control of temperature in the management of heat stroke and did not recognise the need for initial rapid cooling and/ or the need for careful temperature monitoring.

Discussion

The

a) Pathophysiology of heat stroke:

• Exposure to high temperature leads to an increase in the cardiac output, cutaneous vasodilation and sweating.
• Dehydration by sweating leads to hypovolemia and salt loss
• In the absence of plentiful water and salt, sweating becomes impossible and thermoregulation is thus impaired.
• As the convective cooling is now impossible, the core body temperature increases.
• As the core temperature increase, enzyme function is altered and cellular energy production becomes impaired
• Direct heat-related tissue damage results in cytokine release
• At the same time, hypovolemia and shock lead to bacterial translocation from the gut, leading to endotoxaemia
• The cytokine response to this endotoxin load results in a systemic inflammatory response
• Due to this SIRS, the vascular endothelium is damaged, leading to multi-organ system failure and DIC.

b) Factors that affect prognosis of heat stroke:

• LDH, CK and AST levels (when extremely high) were predictive of non-survivors in a study of heat-stroked Haj pilgrims (Alzeer et al, 1997)
• Failure to decrease the core body temperature to below 38.9° within the first 30 minutes of presentation.
• A hyperdynamic circulation is protective, but a sluggish hypodynamic circulation is associated with a poorer survival
• Found collapsed at home (as opposed to public place or care facility)
• Preexisting cardiac disease
• Use of diuretics
• High body temperature
• Low Glasgow Coma Score
• Low platelet count
• Prolonged prothrombin time
• High serum creatinine
• High SAPS II score
• Use of vasoactive drugs within the first 24 hrs in the ICU

c)  List the expected changes on routine investigations in the presence of heat stroke.

• ABG: acidosis, probably mixed metabolic.
• FBC: haemolysis, thrombocytopenia and anaemia
• EUC: renal failure, hyperkalemia
• CMP: hyperphosphataemia
• LFTs: raised transaminases and bilirubin. Specifically, AST and LDH will be raised.
• CK: elevated
• Urinary myoglobin
• Coagulopathy (DIC): raised PT and APTT

d) Outline the management of a patient with heat stroke.

• Goals of therapy:
  • Early, aggressive cooling to under 39°C
  • Support of multiple failing organ systems
• Options for cooling methods:
  • Evaporation of cold water sponges
  • Ice packs
  • Immersion in ice water
  • Contact cooling by blankets and jackets
  • Iced gastric, colonic, bladder, or peritoneal lavage
  • Infusion of cold intravenous fluids
  • Invasive technique such as cooling of the dialysis circuit, or ECMO
• Supportive management:

1. Intubate to protect the airway, if unconscious
2. Ventilate with lung protective ventilation, anticipating ARDS
3. Manage haemodynamic instability aggressively, with a mixture of cold IV fluids and vasopressor agents
4. Protect from seizures (no specific evidence to recommend benzodiazepines or any other conventional agents)
5. Control hyperkalemia and hyperphosphataemia of rhabdomyolysis
6. Consider early dialysis. Watch for myoglobinuria
7. Early trophic feeds to maintain gut integrity
8. Correct the coagulopathy of DIC

References

Bouchama, Abderrezak, and James P. Knochel. "Heat stroke." New England Journal of Medicine 346.25 (2002): 1978-1988.

Grogan, H., and P. M. Hopkins. "Heat stroke: implications for critical care and anaesthesia." British Journal of Anaesthesia 88.5 (2002): 700-707.

Glazer, James L. "Management of heatstroke and heat exhaustion." Am Fam Physician 71.11 (2005): 2133-2140.

Bricknell, M. C. "Heat illness--a review of military experience (Part 1)." Journal of the Royal Army Medical Corps 141.3 (1995): 157-166.

Bricknell, M. C. M. "Heat illness-A review of military experience (Part 2)." Journal of the Royal Army Medical Corps 142.1 (1996): 34-42.

Leon, Lisa R., and Bryan G. Helwig. "Heat stroke: role of the systemic inflammatory response." Journal of applied physiology 109.6 (2010): 1980-1988.

Alzeer, Abdulaziz H., et al. "Serum enzymes in heat stroke: prognostic implication." Clinical chemistry 43.7 (1997): 1182-1187.

Bouchama, Abderrezak, Mohammed Dehbi, and Enrique Chaves-Carballo. "Cooling and hemodynamic management in heatstroke: practical recommendations." Crit Care 11.3 (2007): R54.

Misset, Benoît, et al. "Mortality of patients with heatstroke admitted to intensive care units during the 2003 heat wave in France: A national multiple-center risk-factor study*." Critical care medicine 34.4 (2006): 1087-1092.

College Answer

a)

The root of the neck is the junction between the thorax and the neck. It opens into, and is the cervical side of, the superior thoracic aperture, through which pass all structures going from the head to the thorax and vice versa. The root of the neck is bound laterally by the first rib, anteriorly by the manubrium, and posteriorly by the T1 vertebrae.

From anterior to posterior, the major contents are:

Subclavian artery and branches

• vertebral artery
• internal thoracic artery
• thyrocervical trunk
• costocervical trunk

Subclavian vein and tributaries (EJV)

Trachea

Oesopahagus

Vagus nerve

Recurrent Laryngeal nerve

Dome of pleura

Brachial plexus

Lymphatics and thoracic duct

Phrenic nerve

Sympathetic chain, stellate ganglion

Scalene muscle.

Clavicle

b)

Requires management at a trauma centre with appropriate expertise. May require multiple speciality input - interventional radiology, ENT, vascular, cardiothoracic.

Airway issues:

• The possibility of laryngeal/ tracheal injury and the risk of intubating the “false airway passage”. Consider tracheostomy under local anaesthesia.

Urgent surgical exploration required for haemodynamic compromise, expanding or pulsatile haematoma, extensive subcutaneous emphysema, stridor, or neurological deficit with intra op bronchoscopy/ endoscopy/ angiography if available.

If    no    indication  for    urgent    surgical    exploration    requires    CT    angiography    (or    equivalent)    with    close
observation  in    ICU  +/-  flexible  laryngoscopy  +/-  endoscopy  +/-  oral  contrast  swallow  study.

Additional Examiners’ Comments:

Most candidates were not aware of the issues and management priorities associated with this type of trauma.

Discussion

Anatomy is not our strong suite. This question describes injury to Zone 1 of the neck, where all the important stuff seems to be. For an excellent revision of the important issues, the interested trainees are directed to Karim Brohi's 2002 write-up of neck wounds on trauma.org.

Generic approach to management:

1. Assess for airway compromise (eg. by expanding haematoma)
   Assess for airway injury (eg. subcutaneous emphysema)
   Organise expert help.
   Awake fiberoptic intubation by an experienced operator would be ideal, with an ENT surgeon on standby. Risks include intubating a false passage, or causing complete tracheal disruption.
2. Assess for respiratory compromise.
   Ausculation and percussion may reveal pneumothorax due to injury of the dome of pleura, or the raised hemidiaphragm of a phrenic nerve injury
3. Assess the circulation in the arm on the affected side. There may be vascular compromise.
   Angiography is very important; occlusion balloons may be very useful in controlling haemorrhage from deep vessels.
4. Assess the neurology of the patient, starting with GCS.
   Verterbral artery damage may present with spinal syndromes (eg. Brown-Sequard) or brainstem stroke signs
   Carotid artery damage may present with hemispheric stroke signs

Specific concerns in a Zone 1 injury:

• massive haemothorax
• arteriovenous fistula (subclavian vessels)
• Thoracic duct damage (if it was the left side of the neck, as it tends to be with a right-handed attacker coming from the front)
• brachial plexus damage
• Horner's syndrome

Reasons for urgent surgical exploration:

• airway compromise (stridor, etc)
• haemorrhgic shock
• expanding haematoma (or, especially if it is pulsatile)
• stroke-like symptoms

References

College Answer

Medical Measures to control bleeding

Activate Massive Transfusion Protocol as per local hospital guidelines. Close liaison with surgeon and haematologist is warranted.

Local pressure including adjunctive tourniquet use to control bleeding from the left leg wound.

Target lower systolic blood pressure (e.g. 80 mmHg) until major bleeding has been stopped (absence of brain injury permits the same). Permissive hypotension is tolerated and has shown survival benefits in some studies.

Correct hypothermia and acidosis.

Packed cells transfusion to target haemoglobin concentration 70 – 90 g/L to achieve adequate tissue perfusion.

Fresh Frozen Plasma to maintain INR & APTT < 1.5 x mean control. Usual dose 15 mL/kg.

Cryoprecipitate to maintain Fibrinogen levels > 1.5 g/L. Usual dose is 3-4 g or 50 mg/kg. (Fibrinogen

concentrate is also allowed).

Platelet transfusion to keep platelets > 50 x 109/L. With multiple injuries and suspicion of micro-vascular bleeding; platelet count can be aimed at > 100 x 109/L.
Supplemental Calcium to maintain ionised calcium > 1.1 mmol/L

Fluid Resuscitation with warmed crystalloid solutions. Aggressive fluid resuscitation is no longer recommended due to risk of pulmonary oedema, worsening of thrombocytopenia and coagulopathy due to haemoduilution.

Use of ROTEM/TEG targets Tranexamic Acid (see below)

Recombinant Factor VIIa: Not indicated at this stage (prior to surgery).

b)

Tranexamic Acid (TXA) is a synthetic lysine analogue that is a competitive inhibitor of plasminogen. TXA is distributed throughout all tissues with plasma half-life of 120 minutes.

