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An 80 year old male is bought to your ED via ambulance following a syncopal episode. He reports sitting on a church pew, when he apparently collapsed without prior warning. According to bystanders he was unresponsive on the ground looking pale then ‘blue’. He was making some respiratory effort and eventually recovered without intervention.

By the time you examine him, he is alert and oriented (though, amnestic to the actual event). His pulse is 60, he is warm and perfused (with a BP of 138/66). There is no evidence of cardiac failure and his neurological exam is unremarkable. You do note a pacemaker box in his upper left chest and his CXR shows that this is a ‘dual-lead’ variety….

This is his ECG.

What’s going on here ?
How do you explain his syncope ??
What needs to happen now ???

ECG.

• Atrial paced rhythm @ 60/min
• Left Axis Deviation
• PR 280-300msec. QRS 150msec (RBBB pattern). QTc ~460msec
• Left Anterior Fascicular Block (LAD, ‘rQ in inferior leads)
• No obvious pronounced ischaemia.

 Impression.

• Atrial paced rhythm
• Trifasicular block.

?Syncope secondary to complete heart block (whilst atrially paced)
- why didn’t his ventricular pacing kick in ??
- is there a pacemaker malfunction ??
??tachydysrhythmia

He is admitted to Coronary Care for telemetry whilst he awaits a pace-maker interrogation…..

Pacemakers. 

In short, this case prompted some further reading on PPMs & AICDs, particularly the codings, the variety of settings available & how each functions to assist native cardiac activity (or lack thereof…..).

What’s in one … ??

• Pulse generator (& battery), electronic circuitry and leads.
• Lithium power (lasting 4 to >10 years)
• Leads are placed into ventricular (+/- atrial) endocardium
  • Can be unipolar or bipolar
  • Bipolar leads are compatible w/ AICD systems, but are larger & more prone to fracturing.

What does it do … ??

• Two basic functions:
  • stimulate the heart electrically.
  • sense the intrinsic cardiac activity (native rhythm)
• Additional functions:
  • Overdrive pacing
  • Deliverance of shock/defibrillation

Who gets it … ??

• 3rd-degree & advanced 2nd degree AV block w/
  • symptomatic bradycardia (incl. heart failure) or ventricular dysrhythmia
  • symptomatic bradycardia (secondary to drugs required for dysrhythmia therapy)
  • Documented asystole (>3sec) or escape rhythm (<40bpm) or escape rhythm (below AV node) in an asymptomatic individual
  • After catheter ablation of the AV node, or if post-operative AV blockade is unlikely to resolve.
  • Neuromuscular disease w/ AV block (eg. muscular dystrophy)
• Symptomatic bradycardia from 2nd-degree AV block
• Asymptomatic, persistent 3rd-degree block
• Chronic bifascicular or trifascicular block w/ intermittent 3rd-degree block (or Type II 2nd-degree block)
• 2nd or 3rd degree block w/ exercise

What do those codes mean … ??

Examples:

• AAI:
  • Atrial pacing and sensing.
  • Intrinsic atrial activity inhibits pacemaker firing & natural/native conduction occurs.
  • Lack of intrinsic activity (beyond a programmed time frame) triggers an atrial paced beat (which results in normal AV conduction and ventricular contraction).
• VDD:
  • Capable of pacing ventricle only.
  • Senses both atrial & ventricular native depolarisation
  • If intrinsic ventricular depolarisation occurs; responds by dual inhibition of both atrial & ventricular pacing.
  • A paced ventricular beat is triggered in response to a sensed intrinsic atrial depolarisation.
• VVI:
  • Ventricular (only) pacing and sensing.
  • A paced ventricular beat will be triggered if an intrinsic depolarisation fails to occur during a set, programmed interval.
  • A native ventricular beat will inhibit pacemaker firing.
• DDD:
  • Can sense & pace both atrium and ventricle.
  • Atrial pacing initiated if native atrial contraction fails to occur in given time frame.
  • Ventricle is paced if native ventricular contraction fails to occur for a given time frame following atrial activity.
  • Native sinus rhythm inhibits both atrial and ventricular pacing.

What about the magnet … ??

Magnet application (placed externally over the pulse generator in the chest wall) causes closure of a reed-switch within the pace-maker circuitry, converting the pacemaker to an asynchronous or fixed-rate pacing mode (set by the manufacturer), and the pacemaker is no longer inhibited by the patient’s intrinsic electrical activity.

• Most commonly used when the patient’s intrinsic heart rate exceeds the pacemaker’s set rate and pacemaker function is inhibited.

the conclusion.

Well our fella’s pacemaker was interrogated a few hours later in the CCU.

