Th DRE is performed to detect the following key findings:

• rectal hemorrhage
• rectal mucosal injury or wall defects
• loss of anal tone suggesting spinal cord injury
• palpable pelvic fractures
• a high riding prostate suggestive of posterior urethral disruption

No

Traditional ATLS teaching was that a DRE is mandatory in trauma patients: “a finger or tube in every orifice”. This is no longer the case. The 8th edition of ATLS recommends that ‘DRE be performed selectively before inserting an indwelling urinary catheter’ (Kortbeek et al, 2008).

Over the past 10 years or so, the published literature has consistently downplayed the role of the DRE in the assessment of trauma patients. It is clear that:

DRE rarely changes the management of trauma patients.

• DRE was felt to change management in only in 1.2% of cases in Porter and Ursic’s prospective observational study (2001) and only 4% in Esposito et al’s prospective study (2005).
• Espsoito et al (2005) found that none of 512 patients would have had a significant injury missed had the DRE been omitted.

The DRE is not a useful screening test in trauma patients.

• In a retrospective study of over 1400 patients, Shlamovitz et al (2007) found that the DRE was only 23% sensitive for a composite of significant injuries in trauma patients.
• This means that about three-quarters of the time the DRE will miss significant injuries (such as GI perforation, rectal mucosal injury, urethral rupture, pelvic fracture and spinal cord injury).

Some have argued that despite the poor sensitivity of the DRE, it should still be performed as part of a complete examination as it is “cheap, quick and non-invasive”.

I disagree…

DREs should only be performed selectively

and I certainly don’t consider DREs to be ‘non-invasive’.

Downsides of performing DREs in trauma patients include:

• physical discomfort
• emotional distress
• risk of verbal and/ or physical violence from an agitated patient
• litigation
• possible infection risk — e.g. contamination of local wounds; risk of transmission of infection to the clinician (likely to be extremely low)
• injury — potential for worsening of the patient’s injuries (e.g. unstable pelvic fracture, rectal defects); and also risk of injury to the clinician (e.g. foreign bodies, bone fragments)
• the occurrence of false postive and false negative DRE findings

Factors contributing to DREs being unreliable include:

• DREs are often performed by junior staff
  — either because it is considered a menial task, or so that the junior staff ‘gain more experience’.
• positive findings on DRE are rare… anyone ever felt a ‘high riding’ prostate?… (i.e. before the diagnosis of posterior urethral disruption was confirmed by some other means…)
• the findings on DRE have poor inter-observer agreement
  — this is well document for the assessment of prostate size and the detection of rectal tumours… even when performed by ‘experts’ such as urologists and proctologists.

Yes… 

DRE findings may be falsely positive or negative.

• Esposito et al (2005) found that 6% of DREs in trauma patients had findings that were later shown to be false (either positve or negative) when other investigations or follow up over time was performed.
• Shlamovitz et al (2007) found high rates of falsely negative DREs:

• 63% for decreased anal sphincter tone
• 94% for the presence of gross rectal blood
• 67% for disruption of the rectal wall integrity
• 100% for palpation of bony fragments
• 80% for abnormal position of the prostate.

False negative DREs may lead to

• injuries being missed, resulting in increased morbidity and/ or mortality
• delays in performing necessary investigations  and/ or interventions

False positive DREs may lead to:

• unnecessary investigations (cost, time, radiation, contrast exposure, decreasing access for other patients, etc)
• unnecessary interventions (the possibilities include prolonged time in a c-spine collar, unnecessary fasting, being cut open for no reason, etc)
• prolonged observation (possible increase in hospital length of stay)

Probably not… You can usually rely on other clinical findings and a (gentle) attempt at IDC insertion will reveal all.

Ball et al (2009) found that in patients with posterior urethral disruption, 60% of the time there there were no clinical signs prior to urinary catheter insertion (41 urethral injuries were included in this retrospective study). Possible clinical signs and their sensitivities are shown below:

• blood at the urethral meatus (20% sensitivity)
• gross hematuria prior to catheter insertion (17% sensitivity)
• abnormal prostate position (2% sensitivity)
• scrotal or perineal echymosis
• inability to void

(Unfortunately likelihood ratios could not be calculated from the data provided in the paper.)