Evidence: Recently published CRASH 2 trial; a multi-centre randomised, controlled trial examined the role of TXA against placebo in trauma patients, with, or at risk of significant haemorrhage. In more than 20,000 patients; TXA demonstrated a significant reduction in all-cause mortality at 4 weeks after injury (14.5% vs. 16%; RR = 0.91, P = 0.0035) and risk of death from bleeding (4.9% vs. 5.7%; RR=0.85, p=0.00077).

The risk of precipitated thrombosis with the use of the lysine analogues has been of major theoretical concern; however, CRASH-2 showed that the rate of thrombosis, especially myocardial infarction, was lower with the use of TXA. No adverse events were described with the use of TXA in CRASH-2, although an increased rate of seizures has been described in patients receiving a high dose of TXA when undergoing cardiac surgery.

A further analysis of CRASH-2 data showed that early treatment (< 1 hour and 1-3 hour from injury) significantly reduced the death rate of bleeding but treatment administered after 3 hours; increased the risk of death due to bleeding. Hence, TXA should be administered within 3 hours of injury.

TXA should be considered as adjunctive therapy in patients with traumatic haemorrhage in the setting of overall patient management; including strict attention to the control of bleeding, physiological and metabolic parameters, coagulation and temperature maintenance.

Additional Examiners’ Comments:

Most candidates answered this question well although knowledge relating to the evidence for tranexamic acid was overall limited. Some gave a reasonable discussion of the medical management of bleeding but omitted surgical strategies.

Discussion

The mess we're in:

• Anaemia (Hb 65)
• Thrombocytopenia (plts 46)
• Coagulopathy (INR 1.9, APTT 43, Fibrinogen 1.1)
• Metabolic acidosis (pH 7.29, SBE -11)
• Hypothermia (temp = 34.7°C)

Immediate resuscitation:

• Primary survey should include the assessment of core temperature.
  • Haemostasis by direct pressure wherever this is possible
• ABG to determine the pH, lactate, haemoglobin level and ionised calcium
• Activate the massive transfusion protocol in liason with local blood bank and haematology service
• Organise transfusion: 1:1:1 FFP, platelets, PRBCs.
  • Haemoglobin level is not a valid transfusion trigger, nor can transfusion wait for haemoglobin levels to become available. 
  • Any transfused blood products should be warmed with a heater. Six units of RBCs at 4ºC will reduce the body temperature of an average 70 kg adult by 1ºC.
  • Crystalloid is to be avoided unless there is no other option and haemodynamic performance if life-threateningly poor
• Tranexamic acid 1g over 10 minutes
• Correct ionised calcium
• Commence warming the patient externally
• Practice permissive hypotension if permitted by the absence of neurotrauma

Within the first 6 hours:

• Serial repeated Hb measurements
• Coags data, plus/minus TEG or ROTEM (its utility and cost effectiveness over traditional coags is still being questioned) will guide the ongoing use of blood products.
• FFP 15ml/kg if APTT remains elevated
• Tranexamic acid 1g over 8 hours to chase the first dose (as per CRASH-2 protocol)
• Cryoprecipitate 3-4g (or, 50mg/kg) should be given if the fibrinogen level is below 1.5
• Recombinant Factor VIIa (Novoseven) should be thought about if the coags are trending towards normal, and the patient is still exsanguinating (the dose should be 90 μg/kg)

Endpoint goals within the first 6 hours:

• No further haemorrhage
• SBP = 80-90
• MAP = 50
• Temperature >35.0°C
• pH >7.30
• Hb >70
• INR <1.5
• APTT <40
• Fibrinogen >1.0
• Platelets >50 (100 if there has been intracranial haemorrhage)
• iCa²⁺ >1.10 mmol/L

Use of ROTEM or TEG:

• No clear advantage to their use (Sankarankutty et al, 2011)
• Positive experience with both systems has been reported
• Slightly different transfusion strategies will result, depeding on which modality is used
• A major advantage over traditional coags is immediate access to fibrinolysis data

Evidence for the use of tranexamic acid in trauma

• CRASH-2 Trial (2010):  multi-centre international RCT; 20,211 patients in total. The trial-based dosing regimen was 1g of tranexamic acid within the first 3 hrs, followed by an infusion of 1g over the following 8 hours.
  • The all-cause mortality improvement was small (14.5% vs 16%) but reached significance because of the truly massive number of enrolled patients.
  • Similarly, the improvement in mortality from bleeding was also small (4.9% vs 5.7%)
  • The greatest improvement in mortality was seen in patients who received it earlier: 1 hour after the trauma was ideal. 
  • Analysis of cost-benefit had concluded that tranexamic acid was a very cheap way of saving many lives (Roberts et al, 2013).
  • Concerns regarding the increased risk of thrombosis were not supported by the analysis (in fact the tranexamic acid group had a lower rate of thrombosis and myocardial infarction)
• MATTERS study (2012): single centre observational study, 896 admissions with combat injury to a surgical hospital in southern Afghanistan. Mortality was improved in the intervention group (17.4% vs 23.9%) and the benefit was greatest among those who had massive transfusion
• MATTERS II study (2013)-  also a military retrospective observational study; 1332 patients over 5 years. Looking at whether administering tranexamic acid together with fibrinogin (cryoprecipitate) has any influence on mortality. Mortality was lowest in the tranexamic acid + cryoprecipitate group (11.6%), then the tranexamic acid group (18.2%), then the  cryoprecipitate alone group (21.4%) and finally the "nothing" group (23.6%).

Criticism of this evidence

• Reduction of fibrinolysis was the proposed goal, but no attempt to measure fibrinolysis was made.
• Tranexamic acid has an anti-inflammatory effect, which may account for some of the mortality difference (Volpi et al, 2015).
• In the CRASH-2 trial, doctors could choose to randomize or not randomize based on treatment certainty. Also, of the dead patients, only approximately 5% had bleeding as a cause of death. Approximately half of the patients in the trial did not even require a transfusion. in short, there are serious methodology concerns.
• Much of the trial intervention occurred in the pre-hospital environment, which makes it difficult to generalise the findings.
• If  the tranexamic acid was given later than 3 hours after the injury, it was associated with an increased risk of death from bleeding.
• The CRASH-2 trial did not find much evidence of increased risk of thrombosis, but the observational MATTERS study (2012),  which was conducted among "proper" trauma patients,  demonstrated that DVT/PE rates among patients who received tranexamic acid were 9 and 12 times higher (for PE and DVT respectively)

References

Sankarankutty, Ajith, et al. "TEG® and ROTEM® in trauma: similar test but different results." World J Emerg Surg 7.Suppl 1 (2012): S3.

Shoemaker, William C. "Comparison of the relative effectiveness of whole blood transfusions and various types of fluid therapy in resuscitation." Critical care medicine 4.2 (1976): 71-78.

El Sayad, Mohamed, and Hussein Noureddine. "Recent Advances of Hemorrhage Management in Severe Trauma." Emergency medicine international 2014 (2014).

Castellucci, Lana Antoinette. Evaluating Risk of Delayed Major Bleeding in Critically Ill Trauma Patients. Diss. University of Ottawa, 2016.

Stensballe, Jakob, and John B. Holcomb. "Hemostatic resuscitation is neither hemostatic nor resuscitative in trauma hemorrhage—But did they in fact test the effect of hemostatic resuscitation?." Journal of Trauma and Acute Care Surgery 78.6 (2015): 1237.

MacLeod, Jana BA, et al. "Early coagulopathy predicts mortality in trauma." Journal of Trauma and Acute Care Surgery 55.1 (2003): 39-44.

Lier, Heiko, et al. "Preconditions of hemostasis in trauma: a review. The influence of acidosis, hypocalcemia, anemia, and hypothermia on functional hemostasis in trauma." Journal of Trauma and Acute Care Surgery 65.4 (2008): 951-960.

College Answer

a)

• Type of circuit – AC current worse than DC
• Duration of exposure
• Resistance of tissues : higher the resistance greater the thermal energy produced and greater the damage to the tissues
• Voltage: > 1000 V is high voltage and causes greater tissue damage. Current
• Pathway of current: affects the part of the body that is damaged

b)

• Chest compartment syndrome due to circumferential trunk burns,
• Tight burns dressing on the chest
• Pulmonary oedema due to cardiac involvement
• Pulmonary aspiration
• Lung contusions due to trauma associated with incident
• Abdominal compartment syndrome
• Undersedation/ventilator dysynchrony

c)

• Examine the patient to rule out compartment syndrome.
  • Surgical opinion and fasciotomy should be considered early
• Prevention of AKI Correction of volume depletion: if present rigorous fluid repletion until it is clear from sequential laboratory values that the plasma CK level is stable and not increasing
  • Prevention of intratubular cast formation- a forced alkaline diuresis, in which the urine pH is raised to above 6.5, may diminish the renal toxicity of haem proteins.
  • Diuresis with mannitol can be considered – currently no evidence
• Treatment of Established Renal Failure:
  • CRRT

Discussion

a)

Factors determining the severity of electrical injuries in general (Kombourlis et al, 2002)

• Size of the current: the greater the current (in amperes) the worse the injury. This is the most important determinant of electrical injury; the severity is the most directly related to amperage. Current in excess of 5A can cause sustained asystole.
• Duration of the current: the longer the duration of exposure, the worse the burn
• Magnitude of the voltage: the higher the voltage, the greater the damage
• Tissues traversed by the current: the most important examples being the brain and heart.
• Contact conduction vs. arcing: i.e. current arcing though ionised air causes surface flash burns which may be diffuse, whereas contact with an electrode causes burns at the specific site of contact.
• Presence of a surface conductor, eg. water. Wet skin has its normally high resistance reduced a hundred-fold, with a much larger
• Subcutaneous conduction: most of the resistance to current is by the dry skin. Once it is penetrated, the resistance is greatly reduced. Resistance of the blood and muscles is approximately 20-50 times less than that of the skin (500-1000 Ohm vs 100,000 Ohm). Microshock can be the consequence, which is a risk to ICU patients who have various conductive materials suspended in their bodies.