• Turn’s out he was in an MVP-mode (technically a combination of AAI-DDD)
• Had had a few episodes of Wenchebach and two short runs of VT (‘weeks ago’).
• There was no dysrhythmic event at the time of his syncope.
• He was changed to DDD mode & discharged home 48 hours later with a presumptive diagnosis of vasovagal syncope.

MVP mode (a Medtronic program) is designed to reduce the risk of AF in patients with permanent pacemakers.

• MVP = managed ventricular pacing
• MVP is atrial-based pacing (aimed to significantly reduce unnecessary right ventricular pacing.
  • Primarily operates in AAI whilst providing a safety-net of a dual-chamber back-up mode, if required
• Why ??
  • Risk of AF doubles w/ ventricular pacing (DDD-L or DDD-S) versus atrial pacing (AAI-R).

References.

1. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
   
2. Pacemaker Rhythms – Normal Patterns @ lifeinthefastlane.com
   - This page is a fantastic resource for further reading on pacemakers (particular ECG interpretation).
3. Managed Ventricular Pacing – Medtronic.com
4. Nielsen JC et al. A randomized comparison of atrial and dual-chamber pacing in 177 consecutive patients with sick sinus syndrome: echocardiographic and clinical outcome. J Am Cardiol. August 20, 2003;42(4):614-623.

The Case.

A 59 year old male undergoes an elective radical prostatectomy. He is previously well, however takes some ‘herbal Chinese medicines’ that he stopped 2 weeks prior to surgery. His surgery appears to go without a hitch, except for the 1200mL of blood in the surgical suction container at the end of the case. He has received 2 liters of Hartmann’s & 500mL Volvuven during his OT time. He is extubated and taken to recovery at the end of the case where he reports feeling quite comfortable.

I am called back to recovery about 20-25 minutes later to address his hypotension.

On return to recovery, he looks pretty horrible. He is pale & clammy with cool hands. His pulse rate is 95 (sinus rhythm) with a blood pressure of 82/40. I give him two boluses of fluid (500mL each) & his BP promptly improves to 105 systolic….

…..If only it was that simple! I am called 10 minutes later for further hypotension. 80’s on 40’s again…. This time I take a Hemocue which shows a Hb of 68 (was 128 pre-op).

• 4 units of PRBCs are cross-matched; 2 units given stat
• repeat Hb 84.
• Surgeon’s asked to review [blames Chinese medicines, mutters something about post-anaesthetic hypotension, venous oozing & need for further resuscitation, heads back to do the next cystoscopy]…

By this time my boss perches me in recovery to keep a permanent eye on this fella whom I am confident has haemorrhagic shock…

Morning becomes afternoon;

• Ongoing episodes of hypotension, responding to fluids
• Declining urine output.
• Patient remains clammy and at times frankly diaphoretic
• Bedside USS showed a flat IVC and a hyperdynamic left-ventricle. There was free fluid (~0.6cm) in Morrison’s pouch as well as over the diaphragmatic surface of the liver & spleen…
• Hb drops back to 60.
• Massive transfusion formally commenced… (he needs to go back to theatre)
• Anaesthetic consultant agrees… Urology registrar notified again & again (no action, very reluctant to consider a return to theatre)…

Crisis precipitates action;

• With ongoing periods of hypotension, our patient eventually reaches a peri-arrest state following an episode of abdominal pain and vomiting, with altered mental state and a systolic BP of 50-something.
• Anaesthetic consultant and fellow join me at the bedside…
• MTP continues….
• Formal repeat bloods show worsening metabolic acidosis with acute kidney injury and hyperkalaemia.
• Sick of waiting for the registrar to take action, I call the Urologist himself & we finally get a decision to go back to theatre for exploration.

Not over yet;

• He has one of the more scary inductions I have witnessed.
  • 2mg Midazolam, 100mcg Fentanyl & Cisatracurium (he had received Sugammadex for reversal at the end of his first surgery).
  • This was enough to drop his BP from 130 –> 65 mmHg.
• He has a large pelvic haematoma evacuated and a further 1500mL of blood in his suction container.
• Before leaving to theatre (destination: ICU) he has received;
  • 12 units RBC
  • 12 units FFP
  • 2 pools of PLTs
  • 18 units of cryoprecipitate
  • Calcium (20mmol gluconate)
  • Tranexamic acid….

The Reflection.

This case was obviously frustrating for a lot of people involved (and incredibly emotional  & exhausting for the recovery staff who provided him with so much time and attention). My subsequent reflection on this scenario has lead to a few realisations….

1) You are a much stronger performer in your own environment….

• This diagnosis was easy. There was very little else that could have explained this patients’ clinical state, but I appeared to doubt my diagnosis of haemorrhagic shock over & over. Was this because I was in the post-op setting now ?? Bleeding is bleeding….
• I was obviously uncomfortable in the new surroundings, particularly when it came to escalating my concerns for this patient and advocating for his return to the OT. Perhaps I was afraid of ‘ruffling to many feathers’. I strongly believe that in the face of a registrar’s inaction I would have called a Consultant sooner had I been in my ED.
• I have no doubt that if this scenario took place  on my home-turf of the ED resus bay, that my assertiveness and push for action would have been with a louder and more confident voice.