Why is DRE to detect ‘abnormal prostate position’ such a poor test? In addition to the reasons discussed in Q4, examination is often limited by tenderness or the finding of a ‘high riding prostate’ may be concealed by hematoma formation from a coexistent pelvic fracture or vessel injury.

Abnormal prostate position is near useless for detecting posterior urethral injury.

Consider posterior urethral disruption if a pelvic fracture is present.

Current ATLS guidelines advise that a retrograde urethrogram be performed before inserting an indwelling urinary catheter (IDC) in trauma patients if posterior urethral injury is suspected. In practice, this rarely occurs. This is partly because posterior urethral injury is often first suspected once frank blood is returned following attempted IDC insertion, or if the IDC is difficult to pass. It probably doesn’t matter in the long run if posterior urethral disruption is diagnosed this way — just be very gentle when you’re passing an IDC!

Suspect posterior urethral disruption if there is hematuria on IDC insertion or if the IDC doesn’t pass easily.

Michael McGonigal describes how to perform a retrograde urethrogram on the excellent Trauma Professional’s blog.

Perform a retrograde urethrogram to confirm posterior urethral disruption.

Probably not, unless the patient has a neurological deficit.

If the patient is otherwise neurologically intact on clinical examination, anal tone is very unlikely to be altered.

Normal anal tone does NOT exclude spinal cord injury.

Sensitivity is too low for DRE to have have much bearing on making a serious diagnosis like spinal cord injury:

• Shlamovitz et al (2007) found DRE was only 37% sensitive with a negative likelihood ratio (LR) of 0.66
• Guldner et al (2006) had similar findings, with a negative LR of 0.5.

Of course, a positive DRE finding of decreased anal tone is more useful, but these patients are likely to have other reasons for suspecting spinal cord injury (such as paralysis…).

• Shlamovitz et al (2007): positive LR = 8.5
• Guldner et al (2006): postive LR = 6.8

Two important points about the use of DRE in patients with suspected spinal cord injury:

• Assessing rectal tone is of little use if the patient has been given neuromuscular blockers following intubation. Tone may also be reduced in the unconscious patient, as a result of post-intubation sedation or traumatic brain injury for instance.
• In the patient with neurological deficits, assessment for sacral sparing is important. This can be assessed by checking anal tone, but anal wink or the bulbocavernosus reflex are alternatives and may be more useful and/or better tolerated.

Usually not… sensitivity is poor and other investigations are likely to be needed.

The DRE is only 6% sensitive for bowel injury (LR- 0.95), and only 33% sensitive for rectal mucosal tears (LR- 0.65 with confidence intervals that crossed 1) according to Shamlovitz et al (2007). As such it cannot be used a screening test in trauma patients to exclude either of these types of injuries.

Don’t rely on a negative DRE in a patient at high-risk of a bowel or rectal injury. Such patients need further investigation.

On the other hand, Shlamovitz et al (2007) found that a positive DRE was more useful for bowel and particularly rectal injury.

• 98.9% specific for bowel injury (i.e. PR hemorrhage detected) (LR+ 5.2)
•  99.8% specific for disrupted rectal wall integrity (LR+ 996)

But we need to take into account the fact that patients with these positive findings are likely to require further investigation anyway based on other findings (such as the spear sticking out of his or her perineum…).

There probably is a subgroup of trauma patients (as yet poorly defined) for whom a DRE is useful and may change management.

This subgroup may include patients with:

• pelvic fractures (complications and associated injuries may be detected)
• abnormal neurological findings
• hypotension
• penetrating abdominal or perineal trauma with possible rectal or other GI involvement
• abdominal tenderness

Again, even in these patients further investigations are typically indicated anyway, which may render the DRE findings redundant. I suspect that most clinicians err on the side of performing a DRE given that, throughout the ages, we have been beaten over the head with the notion that failure to perform a DRE is a sign of gross incompetence (“if you don’t put your finger in it, you’ll put your foot in it”).