Factors determining the severity of electrical burns specifically:

• As per Kombourlis, "The severity of the burn depends on the intensity of the current, the surface area, and the duration of exposure."
• Magnitude of the current is most important factor. Current in excess of 1A is enough to cause skin burns.
• Duration of exposure is the next most important factor.
• Surface area of exposure is an important determinant of burn severity and depth: if one has a wide surface area exposed, the current is distributed across all of it, and the damage is relaitvely minor- whereas if all of the current was concentrated in a small area, the burn would be deep and severe. This is the ratonale behind making big wide electrode pads for cardioversion.
• Magnitude of the voltage does not seem to matter (Ferreriro et al, 1998)

b)

" List the potential causes of poor lung compliance", they asked. This is weird, because according to Koumbourlis, "there are no specific injuries to the lungs or the airways directly attributable to electric current." In view of this, the author was forced to concoct an imaginative list of respiratory complications for a condition which usually has none.

• Pulmonary oedema due to heart failure or enthusiastic fluid resuscitation
• Pneumothorax from CPR
• Burns causing reduced chest wall compliance
• Thoracic compartment syndrome (myonecrosis of the intercostal muscles, or circumferential burns)
• Abdominal compartment syndrome (myonecrosis of the abdominal muscles, or circumferential burns)
• Sustained tetany: especially with AC at household frequency (50-60Hz), which can induce "an indefinite refractory state at the neuromuscular junction" (Koumbourlis, 2002), causing sustained tetanic contraction.
• Fractured ribs from CPR or due to a fall
• Lung contusions from CPR, being thrown, or blast damage
• Inhalational injury from burned material (see above).
• Aspiration due to unconsciousness

c)

Something specific to high voltage electrical injury is the need to debride the necrotic muscle.  Occasionally, the whole limb is unviable and must be amputated.

As far as generic mangement of rhabdomyolysis, a recent meta-analysis of management strategies has presented the following conclusions:

• Commence IV fluids within 6 hours - as early as possible
• Aim for a urine output greater than 300ml/hr
• Use of sodium bicarbonate is only indicated to correct systemic acidosis. There is no evidence for any benefit in rhabdomyolysis-induced AKI except for some uncontrolled case series, which does not stop people from recommending it anyway. It appears in the 2010 college answer, which pre-dates the 2013 meta-analysis. The savvy trainee seeking to remain in the good books with examiners who use forced alkaline diuresis will want to mention this therapy in their answer, with the caveat that it is may not be helpful, but is also probably not harmful.
• Use of mannitol is only indicated if urine output >300ml/hr cannot be maintained

References

Bernstein, Theodore. "Electrical injury: electrical engineer's perspective and an historical review." Annals of the New York Academy of Sciences 720.1 (1994): 1-10.

Koumbourlis, Anastassios C. "Electrical injuries." Critical care medicine 30.11 (2002): S424-S430.

Kisner, Suzanne, and Virgil Casini. "Epidemiology of electrocution fatalities." (2002).

PITTS, WILLIAM, et al. "Electrical burns of lips and mouth in infants and children." Plastic and reconstructive surgery 44.5 (1969): 471-479.

Rosen, Carlo L., et al. "Early predictors of myoglobinuria and acute renal failure following electrical injury." The Journal of emergency medicine 17.5 (1999): 783-789.

Brumback, Roger A., Daniel L. Feeback, and Richard W. Leech. "Rhabdomyolysis following electrical injury." Seminars in neurology. Vol. 15. No. 04. © 1995 by Thieme Medical Publishers, Inc., 1995.

Price, Timothy G., and Mary Ann Cooper. "Electrical and lightning injuries." Marx et al. Rosen’s Emergency Medicine, Concepts and Clinical Practice, Mosby, 22 (2006): 67-78.

College Answer

                a)                                                                                                                                              

The key clinical signs to indicate a patient has sustained traumatic asphyxiation include:

• Facial and upper chest petechiae
• Sub-conjunctival hemorrhages
• Cervical cyanosis
• Neurological signs due to cerebral edema
• Temporary loss of vision as a result of retinal edema

b) 

Resuscitative thoracotomy is a procedure of last resort that is nearly always performed in the emergency department and involves gaining rapid access to the heart and major thoracic vessels through an anterolateral chest incision or clam shell incision to control exsanguinating haemorrhage or other life-threatening chest injuries   

What are the indications for resuscitative thoracotomy? 

• Extremely controversial

Accepted Indications                                                               

• Penetrating / Blunt thoracic injury
• Traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)
• Unresponsive hypotension (BP < 70 mmHg)
• Rapid exsanguination from chest tube (> 1500 mL)

 Relative Indications                                                                 

• Penetrating thoracic injury
• Traumatic arrest without previously witnessed cardiac activity
• Penetrating non-thoracic injury and  Blunt thoracic injuries
• Traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)

Contraindications to resuscitative thoracotomy            

• The patient has no signs of life at the scene of injury
• Asystole is the presenting rhythm and there is no pericardial tamponade
• Prolonged pulselessness (> 15 minutes) occurs at any time
• Massive, non-survivable injuries have occurred

Discussion

This SAQ was not passed by anybody, which again brings into question the utility of asking trainees about such esoterica as traumatic asphyxia or pyroglutamic acidosis. Does one's inability to discuss these topics really act as a sensitive discriminator to tell "junior consultant" from "competent senior registrar"?

Anyway.

a) "Traumatic asphyxia" is defined as "a form of suffocation where respiration is prevented by external pressure on the body". It is essentially a crush injury of the thorax, with impaired respiration as the result of greatly decreased chest expansion. Failure of venous return from the upper body results in the characteristic clinical findings, all of which can be attributed to greatly increased venous pressure. This list of signs is composed on the basis of articles by Byard et al (2006) and  Eken et al (2009)

Common features:

• Cyanosis of the upper body, especially the face
• Conjunctival haemorrhage
• Conjunctival oedema
• Petechial haemorrhages and purpura over the face, neck and upper face
• Oedema and congestion of the head
• The "brassiere sign" - petechhii and congestion of asphyxia spare those areas of the thorax which were covered by tight-fitting clothing, as it obstructs cutaneous blood flow and prevents the formation of petechii. This is typically observed in women who were wearing a bra during their crush injury, or a tight-fitting singlet as in the case of the moustachioed gentleman in the picture.

Uncommon features:

• Chemosis
• Exophthalmos
• Retinal haemorrhages and visual loss
• Vitreous haemorrhagic exudates (Purtscher’s retinopathy- Choi et al, 2010 )
• Retrobulbar (posterior orbital) haemorrhages
• Haemotympanum

Other sequelae:

• Loss of consciousness
• Seizures
• Blindness
• Hearing loss
• Cerebral venous infarction

b) Resuscitative thoracotomy is defined as a left-sided clamshell thoracotomy performed for the specific purpose of gaining rapid access to the heart and major thoracic vessels.

Indications for resuscitative thoracotomy  (Rabinowici et al, 2014)

• The patient is in cardiac arrest
• The cause is blunt or penetrating chest trauma (evidence is strongest for penetrating cardiac trauma, where the survival rate is apparently 40% - JACS, 2001)
• Arrest is after arrival to hospital, or shortly before. The "down-time" should be less than 10 minutes for blunt trauma and less than 15 minutes for penetrating trauma.
• There is suspicion that reversible pathology is present in the chest, which includes cardiac tamponade or injury to the greater vessels
• Massive haemothorax (1500ml of blood in the hemithorax)
• There is sufficient surgical expertise available to carry on with a more formal damage control surgery after the patient is stabilised (otherwise, there is no point opening the chest)

Contraindications for resuscitative thoracotomy

• No signs of life witnessed in the pre-hospital setting
• Prolonged pre-hospital CPR
• Asystole on presentation, and no cardiac tamponade
• Massive extrathoracic injuries which may be unsurvivable

References

Morrison, Jonathan J., et al. "Resuscitative thoracotomy following wartime injury." Journal of Trauma and Acute Care Surgery 74.3 (2013): 825-829.

Burlew, Clay Cothren, et al. "Western Trauma Association critical decisions in trauma: resuscitative thoracotomy." Journal of Trauma and Acute Care Surgery 73.6 (2012): 1359-1363.

Ohrt-Nissen, S., et al. "Indication for resuscitative thoracotomy in thoracic injuries—Adherence to the ATLS guidelines. A forensic autopsy based evaluation." Injury 47.5 (2016): 1019-1024.

Rabinovici, Reuven, and N. Bugaev. "Resuscitative thoracotomy: an update." Scandinavian Journal of Surgery (2014): 1457496913514735.

CALS program manual: "Emergency Thoracotomy (Circulation Skills 4)"

Working Group, Ad Hoc Subcommittee on Outcomes. "Practice management guidelines for emergency department thoracotomy." Journal of the American College of Surgeons 193.3 (2001): 303-309.