2) There is no place like home….

• When the proverbial hit the fan and this guy decompensated I quickly realised that I had absolutely no idea where the resuscitation equipment, drugs & fluids etc were & I had to rely solely on the staff around me to ‘go fetch’ as I kept barking orders.
• This was a stark reminder of what Cliff Reid has been talking about for years, in the need to know and control your resuscitation environment.
• I have subsequently spent my own time going through various parts of the department familiarising myself with the resus equipment and its location (not only in the operating theaters and recovery, but also on the ward resus-trollies where we attend medical emergencies).

3) Our ED training is great to fall back on…

• Faced with a persistently hypotensive patient, I did what felt comfortable and what came naturally… I took ultrasound to the bedside.
• Whilst this didn’t add anything new to the case, it backed up my suspicions at a time when I was doubting myself…

4) The patient in haemorrhagic shock can fall in a heap on induction…

• Midaz/Fentanyl was all that was needed to reach reasonable sedation for induction.
• I am left to ponder what would have happened if he was given a more ‘generous’ induction agent (eg. ketamine).

The Conclusion.

Well, this is fortunately the boring part of the story. Our fella is delivered to ICU with stable haemodynamics, a temperature of 36.2*C & a normal pH/bicarb. His INR is 1.1 & Hb is 72.

He receives a further 2 units of RBCs overnight in the ICU & is extubated the following day.

By day 3 (post-op) he is back on the ward and makes a progressively uneventful recovery to hospital discharge.

So, there you go.
I’d love to hear peoples feedback and comments on this case.

Sorry for the long hiatus. I’ll be ‘dissecting’ more frequently again, promise.

Chris.

A 3 week old infant is bought into your ED late at night. She is febrile and looks incredibly unwell. Her parents report a 36 hour history of increasing vomiting and poor oral intake. She has not had a wet nappy for 12 hours or so and the parents now report a fever of 39.5*C.

She was born at 39 weeks gestation following an unremarkable pregnancy and delivery. They were only in hospital for 2 days as everything was going so well…..

When you approach this child in resus, you immediately identify that she is in a whole world of trouble. She is flat and listless, tachypnoeic at 70/min (with moderate work of breathing) and tachycardic at 204 bpm. Her capillary return is 5-6 seconds and her skin is mottled. Her abdomen is quite obviously distended.

Amongst the flurry of activity at the bedside the following x-ray is taken….

What’s going on here ?
What are your differentials ??
What are you going to do next ???

Based on the clinical picture above, we were left with a few differentials including;

• Sepsis, sepsis, sepsis…
• Pyloric stenosis
• ‘something nasty in the belly’…
  • obstruction
  • malrotation-volvulus

There are a number of things going on in this xray….

1. a healing left-sided clavicle fracture, with callous formation.
2. small right pneumothorax.
3. intestinal dilatation. nasogastric tube insitu.
4. pneumatosis intestinalis.
5. portal vein gas.

These xray findings were almost diagnostic of necrotising enterocolitis ….

Necrotising Enterocolitis (NEC).

The most common gastrointestinal emergency in neonates and the most common cause of intestinal perforation occurring in the neonatal period. It is a condition of intestinal necrosis in previously well infants and whilst it is predominately a disease of prematurity & most cases occur whilst the child is in the NICU, up to 10% of cases occur in full term infants. As today’s child-delivery practices change (home-births, very early discharges from labour wards – some as early as 4 hours) this is potentially a problem that can make its way into the Emergency Department.

The exact pathophysiologic mechanism behind NEC remains unknown, but appears multifactorial. The primary event may be inflammation or injury to the intestinal wall, which begins in the mucosa and then extends transmurally. The distal ileum and proximal colon are more commonly affected, and the involvement may be continuous or patchy.

Risk factors include;

• Prematurity (90% of cases)
• Aggressive enteral feeding
• Birth-related hypoxic or ischaemic insults (including congenital heart disease)
• Infectious causes

The development of NEC is closely related to gestational age;
          * 24-28 weeks: NEC w/in 2-4 weeks of life.
          * 29-32 weeks: NEC w/in 1-3 weeks of life.
          * Full term infants: NEC in 1st week of life.

Clinically…

The classic symptoms are that of food intolerance (poor feeding) and vomiting (either bilious or non-bilious). Examination may reveal palpable loops of bowel (oedematous & distended with air), as well as erythema & discolouration of the abdominal wall. Other symptoms and signs include; haematemesis, PR bleeding, shock and apnoea.