Perhaps it is easier to say which trauma patients don’t need a DRE…

Gulder et al (2004) published an as yet unvalidated clinical decision rule for performing DRE in trauma patients, based on an observational study of 862 patients. They found that there is a 0 to 0.8% probabilty of a ‘true positive’ abnormal DRE in patients with all three of:

• a normal neurological exam
• aged <65 years
• absence of blood at the urethral meatus

The take home messages for me are that DREs in trauma patients:

• should be performed selectively
  — you must have a reason for performing this invasive examination… don’t feel you have to do it! But make sure your reasoning for not performing a DRE is equally sound. In most patients the DRE won’t be useful.
• can often be delayed or be performed at the time of a subsequent investigation (e.g. colonoscopy) or intervention (e.g. laparotomy) if necessary
• may be redundant in light of other clinical findings or if further investigation is indicated by other clinical findings
• may be best performed by an experienced practitioner (although there is little or no evidence that their findings are any better than those of their junior collegues)… and only once!

Step 1

• Effectively manage the airway and optimise oxygenation.

Step 2

• Identify and control immediate threats to central perfusion.

Step 3

• Identify and address severe intracranial injuries.

Step 4

• Identify and control other potentially life-threatening thoracic and abdominal injuries.

Step 5

• Identify and control potentially limb-threatening injuries.

Step 6

• Identify and treat noncritical injuries.

From a physiological standpoint, shock results when oxygen delivery is inadequate to meet tissue demands.

Key points in treating shock are:

The correct approach to treating shock is to restore tissue perfusion rather than to simply achieve a higher systolic blood pressure.

1. The presence of shock should never be simplistically equated with a systolic blood pressure reading<90mmHg.
2. The recognition of clinical shock requires complex integration of numerous data points  including the mechanism of injury and patient’s overall appearance, vital signs , level of mentation, peripheral perfusion and urine output.
3. These clinical parameters alone do not adequately quantify the degree of shock or the response to shock therapy. This principle is especially pertinent in elderly patients and in those with limited cardiovascular reserve.
4. In severely injured blunt trauma patient, clinical parameters should be coupled with objective makers of tissue perfusion eg, serum lactate or base deficit).

Haemorrhagic:

• External bleeding
• Haemothorax
• Haemoperitoneum
• Retroperitoneum (pelvic fracture/renal injury)
• Long bone fracture

Non-Haemorrhagic:

•  Tension pneumothorax
• Pericardial tamponade
• Myocardial contusion
• spinal cord transection/injury
• Coincident medical event (cardiac event, GI bleed, vasoactive medications)

1. Chest radiography:

• Look for tension pneumothorax or massive haemothorax.
• Is there evidence suggestive of aortic injury?

2. Pelvis radiography:

• Is there pelvic ring disruption?

3. Focused assessment with sonography for trauma (FAST):

• Is there sonographic evidence of:

1. Pneumothorax?
2. Haemothorax?
3. Haemopericardium?
4. Haemoperitoneum?

4. Diagnostic peritoneal aspiration (DPA):

• Is there haemoperitoneum?

• The determination that a trauma patient is “in shock” is a complex one, and it is not always synonymous with a systolic blood pressure <90mmHg.
• The accurate diagnosis of the cause(s) of shock begins with a targeted physical examination and the thoughtful use of diagnostic testing (including chest radiography, pelvis radiography, and ultrasound). The use of objective serum makers of tissue perfusion (eg. serum lactate or base deficit) can be helpful in identifying “subclinical” shock and in following the patient’s response to resuscitation.
• In patients requiring massive transfusion (defined as the administration of > 10 U of PRBCs in 24 hours), institutional protocols defining blood product ratios have improved outcomes. When massive transfusion is employed , use of PRBC to platelet to FFP ratio of approximately 1:1:1 may result in decreased need for blood products. (Remember to give calcium as well in patients requiring massive transfusion to prevent citrate toxicity).