Keller, Deborah, et al. "Life after near death: long-term outcomes of emergency department thoracotomy survivors." Journal of Trauma and Acute Care Surgery 74.5 (2013): 1315-1320.

College answer

a) Type of fluid: 
Fluid resuscitation of patient with moderate to severe burns consists of an isotonic crystalloid solution, such as Hartmann‟s solution or plasmalyte. Large volumes of 0.9% NaCl may be associated with hyperchloremic metabolic acidosis. 
The colloids (albumin) are more expensive, and do not improve survival, compared to crystalloids. 
The use of hypertonic saline does not provide better outcomes than isotonic saline. 
 
    Estimating fluid requirements:                                
No formula provides a precise method for determining the burn victim's fluid requirements; the formulas described provide only a starting point and guide to initial fluid resuscitation. Patient age, severity of burns and co-morbidities can substantially alter the actual fluid requirements of individual patients. 
Parkland (or Baxter or consensus) Formula (most widely used):  
Fluid requirement (ml) = 4 x body weight x percentage of burns. (Only deep) 
One half of the calculated fluid is given over the first eight hours and the remaining over the next 16 hours. 
The rate of infusion should be as constant as possible; sharp decrease in infusion rates can cause vascular collapse and increase in edema. 
Modified Brooke Formula: Fluid requirement (ml) over the initial 24 hours = 2 x body weight x percentage of burns. 
This formula may reduce the total volume used in fluid resuscitation without causing harm. 
Following initial resuscitation, IV fluids are administered to meet baseline fluid needs and maintain urine output. 
Care should be taken to avoid fluid overload, as associated with pulmonary edema, peripheral edema leading to compartment syndrome. 
Inadequate resuscitation suggested by poor urine output should be managed by judicious fluid boluses and an increase in the infusion rate. 
 
b) List the diagnostic possibilities  
Cardiogenic Shock (severe myocardial suppression caused by burns, pre-existing myocardial dysfunction) 
Cyanide toxicity 
Compartment Syndrome, including abdominal compartment 
Carbon monoxide poisoning 
Blast injury 
Ingestion of toxins (ethylene glycol, methanol, salicylates) 
Acute Liver Failure 
 
Additional Examiners' Comments: 
Most of the candidates answered this question very well. Candidates who did not pass showed knowledge gaps, poor synthesis of knowledge and poorly structured answers. 

Discussion

This question closely resembles Question 21 from the first paper of 2014, with the exception of the fact that this time an ABG was also offered.The ABG does not add very much to the process of answering this question, and therefore the discussion section for Question 21 is reproduced here with minimal modification.A detailed dissection of fluid resuscitation for the burns patient  is performed in the Required Reading section. Physiologic consequences of burns is also covered there. The ABG looks like a metabolic acidosis, which would accompany any sort of shock state - and so the "Causes of Shock in the Acute Burns Patient" table was still relevant here.

a)

In brief:

Fluid resuscitation end point:

• urine output of 0.5-1.0 ml/kg/hr (Paratz et al, 2014)
• MAP >65mmoHg

Choice of fluids:

• Resuscitation should use a balanced solution to avoid hyperchloraemic acidosis (Walker et al, 2001)
• Most formulae recommend Ringer's Lactate; the locally available version is Hartmanns
• The disadvantage of crystalloid is the potential need for massive volume
• Historically, significantly more fluid is given to burns patients  then is predicted by any formula (Mitra et al, 2006). This is known as "fluid creep" and is associated with significant complications, of which the most serious is abdominal compartment syndrome.
• Colloid (eg. albumin) is also recommended by many of the formulae
• The advantage of colloid is that it may alleviate "fluid creep" and achieve haemodynamic goals more rapidly and with less volume
• There is no evidence that albumin improves survival or organ dysfunction (Melinyshyn et al, 2013)
• The theoretical advantage of hypertonic saline is earlier achievement of haemodynamic goals and the avoidance of burns-associated hypernatremia. However, hypertonic saline solutions were associated with a fourfold increase in the risk of renal failure and a twofold increase in the risk of death (Huang et al, 1995)

Resuscitation formulae

It is probably worth adding that this patient is at high risk of inhalational injury. He was unconscious, and sharing a small enclosed space with his fire. Naver et al (1985) demonstrated that patients with smoke inhalation injury and airway burns require a larger volume of fluid resuscitation. The total volume is increased up to 35% - 65%.

b)

Causes of shock in the unconscious burns patient with metabolic acidosis

Let this be an exercise in generating differentials.

• Wrong BP measurement (eg. arterial line is not zeroed)
• Cardiogenic shock
  • Due to cytokine storm of severe burns
  • Due to carbon monoxide toxicity (i.e. severe tissue hypoxia)
  • Due to cyanide toxicity (i.e. mitochondrial failure)
  • Due to a myocardial infarction (due to increased myocardial oxygen consumption in context of burns, on top of pre-existing ischaemic heart disease)
• Abdominal compartment syndrome (over-resuscitation)
• Tension pneumothorax (explosion)
• Spinal injury neurogenic shock (unrecognised due to unconsciousness)
• Blood loss from some internal injury or due to DIC
• Under-resuscitated burns shock (i.e. fluid shifts)
• SIRS vasoplegia
• Anaphylaxis to some drug given in hospital

In more detail:

References

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.

Bak, Zoltan, et al. "Hemodynamic changes during resuscitation after burns using the Parkland formula." Journal of Trauma and Acute Care Surgery 66.2 (2009): 329-336.

Blumetti, Jennifer, et al. "The Parkland formula under fire: is the criticism justified?." Journal of burn care & research 29.1 (2008): 180-186.

Baxter, Charles R., and Tom Shires. "Physiological response to crystalloid resuscitation of severe burns." Annals of the New York Academy of Sciences 150.3 (1968): 874-894.

Saffle, Jeffrey R. "The phenomenon of “fluid creep” in acute burn resuscitation." Journal of burn care & research 28.3 (2007): 382-395.

Naver, P. D., J. R. Saffle, and G. D. Warden. "Effect of inhalation injury on fluid resuscitation requirements after thermal injury." Plastic and Reconstructive Surgery 78.4 (1986): 550.

Arlati, S., et al. "Decreased fluid volume to reduce organ damage: a new approach to burn shock resuscitation? A preliminary study." Resuscitation 72.3 (2007): 371-378.

Bittner, Edward A., et al. "Acute and Perioperative Care of the Burn-Injured Patient." Survey of Anesthesiology 59.3 (2015): 117.

Melinyshyn, Alex, et al. "Albumin supplementation for hypoalbuminemia following burns: unnecessary and costly!." Journal of Burn Care & Research 34.1 (2013): 8-17.

Cooper, Andrew B., et al. "Five percent albumin for adult burn shock resuscitation: lack of effect on daily multiple organ dysfunction score." Transfusion 46.1 (2006): 80-89.

Wilkes, NICHOLAS J. "Hartmann's solution and Ringer's lactate: targeting the fourth space." Clinical Science 104.1 (2003): 25-26.

MONAFO, WILLIAM W. "The treatment of burn shock by the intravenous and oral administration of hypertonic lactated saline solution." Journal of Trauma and Acute Care Surgery 10.7 (1970): 575-586.

Huang, Peter P., et al. "Hypertonic sodium resuscitation is associated with renal failure and death." Annals of surgery 221.5 (1995): 543.

Sun, Ye-Xiang, et al. "Effect of 200 mEq/L Na+ hypertonic saline resuscitation on systemic inflammatory response and oxidative stress in severely burned rats." Journal of Surgical Research 185.2 (2013): 477-484.

Paratz, Jennifer D., et al. "Burn Resuscitation—Hourly Urine Output Versus Alternative Endpoints: A Systematic Review." Shock 42.4 (2014): 295-306.

Walker, Steven C., et al. "Balanced Electrolyte Solution Reduces Acidosis as Compared to Normal Saline in the Resuscitation of Perioperative Burn Patients." Anesthesiology 95 (2001): A375

College answer

a) Differential diagnoses

• Iatrogenic fluid volume overload due to blood product/ resuscitation fluid
• Atelectasis/Collapse/ sputum plugging
• Unrecognised pulmonary contusions
• Unrecognised pneumothorax – Mech vent, line insertion
• Aspiration at time of MBA or at intubation
• Endobronchial intubation
• Transfusion related acute lung injury (TRALI)
• Cardiogenic pulmonary oedema/myocardial event
• Fat embolism syndrome
• Anaphylaxis
• PE

b) Assessment

• History
  • Details of accident
•  PMH
  • Allergies
• Clinical examination
  • Ensure adequate tertiary survey
  • Detailed respiratory examination
  • Review fluid balance and urine output
  • Evidence of generalised allergic reaction FBE – Hb, WCC, eosinophilia
• Investigations
  • Coags – ongoing coagulaopathy, 
  • Chest XRay – infiltrates, ETT position, hardware, PTx, pleural effusions
  • Cardiac enzymes – TnI
  • ECG – ischaemic changes, arrhythmia, R heart strain
  • Echocardiogram – if suspect cardiogenic component, assess LVF, or RVF for PE
  • CTPA – early for PE but possible if patient delayed in ED
  •  Bronchoscopy – if evidence of localised collapse or unexplained infiltrates

Discussion

The possible differentials must be broad. Why?

• Old guy with ischaemic heart disease
• Long bone injuries
• Extensive blood loss (thus, likely a massive transfusion)

Thus, perioperative hypoxia could have resulted from any combination of the following differentials:

• Fat embolism
• Acute MI with pulmonary oedema
• Transfusion-associated circulatory overload
• Trasfusion-associated lung injury

To discriminate among them, the following investigative steps might be taken:

History from the anaesthetist:

• Exact timing of onset of hypoxia, as related tos urgical manipulation
• Any changes in ST segments or arrhythmias intraoperatively
• Exact volume of blood products and fluid resuscitation
• Any perioperative TOE findings (if they did one)
• Ventilation mechanics and EtCO₂ trends - anaesthetists often note a sudden drop in end-tidal CO₂ concentration during a stable steady state

Examination of the patient, looking for

• Respiratory features: moist crepitations over all lung fields, hypoxia, cyanosis
• Characteristic petechial rash, usually over the anterior axillary fold and at the root of the neck, as well as on the buccal mucosa and the conjunctiva. This distribution can be explained by fat droplets accumulating in the aortic arch prior to embolisation to nondependent skin via the subclavian and carotid vessels.
• Fever
• Tachycarda
• Retinal haemorrhages
• Visible fat droplets on ophthalmoscopy
• Jaundice
• Renal impairment

Laboratory tests,  looking for:

• Thrombocytopenia
• Anaemia (sudden decrease)
• High ESR
• Fat macroglobulinaemia
• Troponin

Imaging

• ECG looking for ischaemic changes
• TTE looking for right sided strain and LV function 
• CXR looking for pulmonary oedema

References

College answer

A. General; compliance with CICM/ANZCA/ACEM guideline;

 Possible clinical impact of the transport environment (in this case flight environment may be particularly deleterious if patient is exposed to sub-atmospheric pressure).

• Urgency of intervention – urgent
• Road transport times and road conditions  
• Weather conditions and aviation restrictions for airborne transport  
• Aircraft landing facilities  
• Range and speed of vehicle                                

 a) Team with suitable training and experience

• Clinical – adequate seniority
• Logistic – aircraft safety training and familiarity with transport equipment/environment 

 
b) Equipment- appropriate ventilator, monitors, alarms, devices for manual handling, pumps to maintain infusions. Full list from the CICM guideline not required but key elements needed

• Respiratory support equipment (doesn’t need extensive expansion other than ventilator, manual ventilation equipment, appropriate gear for reintubation)
• Circulatory support equipment:
  • Monitor/defibrillator/external pacer combined unit  
  • Multifunction monitor including capnograph
  • Intravenous fluids and pressure infusion set  
  • Infusion pumps
  • Syringes and needles
  • Pericardiocentesis and thoracostomy equipment
• Other equipment:  
  • Personal protective equipment
  • Nasogastric tube and bag
  • Urinary catheter and bag
  • Thermal insulation and temperature monitor  
• Consideration should be given to alternative vascular access such as intraosseous devices  

 
c) All drugs should be checked and clearly labelled prior to administration. The range of drugs available should include all drugs necessary to manage acute life-threatening medical emergencies and those specific to the patient’s clinical condition 
 
d) Liaison with the receiving centre ensuring key details have been conveyed, especially relevant in this case 
 
e) Final preparation of the patient should be made prior to transport, with anticipation of clinical needs. Examples include giving appropriate doses of muscle relaxants or sedatives, replacing  near-empty inotrope and other intravenous solutions with fresh bags, and emptying drainage bags

 B. Specific to condition;  Need to consider mode of transport

• 300km essentially obviates road  
• Fixed wing has potential for sea level cabin but requires increased handling
• Helicopters not pressurised and may not be suitable unless terrain allows low-level flight 

The candidates needed to be aware that minimal cabin altitude is a key part of management. 

• Airway
  • ETT secured, CXR to confirm the position
  • May need suctioning if prolonged delay to retrieval
• Ventilation
  • 100% FiO2
  • Minimise PEEP (5cm H2O)
  • Check ABG, and ventilate at TV 6-ml/kg, SIMV, rate to maintain normocarbia
  • CAGE may be associated with other barotrauma so CXR to exclude pneumothorax •
• Circulation
  • Try to maintain euvolaemi
  • As on vasopressors will need CVC. CVC needs to be well secured. Probably dilute vasopressors according to retrieval regimen to ensure smooth transition
• Neurological
  • Maintain normothermia
  • Will need sedation and paralysis for transport, again dilutions as per retrieval
  • Regular check of BSL, aim 6-10
  • Should have CT to exclude differential diagnosis.
  • Copy will need to go with patient (hard copy or digital copy) 

 C. Interim management in liaison with hyperbaric unit

Additional Examiners’ Comments: This answer template is long and detailed and it was not expected that candidates needed to reproduce it all to obtain a pass. Important points were the awareness and compliance with guidelines on transport of critically ill patients, and the awareness that minimising flight altitude is essential. 

Discussion

Preparation, planning and implementation of transfer sounds a lot like a question on aeromedical retrieval. However, for some reason this gas embolism question ended up in the Trauma category.

Administrative/logistic planning of the transfer:

• Consider the urgency of transfer, depending on clinical need.
• Transfer options which are available in this scenario all have some advantages and disadvantages:
  • The timing of the transfer is less important than the safety of the patient, as recompression therapy still has a role to play even 24-48 hrs after the injury; therefore there is no imperative to transfer by air immediately.
  • If the dive was recent (within the last 24 hrs), exposure to altitude in a commercial aircraft cabin could give rise to new gas emboli.
  • One may use a pressurised cabin instead. The additional weight and the need to fly at a lower altitude increases the amount of fuel required by up to 30%, and the travel time is longer.
  • Travel by road may be up to 4 hrs. During this time, vibration in the vehicle may give rise to increased tribonucleation, whereby gas bubbles precipitate out of a solution. 

• Which of the possible options are chosen (road, fixed wing, helicopter, pressurised vs. depressurised cabin) depends on the clinical state of the patient.
• If the patient is stable on vasopressors and mechanicaly ventilated, road transport may be the safest option (i.e. one which does not promote any new neurological injury). The next best option is retrieval by an aircraft with a sea-level pressurised cabin.

Preparation of the patient

• Secure the airway with immobiliser devices to ensure the patient is not accidentally extubated in transit
• Trial the patient on the retrieval transport ventilator for ~ 30 minutes prior to transfer, to ensure that this is well tolerated
• The patient will be on 100% FiO₂ throughout this transfer; there should be no hiatus in therapy. Ensure that the transport vehicle has enough oxygen supply to last for two such trips  
• Ensure all vascular access is established before transfer, and all ports easily accessible.
• Administer thiopentone - ensure the cerebral metabolic rate is lowest in the event of worsening cerebral ischaemia. This also protects against seizures.
• Administer long-acting muscle relaxant
• Perform one last pre-transfer assessment.

Preparation of personnel and family

• Brief senior retrieval staff (this complex job is not for the junior trainees)
• Ensure accepting hospital have received a detailed handover about the patient
• Next of kin need to be updated about the trasnfer
• Medical documentation travels with the patient
• Receiving unit receives updates on transfer status (i.e. call them as you are about to leave)

References

College answer

1. Spurious

1. Damped or poorly functioning, zeroed, arterial line
2. Inappropriate sized cuff
   1. Check line, cuff size
   2. Measure second site, alternative modality

2. Hypovolemia

1. Review volumes of administered fluids to date
2. Confirm size and depth of burn
3. Check calculations for fluid resuscitation are correct
4. Rising haematocrit, ECHO findings

i. Increase fluid resuscitation rate

3. Bleeding from occult/missed injury

a. Review/repeat trauma imaging

i. Blood product resuscitation, correction of coagulopathy ii. Operative/Interventional radiology interventions to treat cause

4. Sepsis             
   1. Too early for burn sepsis – possible intraabdominal or thoracic blast injury
      1. Broad spectrum antibiotics and source control
5. Distributive
   1. High cervical spine injury
      1. Review imaging, vasopressors
   2. Anaphylaxis to drugs
      1. Review history, examine for rash/bronchospasm, adrenaline c. Cyanide toxicity

i. Mixed venous oxygen, empirical antidote administration

Cardiogenic

1. 1. Takustubo, underlying cardiac disease, blast injury, myocardial toxins
      1. ECHO, ECG, Inotropic support

5. Obstructive
   1. Tension pneumothorax
      1. CXR, drainage

b. Abdominal compartment syndrome

i. Bladder pressure, escharotomies, laparotomy/laparostomy

c. Tamponade

i. Echo and pericardiocentesis

Examiners comments: 

 Most candidates were not able to amalgamate the three crucial aspects of this patient i.e., trauma in a burns patient in the setting of a closed area explosion.

 Many focused solely on the burns with little reference to the trauma. 

 Many used a generic ABCD template without applying it to the patient.

 Many answer structures were haphazard with an initial list of the causes followed by the management, with the result that the management for a number of the differentials were missed.

 The best answers used a table or bulleted list approach taking about causes as well as management.

Discussion

Though the college describes this as an "explosion", it is highly unlikely that this patient was exposed to a blast wave (as usually household explosions are of the deflagration variety) and so the discussion will focus mainly on the investigations and management of burns-related hypotension. Blast injury is mentioned in the list as an aside, in response to the comment that most answers "focused solely on the burns with little reference to the trauma".