• A blunt aortic injury is a potentially lethal injury that should be considered in all blunt trauma patients who experience major deceleration, including motor vehicle crashes, automobile-versus-pedestrian injuries, and falls from a significant height.
• A CT scan is the current criterion standard in the diagnosis of BAI. Although TEE can be useful,although it is operator dependent.
• Chest radiography is a useful screening tool in then diagnosis of BAI. In large trials, the most important radiographic findings suggestive of BAI were: (1) widening of the mediastinum (>8cm), (2) blurring of the aortic knob, and (3) loss of aortopulmonary window.
• A BAI seldom occurs in isolation. A diligent search for other potential causes of shock and time-sensitive conditions is essential.
• In the setting of BAI, other causes of ongoing haemorrhage and/or neurosurgical lesions should be rapidly identified. Management of these conditions often’s requires thoughtful staging of interventions and is best done in experienced trauma centers.

• Pelvic ring fractures are a sign of major energy transfer and should be viewed as markers of potentially severe multisystem trauma.
• Pelvic ring fractures can be classified as: (1) lateral compression injuries, (2) AP compression injuries, or (3) vertical shear injuries. Classification is helpful to predict risk of ongoing haemorrhage. Fractures that increase pelvic volume 9ie, AP compression injuries and vertical shear injuries) pose the highest risk of ongoing bleeding.
• Institutional protocols that incorporate stabilisation, aggressive resuscitation, and early definitive therapy improve outcomes.
• For community physicians, the essential steps are to : (1) recognise pelvic injury pattern on plain film, (2) institute aggressive resuscitation early, (3) employ external pelvic stabilisation when pelvic fracture patterns lead to increased pelvic volume, and (4) orchestrate timely transfer to a trauma centre.

• In the haemodynamically unstable blunt trauma patient, ultrasound is the  study of choice for the initial evaluation for haemoperitoneum.
• Persistent or recurrent hypotension in the patient with haemoperitoneum is an indication for immediate laparotomy.
• Computed tomography managing provides valuable information in patients who stabilise with resuscitation and assists with injury staging and planning for definitive management. The most common injuries are to the liver and spleen, and many of these injuries can be managed non-operatively in patients without hypotension or ongoing transfusion requirements.

Definitions vary widely, but a useful definition of emergency thoracotomy is:

“a thoracotomy performed prehospital, in the emergency department or elsewhere that is an integral part of the initial resuscitation of a patient”

The indications and contraindications for emergency thoracotomy are controversial, and may vary between institutions.

In general, the following are considered contraindications to performing an emergency thoracotomy:

• prehospital CPR performed for >15 minutes after penetrating chest injury without response
• prehospital CPR performed for >10 minutes after blunt chest injury without response
• the presence of coexistent injuries that are unsurvivable, e.g. severe head trauma
  (an exception maybe the patient who is a potential organ donor)
• asystole is the presenting rhythm, and there is no pericardial tamponade

Furthermore, it makes little sense to perform an emergency thoractomy in settings where there is no hope of providing definitive surgical interventions following the procedure.

The Moore et al (2011) study, which collected data from 18 US trauma centers, suggests that emergency thoracotomy is not as hopeless as once believed — hence blunt trauma alone is not listed as a contraindication. Also, compared to the recommendations of Hunt et al (2005) — as featured in EMCrit Podcast 36: Traumatic Arrest — longer CPR times are allowed (10 and 15 minutes, rather than 5 and 10 minutes for blunt and penetrating trauma respectively). Even with these increased time allowances there are still a few reported cases of patients with both penetrating or blunt chest trauma who have survived following even longer periods of CPR.

Survival rates directly correlate with the patient’s physiological status. This physiological status needs to be taken into account when considering the indications for an emergency thoracotomy.

According to Lorenz et al (1992) the patient’s physiological status can be classified as follows:

I — no signs of life (see Q4)

II — pulseless electrical activity

III — profound shock: SBP<60 mmHg; transient / no response to fluid resuscitation.

IV — mild shock: SBP 60-90 mmHg; stable response to fluid resuscitation.