Thus:

Possible causes of shock in this patient (table adapted from "Causes of Shock in the Trauma Patient")

Management, therefore, will consist of the following steps:

• Confirm blood pressure measurement invasively (i.e. insert an art line)
• Exclude immediately lifethreatening causes of shock:
  • Tension pneumothorax (examination)
  • Cardiac tamponade (TTE)
• Estimate fluid requirements using the modified Parklands Formula
• Assess fluid responsiveness via multimodal approach (combination of dynamic and static tests, including physical examination, ABG lactate, pulse pressure variation and passive leg raise)
• Offer a combination of crystalloid and colloid (expecting protein losses to be substantial)
• Vasopressors may be required (a vasodilated state formerly known as SIRS may develop)

References

College answer                                                                                                                                       

a)

The potential issues the that need to be considered in this patient include

• Electrocution
• Trauma from the fall
• Hypoxic-ischaemic brain injury
• Aspiration

1. Electrocution
   • Myocardial damage/Unstable rhythm
   • External burns
   • Rhabdomyolysis/ internal tissue burn / compartment syndrome.
   • Electrolyte abnormalities e.g. hyperkalaemia
   • Traumatic injuries as below
   • Hypovolaemia due to fluid extravasation
   • Neurological damage –central and peripheral, including autonomic neuropathy

2. Hypoxic-Ischaemic Brain injury

3. Trauma from the fall
   • Head and or spine injury
   • Blood loss
   • Abdominal injury
   • Rib fractures
   • Long bone/ pelvic injury

4. Aspiration 
   • Pneumonitis
   • Foreign body aspiration

b)                                                                                                                                             

The assessment of factors contributing to AKI in this setting

Pre-renal causes

• Most likely o Ongoing/ new hypovolaemia
  • Low cardiac output secondary to myocardial injury o Renal artery/vein injury from trauma
• Assess volume status
• History, examination, monitoring, investigations
• Check Hb
• * echocardiography
• Urinary fractional sodium excretion

Renal causes

• Most likely o Rhabdomyolysis o Other nephrotoxin o Abdominal compartment syndrome
  • Drug reaction -> interstitial nephritis
• Examination for ongoing compartment syndrome, check CK
• Assess medications and cease any nephrotoxins (NSAIDS, gentamicin, vancomycin)
• Examination of abdomen, measure intra-abdominal compartment pressure, consider renal ultrasound with duplex if retroperitoneal haematoma
• Urinary microscopy to look for casts, assess medications for potential causes (penicillins, cephalosporins, pantoprazole)

Post renal causes

• Most likely IDC obstructed, or clot in renal pelvis, pelvis causing ureteric obstruction
• Ensure IDC not blocked o Flush catheter, bladder ultrasound o Renal ultrasound to exclude obstruction

Discussion

Major issues in the management of the patient:

• Airway:  assess the ETT tip position: he was intubated in the field, and the ETT position may be sub-optimal
• Respiratory management: assess the efficacy of mechanical ventilation; the patient may have developed pulmonary oedema. A CXR would be in order.  
• Cardiovascular management: ECG to assess the effect the current had on the conduction system, and the presence of any ischaemic changes. Ensure pacing is available. The patient will likely go on to develop a global reperfusion injury, and a vasodilated state should be expected.
• Transthoracic echo / inotropes: cardiac function needs to be assessed; depressed contractility may be expected
• Neurological management: this comatose survivor of cardiac arrest may also have hit his head falling off that ladder.
  A CT brain would be in order to exclude intracranial haemorrhage. Once that is done, he may be cooled in by some sort of a therapetic temperature management protocol, down to 36° for 24 hours.
• C-spine: the patient had a fall; C-spine fracture needs to be excluded.
• Electrolyte management: there is a high likelihood of some potassium and phosphate elevation due to muscle breakdown (thus, assess with blood biochemistry). Serum calcium may be low, and may require replacement
• Fluid management: burns and damaged muscle will attract fluid and result in evaporative/exudative loss in the case of the former and third-spacing in the case of the latter. Physical examination and BP monitoring will reveal this. Fluid 
• Musculoskeletal trauma: the fall and violent spasmodic muscle contraction may have given rise to bone fractures. Arcing of high voltage current may have resulted in burns. It would be important to assess these by a whole-body survey. 
• CT of the extremities: myonecrosis may be hidden; deep burns may have no external manifestations
• Rhabdomyolysis: myonecrosis may occur; a CK level will reveal this. The patient should receive a sufficient amount of fluid to promote diuresis, as well as an alkalinising agent such as sodium bicarbonate.
   

Part b) asks about the assessment of renal failure in this patient. That's got to be a 6-mark (60%) answer, so it can't just be "send a CK and urinary myoglobin". Sure, the high voltage injury is likely the cause of some deep myonecrosis and this has probably put the patient into a rhabdomyolysis-induced ATN. However that is not the only possibility. Because the patient is complex and may have multiple problems by Day 4, there may be numerous differentials for this AKI. For instance, the 30 minutes of 'down-time" during the cardiac arrest may have given rise to a global hypoxic-ischaemic reperfusion syndrome, and the ATN might be due to that. Or the burns resulting from the electrocution resulted in a prothrombotic state and the patient has developed renal vein thrombosis. Or the IDC is blocked. In short, one would need to deploy a lightly electric-flavoured version of the usual workup for acute kidney injury.

That would look a little like this:

• Rule out mechanical obstruction
  • Explore the IDC (is it blocked?)
  • Perform a renal tract ultrasound
• Exclude obvious causes of pre-renal failure
  • Exclude abdominal compartment syndrome due to intraabdominal burns
  • Exc
  • Renal vascular disease (one may wish to perform renal doppler studies to exclude renal artery stenosis or renal vein thrombosis)
• Examine the urinary sediment
  • Hyaline casts are not associated with anything specific
  • Fatty and waxy casts are suggestive of long-standing renal disease, whatever its cause.
  • Muddy brown (coarse granular) casts and tubular epithelial casts are associated with ATN
  • Red blood cell casts indicate glomerular disease
  • Shredded-looking RBC fragments also indicate glomerular disease
  • Intact-looking red cells suggest some source of bleeding inside the urinary tract, eg. calculi trauma, malignancy, or the haemorrhagic cystitis of cyclophosphamide therapy.
  • Eosinophils in the urine, especially when they comprise in excess of 5% of the total urinary WCCs, may suggest acute interstitial nephritis
  • White cells in excess, and white cell casts specifically, suggest pyelonephritis
  • Pigmented casts may suggest myoglobin as the cause of ATN
  • Urinary myoglobin levels confirm rhabdomyolysis
  • Urinary crystals suggest some sort of crystalline nephropathy (they might be urate, oxalate, sulfonamides, etc)

• When all else fails
  • A renal biopsy may yield diagnostic information, provided one manages to biopsy something relevant. Potentially, one's sample could be full of uselessly necrotic parenchyma, which all looks the same (therefore there will still be no diagnosis, and now one's patient has a hole in their kidney).

References

College answer

a)

The root of the neck is the junction between the thorax and the neck. It opens into, and is the cervical side of, the superior thoracic aperture, through which pass all structures going from the head to the thorax and vice versa

 The root of the neck is bound laterally by the first rib, anteriorly by the manubrium, and posteriorly by the T1 vertebrae.  

From anterior to posterior, the major contents are:          

• Subclavian artery and branches 
  • vertebral artery
  • internal thoracic artery
  • thyrocervical trunk
  • costocervical trunk
• Subclavian vein and tributaries (EJV)
• Trachea
• Oesopahagus
• Vagus nerve
• Recurrent Laryngeal nerve
• Dome of pleura
• Brachial plexus
• Lymphatics and thoracic duct
• Phrenic nerve 
• Sympathetic chain, stellate ganglion
• Scalene muscle.
• Clavicle

b)

• Requires management at a trauma centre with appropriate expertise. May require multiple speciality input - interventional radiology, ENT, vascular, cardiothoracic.
•  Airway issues: The possibility of laryngeal/ tracheal injury and the risk of intubating the “false airway passage”. Consider tracheostomy under local anaesthesia.
•  Urgent surgical exploration required for haemodynamic compromise, expanding or pulsatile haematoma, extensive subcutaneous emphysema, stridor, or neurological deficit with intra op bronchoscopy/ endoscopy/ angiography if available. 
•  If no indication for urgent surgical exploration requires CT angiography (or equivalent) with close observation in ICU +/- flexible laryngoscopy +/- endoscopy +/- oral contrast swallow study.

Examiners Comments:

Generally, poorly answered. Limited knowledge of anatomy and poor structure to answers. A broad approach with a logical approach to prioritisation of investigations/treatments was all that was required to score well. Few candidates commented on general principles of complex trauma requiring input from multiple teams.

Discussion

This queestion is identical to Question 7 from the second paper of 2015, except this time you have been called to the Emergency Department, not the Emergency Room.  Again, the pass rate was under 30%. For future reference, neck anatomy and penetrating neck injury is described in excellent detail by Phillip Thorek in his chapter for Anatomy in Surgery (1985) which is unfortunately paywalled by Springer. So is "Trauma to the neck region"  by Saletta et al (1973) and the UpToDate article on penetrating neck injury. For the freegan,  Karim Brohi's 2002 write-up of neck wounds on trauma.org is of a high quality.

Brohi divides the neck into three zones, each with its own specific concerns:

(image from trauma.org)

So, this question is about Zone 1, where all the important stuff is. 

b)

A generic approach to management:

1. Assess for airway compromise (eg. by expanding haematoma)
   Assess for airway injury (eg. subcutaneous emphysema)
   Organise expert help.
   Awake fiberoptic intubation by an experienced operator would be ideal, with an ENT surgeon on standby. Risks include intubating a false passage, or causing complete tracheal disruption.
2. Assess for respiratory compromise.
   Ausculation and percussion may reveal pneumothorax due to injury of the dome of pleura, or the raised hemidiaphragm of a phrenic nerve injury
3. Assess the circulation in the arm on the affected side. There may be vascular compromise.
4. Assess the neurology of the patient, starting with GCS.
   Verterbral artery damage may present with spinal syndromes (eg. Brown-Sequard) or brainstem stroke signs
   Carotid artery damage may present with hemispheric stroke signs

Reasons for urgent surgical exploration:

• airway compromise (stridor, etc)
• haemorrhgic shock
• expanding haematoma (or, especially if it is pulsatile)
• stroke-like symptoms

Additional concerns specific to the root of the neck:

• massive haemothorax
• arteriovenous fistula (subclavian vessels)
• Thoracic duct damage (if it was the left side of the neck, as it tends to be with a right-handed attacker coming from the front)
• brachial plexus damage
• Horner's syndrome

References

College answer

First-line measures

Paracetamol

Intravenous opioid PCA

Second-line measures

IV ketamine infusion 4-16 mg/h

Tramadol

These have the advantages of simplicity and familiarity.

Disadvantages include lack of efficacy, and side effects of sedation, impaired cough, respiratory depression, and agitation or delirium.

  Regional anaesthetic techniques

 Thoracic Epidural 

Benefits

Analgesia is better than with PCA

Better MIP (maximum inspiratory pressure) than with PCA 

Avoidance of sedation

Less delirium

Less risk of respiratory depression

 Disadvantages

Insertion requires expertise

Risk of failure

Risk of infection

Risk of epidural haematoma

Hypotension

Bradycardia in case of a high block

Intercostal nerve block

Advantages

Simpler than epidural

May require multiple intercostal levels (risk of local anaesthetic toxicity)

Paravertebral catheter infusion

Less effective than epidural, but lower rate of systemic hypotension. 

Patients can be discharged to home with a paravertebral catheter in place. 

Intrapleural infusion

Relatively contraindicated – NSAIDs, COX-2 inhibitors (risk of renal failure and/or GI bleed)

Although there are no randomized trials comparing the efficacy of these modalities, trauma guidelines recommend epidural analgesia for patients with four or more rib fractures and suggest its use in those with fewer fractures who are older than 65 years or who have significant cardiopulmonary disease or diabetes mellitus.

Other options

Although not a primary analgesic option, invasive or non-invasive mechanical ventilation may reduce analgesic requirements by splinting a large flail segment. Disadvantages of complexity, risks associated with intubation, and IMV, as well as patient discomfort and aspiration risk in NIV

Surgical fixation of the fractures

This has been shown to reduce the chronic pain with non-union and help with the weaning of patients with rib fractures causing flail chest, prevents traumatic thoracoplasty

Disadvantages of invasive procedure with associated risks, may require post-operative ventilation.

Discussion

Anything that asks for you to discuss advantages and disadvantages of a series of therapeutic options would benefit from a tabulated answer.

References

College answer

Precipitants:                                               
Trauma-related 
Orthopaedic (most common) 
Long bone fracture (esp femur) 
Pelvic fracture 
Elective Orthopaedic surgery 
Non-orthopaedic 
Liposuction 
BM harvest/transplant 
Nontrauma-related 
Acute pancreatitis  
Sickle cell disease 
 
Clinical features                                              
Typically develops 24-72 hours following insult. 
Classic clinical triad (neurological, respiratory, cutaneous), none of which is specific for FES. 
•    Respiratory – the most common presenting feature. Dyspnoea, hypoxia, ARDS  
•    Neurological – confusion, reduced level of consciousness, seizure, focal deficit, retinal changes (petechiae) 
•    Petechial rash – usually in non-dependent areas, including neck, axillae, anterior chest, head, subconjunctiva. Only in 1/3 of cases, and often not until 3-5 days after insult. 
Other – fever, thrombocytopenia, coagulation abnormalities (incl DIC), anaemia, tachycardia, myocardial depression, renal/liver dysfunction, high ESR 
 
Diagnosis 
Based on the clinical features in the setting of known precipitant 
CXR may reveal bilateral patchy infiltrates 
No single diagnostic test – BAL sampling for lipids has been described – no other tests shown to be useful 
Several sets of diagnostic criteria proposed 
 
Management                                               
Prevention clearly preferable if possible – e.g. surgical timing (following fracture) and technique Fixation of fracture 
No specific therapy. Supportive only. 
Steroids controversial – proposed anti-inflammatory effect but limited data to support 
 

Discussion

Precipitants

• One long bone fracture: 1-3% chance
• Chance increases in proportion of number of fractures, and size of involved bones
• 33% with bilateral femoral fractures

Clinical features

Symptoms of fat embolism

• Confusion is usually the earliest symptom (60%), but seizures and focal neurological signs have also been reported (all resolve completely)
• Dyspnoea
• Tachypnoea
• Haemoptysis
• Usually, with a latent period (say, some days after the manipulation of a fracture).

Signs of fat embolism

• Respiratory features are present in 95%: moist crepitations over all lung fields, hypoxia, cyanosis. ARDS-like picture develops
• Fat globules may be seen in the sputum!
• Petechial rash (in 30-60%) - alone, enough to make the diagnosis according to Schonfelds criteria.
• Fever
• Tachycardia
• Purtscher’s retinopathy: 
  • cotton wool exudates
  • macular oedema
  • macular haemorrhage
  • retinal haemorrhages
  • visible fat droplets on ophthalmoscopy
• Jaundice
• Renal impairment
• Anaesthetists often note a sudden drop in end-tidal CO₂ concentration during a stable steady state.

Diagnosis

Laboratory features:

• Thrombocytopenia
• Anaemia (sudden decrease) -70% of patients
• High ESR
• Fat macroglobulinaemia
• Hypocalcemia (due to free fatty acids binding calcium)
• Elevated serum lipase
• DIC-like coagulopathy
• ABG: respiratory alkalosis with hypoxia and an unexplained shunt
• ECG: right heart strain, RBBB

Characteristic imaging:

• CXR: florid embolism may develop into a "flocculent" patchy widespread opacities, "snowstorm appearance".
• CT chest: non specific; focal areas of ground glass opacification
• CT brain: diffuse white-matter petechial hemorrhages consistent with microvascular injury.
• TOE: may actually catch the passing of fatty globules within the heart, but afterwards - useless.

Management:

• Specific management not supported by very strong evidence:
  • Corticosteroids
  • Aspirin
  • Heparin infusion (which supposedly encourage lipase activity and discourages the formation of platelet aggregates).
  • N-acetylcysteine (based on rat studies only)
• Boring, non-specific treatment:
  • O₂ supplementation
  • Positive pressure ventilation
  • Correction of coagulopathy
  • Replacement of platelets
  • Correction of the source problem (i.e. reduction of fractures)

References

College answer

a)    Heat stroke is defined as a core body temperature usually in excess of 40ºC with associated central nervous system dysfunction in the setting of a large environmental heat load that cannot be dissipated. Classic (nonexertional heat stroke) affects elderly individuals with underlying chronic medical conditions that impair thermoregulation, prevent removal from a hot environment, or interfere with access to hydration or attempts at cooling. These conditions include cardiovascular disease, neurologic or psychiatric disorders, obesity, anhidrosis, physical disability, extremes of age, and the use of recreational drugs and certain prescription drugs. Exertional heat stroke generally occurs in young, otherwise healthy individuals who engage in heavy exercise during periods of high ambient temperature and humidity.   (2 marks)         
 
b)    The first clinical signs are often neurological and may include restlessness, delirium, seizures and coma. Multiple organ involvement may occur including signs of distributive shock with a hyperdynamic profile with hypovolaemia as a consequence of dehydration and reduced organ perfusion and associated lactic acidosis. There may be hyperventilation with respiratory alkalosis and hypoxia from acute lung injury. The main biochemical abnormalities include hyperglycaemia, hypophosphataemia, raised hepatic and muscular enzymes and an elevation of acute phase proteins. The haematological findings include leucocytosis, thrombocytopenia and activation of coagulation and fibrinolysis.    (4 marks) 
 
c)    Cooling Strategies in Heat Stroke: 
Methods:  
Water and fan: Evaporative and convective cooling: 
Body sprayed with lukewarm water and fans are used to blow air over the moist skin. 
 