According to Hunt et al (2005) ‘signs of life’ include:

• presence of a pulse or spontaneous movements
• GCS>3
• presence of pupillary reflexes, corneal reflexes or gag reflexes
• evidence of cardiac electrical activity on ECG, or contractile activity on bedside ultrasound
  (this information is rarely available in a prehospital setting)

The definition of what constitute ‘signs of life’ in this setting remains surprisingly controversial. As implied by the contraindications listed in Q2, emergency thoracotomy is essentially futile unless the patient has, or recently had, some signs of life.

Only if:

• the patient had definite signs of life at the scene, and
• none of the contraindications listed in Q2 are present.

Only if there is evidence of:

• intrathoracic hemorrhage
• severe extrathoracic hemorrhage
• pericardial tamponade
• systemic air embolism

Only if there is evidence of:

• intrathoracic hemorrhage
• severe extrathoracic hemorrhage
• pericardial tamponade
• systemic air embolism

The indications are the same as for scenario (b) above.

No

If possible, he should be urgently transferred to an operating theatre for an urgent thoracotomy instead.

Emergency thoractomy allows the following therapeutic interventions to be performed:

1. Release of pericardial tamponade —
   improves cardiac output and control of cardiac haemorrhage
2. Control of intrathoracic vascular or cardiac haemorrhage —
   facilitates  fluid resuscitation by ‘turning off the tap’
   improves cardiac output and myocardial perfusion
3. Control of massive air embolism or bronchopleural fistula —
   resolves myocardial ischaemia and hence  improves myocardial contractility as well as prevents neurological injury
4. Open cardiac massage —
   improves resuscitative cardiac output and coronary perfusion especially with limited ventricular filling pressures
5. Occlusion of the descending aorta (cross-clamping) —
   Redistribution of limited blood volume to myocardium and brain as well as limiting subdiaphragmatic losses.

Assess and manage the patient in a setting appropriately staffed and equipped for resuscitation using a coordinated team-based approach.

Perform the following key actions:

1. secure the airway by endotracheal intubation and commence ventilation and oxygenation.
2. seek and treat tension pneumothorax
   e.g. bedside ultrasound and bilateral finger thoracostomies.
3. seek and treat pericardial tamponade
   e.g. bedside ultrasound and emergency thoractomy.

If the patient has arrested and both tension pneumothorax and pericardial tamponade have been excluded, some experts would cease resuscitation at this point. Others would argue that there may be a role for emergency thoractomy if performed within 10 minutes of the arrest and the patient is actively resuscitated during this time.

Closed chest cardiac compressions and standard resuscitation drugs such as adrenaline are ineffective in the resuscitation of arrested trauma patients.

Despite this, CPR is routinely performed in such patients, especially in the prehospital setting. At best, CPR can be viewed as a temporising measure until emergency thoracotomy can be performed. It is far more important to give these patients blood products — not drugs — during resuscitation, while attempting to control the source of hemorrhage.

FACEM SAQ Exam 2011.1 – Question 5

• The overall pass rate for this question was 52/81 (64.2%)
• Pass Criteria (MUST include the following)
• PART A
  
  • Need to secure airway in a safe and timely manner
  • Risk of laryngotracheal injury
  • Risk of injury to at least two other structures including: vascular, neurological, cervical spine, soft tissues with expanding haematoma

• PART B
  
  • Need to balance urgency and optimising personnel (incl Anaesthetist), equipment (e.g. fibreoptics) and location (ED vs. OT)
  • Need for preparation for surgical airway as back up
  • If candidate includes RSI as an option, then fails if does not include the significant risks associated with this technique

FACEM VAQ Exam 2011.2 – Question 3

• The overall pass rate for this question was 67/81 (82.7%)

Question A

• Pass Criteria
  • Interpretation with good diff and important management issues.
  • Describe seat belt pattern and potential consequences e.g. Internal injuries/particular patterns associated with this injury
• Features of unsuccessful answers
  • No Interpretation/minimal synthesis
  • No differential or very poor differential

Question B

• Pass Criteria
  • Understands utility for recognising abdominal bleeding + pneumothorax
  • Some discussion of US limitations/including details not normally seen/guidance for management and poor at ruling out major non-bleeding injuries
• Features of unsuccessful answers
  • Pure list of views and no understudy of limitations of US both technically or for clinical management

An oral commissure burn.