Suppression of heat: 
Agitated and shivering patient can generate heat. That can be suppressed with the use of benzodiazepines (such as lorazepam, midazolam) and chlorpromazine paralysing agents may be required 
 
Cold water immersion:  
Immersion of patient in ice water: non-invasive, rapid but makes patient monitoring difficult 
 
Application of ice packs: 
Ice packs can be placed in axillae, neck and groin: excellent method for intubated patient, poorly tolerated by non- intubated patients 
 
Cold compressors:  
Can be applied on smooth, hairless surfaces like: palms, cheeks, soles: rapid cooling 
 
Cold thoracic, gastric and peritoneal lavage: invasive but rapid 
 
Cooling catheters: invasive, rapid 
 
Cooling blankets: non-invasive, can set the temperature 
 
Cold IV fluids 
 
Cooling recommendations are primarily based on observation studies 
There is no definitive study supporting any particular approach to cooling in classic heat stroke 
Pharmacological agents like dantrolene are ineffective and not indicated in heat stroke 
Alcohol sponge baths should be avoided due to risk of absorption of alcohol through skin  
 

Discussion

Definition of heat stroke

• Failure of thermoregulation due to impaired heat dissipation, characterised by severe hyperthermia, dry skin and a decreased level of consciousness

Exertional heat stroke

• Increased body thermogenesis due to exercise, and the failure of otherwise normal healthy thermoregulatory mechanisms

Non-exertional heat stroke

• Impaired thermoregulatory mechanisms and increased body temperature under condtionals of normal rates of thermogenesis

Clinical signs of heat stroke

• Raised body temperature
• Neurological dysfunction - restlessness, delirium, coma
• Hyperdynamic circulation; distributive shock (Shahid et al, 1999)
• Dry skin (usually)
• Seizures

Characteristic laboratory findings in heat stroke

• ABG: acidosis, probably mixed metabolic; as well as respiratory alkalosis and hypoxia
• BSL: elevated (catecholamines)
• FBC: haemolysis, thrombocytopenia, anaemia, raised white cell count
• EUC: renal failure, hyperkalemia
• CMP: hypophosphataemia and hypocalcemia (Knochel & Caskey, 1977)
• LFTs: raised transaminases and bilirubin. Specifically, AST and LDH will be raised.
• CK: elevated
• Urinary myoglobin
• Coagulopathy (DIC): raised PT and APTT
• Raised acute phase inflammatory markers (CRP, ferritin)

Cooling strategies for heat stroke

• Evaporation of cold water sponges
• Ice packs
• Immersion in ice water
• Contact cooling by blankets and jackets
• Iced gastric, colonic, bladder, or peritoneal lavage
• Infusion of cold intravenous fluids
• Invasive technique such as cooling of the dialysis circuit, or ECMO

There is not specific approach which is thought to be more effective than other approaches. For instance, in a letter to Intensive Care Medicine, Hadad et al (2005) pointed out that in the Israeli Defence Forces, with tap water and a fan one is able to achieve a core temperature rate drop of 1°C every 9 minutes. Costrini (1990), looking at different ways of cooling down overheated athletes, suggested ice water immersion to be the best method. A more detailed discussion of cooling methods is carried out in the chapter on inducing therapeutic hypothermia. The college, in their answer to Question 22 from the second paper of 2018,  mention alcohol sponge baths as a discredited alternative.  This practice has been discredited since the 1960s, when it killed children (Senz et al, 1959) and adults (Wise, 1969) by producing a surprising amount of alcohol absorption (they were using mainly isopropyl "rubbing" alcohol). On the other hand, if your objective is to achieve heroic levels of intoxication, percutaneous obsorption is a valid method (Puschel et al, 1981).

References

College answer

7. Obstructive
   1. Tension pneumothorax
      1. CXR, drainage
   2. Abdominal compartment syndrome
      1. Bladder pressure, escharotomies, laparotomy/laparostomy
   3. Tamponade
      1. Echo and pericardiocentesis

Examiners Comments:

Frequently poorly structured answer, with a list of causes of hypotension, then repeated with diagnosis and management. Worked better when candidates classified each category of shock, then described individual diagnosis and management within each category. Often the question had not been carefully read, and the time already spent in ED and ICU was ignored; then a simplistic EMST initial approach to trauma was given.

Discussion

This question resembles Question 26 from the second paper of 2016, except the patient is not unconscious and there is no ABG to interpret.  

Let this be an exercise in generating differentials.

• Wrong BP measurement (eg. arterial line is not zeroed)
• Cardiogenic shock
  • Due to cytokine storm of severe burns
  • Due to carbon monoxide toxicity (i.e. severe tissue hypoxia)
  • Due to cyanide toxicity (i.e. mitochondrial failure)
  • Due to a myocardial infarction (due to increased myocardial oxygen consumption in context of burns, on top of pre-existing ischaemic heart disease)
• Abdominal compartment syndrome (over-resuscitation)
• Tension pneumothorax (explosion)
• Spinal injury neurogenic shock (unrecognised due to unconsciousness)
• Blood loss from some internal injury or due to DIC
• Under-resuscitated burns shock (i.e. fluid shifts)
• SIRS vasoplegia
• Anaphylaxis to some drug given in hospital

If one were to offer more detail, one would have to tabulate one's answer, which would handily answer complaints about a lack of structure, because nothing says "structure" like a table.

References

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.

Bak, Zoltan, et al. "Hemodynamic changes during resuscitation after burns using the Parkland formula." Journal of Trauma and Acute Care Surgery 66.2 (2009): 329-336.

Blumetti, Jennifer, et al. "The Parkland formula under fire: is the criticism justified?." Journal of burn care & research 29.1 (2008): 180-186.

Baxter, Charles R., and Tom Shires. "Physiological response to crystalloid resuscitation of severe burns." Annals of the New York Academy of Sciences 150.3 (1968): 874-894.

Saffle, Jeffrey R. "The phenomenon of “fluid creep” in acute burn resuscitation." Journal of burn care & research 28.3 (2007): 382-395.

Naver, P. D., J. R. Saffle, and G. D. Warden. "Effect of inhalation injury on fluid resuscitation requirements after thermal injury." Plastic and Reconstructive Surgery 78.4 (1986): 550.

Arlati, S., et al. "Decreased fluid volume to reduce organ damage: a new approach to burn shock resuscitation? A preliminary study." Resuscitation 72.3 (2007): 371-378.

Bittner, Edward A., et al. "Acute and Perioperative Care of the Burn-Injured Patient." Survey of Anesthesiology 59.3 (2015): 117.

Melinyshyn, Alex, et al. "Albumin supplementation for hypoalbuminemia following burns: unnecessary and costly!." Journal of Burn Care & Research 34.1 (2013): 8-17.

Cooper, Andrew B., et al. "Five percent albumin for adult burn shock resuscitation: lack of effect on daily multiple organ dysfunction score." Transfusion 46.1 (2006): 80-89.

Wilkes, NICHOLAS J. "Hartmann's solution and Ringer's lactate: targeting the fourth space." Clinical Science 104.1 (2003): 25-26.

MONAFO, WILLIAM W. "The treatment of burn shock by the intravenous and oral administration of hypertonic lactated saline solution." Journal of Trauma and Acute Care Surgery 10.7 (1970): 575-586.

Huang, Peter P., et al. "Hypertonic sodium resuscitation is associated with renal failure and death." Annals of surgery 221.5 (1995): 543.

Sun, Ye-Xiang, et al. "Effect of 200 mEq/L Na+ hypertonic saline resuscitation on systemic inflammatory response and oxidative stress in severely burned rats." Journal of Surgical Research 185.2 (2013): 477-484.

Paratz, Jennifer D., et al. "Burn Resuscitation—Hourly Urine Output Versus Alternative Endpoints: A Systematic Review." Shock 42.4 (2014): 295-306.

Walker, Steven C., et al. "Balanced Electrolyte Solution Reduces Acidosis as Compared to Normal Saline in the Resuscitation of Perioperative Burn Patients." Anesthesiology 95 (2001): A375

College answer

References

Christie, Robert James. "Therapeutic positioning of the multiply-injured trauma patient in ICU." British Journal of Nursing 17.10 (2008): 638-642.

College answer

References

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

• ABC of burns: Introduction
• ABC of burns: pathophysiology and types of burns
• ABC of burns: Initial management of a major burn: I—overview
• ABC of burns: Initial management of a major burn: II—assessment and resuscitation
• ABC of burns: Management of burn injuries of various depths
• ABC of burns: first aid and treatment of minor burns
• ABC of burns: psychosocial aspects of burn injuries
• ABC of burns: Rehabilitation after burn injury
• ABC of burns: intensive care management and control of infection

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.

College answer

Early recognition and identification of location of bleeding (0.5)

Early haemorrhage control with basic haemostatic measures including: (1)

-Direct pressure

-Use of staples for soft tissue bleeding e.g. scalp bleeding

-Use of tourniquets in traumatic amputations

-Avoiding scene delays

Early definitive haemorrhage control with surgery or angiographic techniques (0.5) Avoidance of excessive crystalloid infusion. (0.5)

“Permissive hypotension” is a fluid restriction strategy that limits dilutional coagulopathy, potentially limits clot dislodgement by maintaining a SBP 80-90mmHg.

Initial RCT single centre research (Bickel 1994 NEMJ) in penetrating torso injures showed mortality benefit in delayed fluid resuscitation. Further multi centre RCT research with blunt trauma confirmed the improved mortality in the permissive hypotension group.

The controversy exists in the presence of TBI (traumatic brain injury) and Spinal cord injury (SCI) and the avoidance of secondary brain injury. Brain trauma foundation guidelines aim for an SBP >90 or CPP > 60 to prevent this. Permissive hypotension is not suitable for these patients. There is no evidence for Hb level. The TRICC trial excluded these patients (1.5)

Avoid the lethal triad of hypothermia, acidosis, and coagulopathy.(0.5 mark each) Ensure an ionised Ca2+ > 1 mmol/l. (0.5)

Maintaining fibrinogen > 1.5 g/L. (0.5)

Maintaining platelets > 100 x 109 /L. (0.5)

Recognition of the presence of medications causing coagulopathy or platelet dysfunction such as aspirin, clopidogrel, warfarin or a novel oral anticoagulant. In this instance the provision of platelets, FFP or prothrombin concentrate complexes may be appropriate. (1)

Point of care testing such as thromboelastography to facilitate rapid and targeted coagulopathy correction. (1)

The use of tranexamic acid < 3 hours (CRASH2). (0.5) Appropriate cessation of the massive bleeding protocol. (0.5)

References

College answer

References