These injuries typically result from biting on an electrical cord (no, not from smoking a cigarette and letting it burn all the way down…). This is one of the most common mechanisms of electrical injury in toddlers, who tend to explore their environment by putting things in their mouths.

Delayed lingual artery hemorrhage

These burns are often full thickness and are subject to the usual complications of burns. They may be disfiguring and result in microstomia. They are often underestimated. A particularly important complication is the potential for lingual artery hemorrhage. This occurs in about 10% of cases, typically about 5 to 21 days after the injury when separation of the maturing eschar occurs.

Click image for source

Consider the possibility of systemic electrical injury.

• look for an ‘exit’ wound. This may suggest the likely path of current through the body.
• a baseline ECG and cardiac monitoring should be considered if current may have passed through the heart.
• musculoskeletal injuries can result from tetanic contractions (e.g. rhabdomyolysis or fractures)
• assess for neurological injury, deep tissues burns and other organ injuries.

Referral to a plastics/ burns surgeon, patients are usually discharged with outpatient follow up.

In the past children were often admitted for observation to ensure that a delayed lingual artery bleed would be detected and treated. However, in modern times, the pressure on bed numbers is such that this is infeasible. Parents should be instructed on how to apply bidirectional direct pressure to the floor of the mouth in the event of lingual artery hemorrhage. If this occurs urgent plastics/ ENT/ maxillo-facial surgery assessment and management is essential.

Admission may be required for analgesia, nutrition (e.g. nasogastric feeding) or for assessment of possible non-accidental injury or neglect. Definitive treatment options include conservative management with an oral commissure split, early reconstruction or delayed excision of the burn site.

The most common source of microwaves in day-to-day life is the microwave oven. Injury may result from:

direct thermal injury due to dielectric heating

indirect thermal injury due to super-heating of fluids

mechanical trauma —
e.g. fragments of of an exploding superheated foodstuff or dropping a microwave oven on your toe!

Another potential hazard is exposure to toxic gases. This can result from the use of inappropriate food containers. For example, polymer fume fever can result from overheating and melting of teflon aka polytetrafluoroethylene (PFTE).

In ‘simple physician-ly’ terms, this is how dielectric heating works:

The microwave energy is absorbed by polar molecules. These molecules rotate and collide as a result. Thus the electromagnetic energy is converted into kinetic energy and generates heat. Polar liquids like water heat up more quickly in the microwave than either polar solids (e.g. ice) or less polar liquids such as oils.

Despite their safety mechanisms, microwave ovens are not fool-proof. There are reports of people managing to sustain direct thermal injury due to dielectric heating. Occasionally people somehow manage to burn their hands in a microwave oven… or, horrifically, a small infant…

Clinically, it is important to realise that:

Injuries sustained by dielectric heating resemble electrical burns in that the degree of internal thermal injury, and resulting necrosis, may be under-estimated due to the lack of external signs of injury.

Super-heating occurs when a liquid is heated to beyond its boiling point.

This can occur in undisturbed liquids in a smooth container that are free of nucleation sites as the formation of bubbles in the boiling process is suppressed by surface tension. Superheating is not limited to ‘pure’ fluids — it also occur in ‘impure’ fluids, like a cup of coffee, infant milk formula, or even an egg. When a superheated liquid is disturbed, rapid boiling may occur, and the result may be a violent explosion… Sanjay Arora MD found this out at last year’s USC Essentials Trauma Review course (see free video here).

Microwave-heated food or drink items are also prone to causing internal thermal injuries following premature ingestion. This can occur because the food or drink may seem cool externally yet be internally superheated.

Most microwave manufacturers advise letting food stand for 2 minutes to allow adequate diffusion of heat — the more viscous the fluid, the longer the time required.

Standing time is particularly important with items that have fluid centres and a solid outer shell — examples include eggs, jelly-filled donuts and bottles of infant formula.