NEC is commonly divided into three stages:
          1) Early or suspected NEC [food intolerance, vomiting, ileus]
          2) Definite NEC [confirmed on radiograph w/ 
               intestinal dilatation & pneumatosis intestinalis]
          3) Advanced disease [perforation, marked abdo distension,
               metabolic acidosis, DIC & shock]

** an example of pneumatosis intestinalis, courtesy of Wikipedia **

A 7 year old boy presents to your ED with a 3-4 day history of fevers, nausea and vomiting. There is some associated non-specific abdominal pain. He has a history of Type 1 Diabetes Mellitus. His blood glucose at triage is reading ‘HI’ and his finger-prick ketones are 6.4 mmol/L. He is therefore taken through to your resus bay, where you achieve IV access and get the following set of results…

How do you approach this child ?
What are your principles of management ??
Would your approach be different if he was 37 years old ???

Well, there are no hidden tricks with this case. This is not a fancy diagnosis, rather a very common one. I feel that if you are in a department that sees children, then you need to know Paediatric DKA back to front & be able to manage it with a certain level of finesse, particularly as there is certainly the potential to do more harm than good.

I wanted to use this case as a vignette to bring the following paper to your attention….

To my knowledge it is the most concise paper that summarises the management of Paediatric DKA. Below are what I consider the pertinent points to take from this guideline….

Diagnosis:

• * Hyperglycaemia 
       - Blood glucose > 11mmol/L (200mg/dL)
  * Venous pH < 7.3 or HCO3 < 15mmol/L
  * Ketonaemia / Ketonuria.

Severity:

• * Mild
       - pH < 7.3  or  HCO3 < 15 mmol/L
  * Moderate
       - pH < 7.2  or  HCO3 < 10 mmol/L
  * Severe  
       - pH < 7.1  or  HCO3 < 5 mmol/L

Goals of Therapy:

• * Correct dehydration.
  * Correct acidosis & reverse ketosis.
  * Restore blood glucose to near normal.
  * Avoid complications of therapy.
  * Identify & treat any precipitating causes.

Fluid Management:

• * Severe volume depletion w/out shock.
       - Volume resuscitation begins immediately w/ 0.9% saline.
       - Aim for 10mL/kg/hr over 1-2 hours
            ~ repeat if necessary.
       - Do not exceed 30mL/kg in first 4 hours.
  
  * DKA w/ shock (rare).
       - 20mL/kg bolus (0.9% Saline or Hartman's) 
       - reassess after each bolus
       - don't forget the intraosseous route !
  
  * Subsequent fluid management (deficit replacement).
       - 0.9% Saline or Hartman's for at least 4-6 hours.
            ~ Thereafter; tonicity > 0.45% (w/ added K+)
       - Calculate fluid deficit (ie. 5 vs 7 vs 10% dehydration).
            ~ Rehydrate evenly over 48 hours
            ~ Avoid rates of > 1.5-2x usual daily maintenance requirements.
            ~ click here for fluid calculation example
       - No need to add urinary losses to fluid calculations.
       - Sodium content may need to be increased 
         (if Na+ not increasing w/ appropriate therapy).

Insulin Therapy:

• * Start insulin infusion 1-2 hours after commencing fluid replacement.
       - ie. after initial volume expansion.
  * Dose = 0.1 units / kg / hour (via infusion).
       - reduce to 0.05 units/kg/hr in those w/ exquisite insulin sensitivity.
       - do not use boluses !!
  * Continue insulin until DKA resolves [ Target BSL ~ 11mmol/L ].
       - ie. pH > 7.3, HCO3 > 15 mmol/ or anion gap is closed.
  * Add 5% Dextrose to IV fluid when glucose ~ 14-17mmol/L
       - consider adding earlier w/ rapid glucose drop (>5mmol/hr).
       - up to 10-12.5% may be required to correct acidosis.

Potassium Replacement:

• * Children w/ DKA have total body deficits of up to 3-6 mmol/kg.
  * Replacement is required regardless of serum K+ concentration.
       - If hypokalaemic;
            ~ start K+ replacement w/ initial volume expansions.
            ~ concentration of 20mmol/L should be used.
       - If normal K+;
            ~ start K+ replacement after expansion, before insulin therapy.
       - If hyperkalaemic;
            ~ defer K+ replacement until urine output is documented.
  
  * Maintenance therapy;
       - Potassium concentration of 40mmol/L.
  * Maximum replacement is ~ 0.5mmol/kg/hr.
  

Phosphate Replacement:

• * No clinical benefit from routine replacement.
  * Severe hypophosphataemia w/ unexplained weakness should be treated.
  * Potassium phosphate can be used with KCl to replace both.
       - Beware inducing hypocalcaemia.

Acidosis:

• * Severe acidosis is reversible by fluid & insulin therapy.
       - Insulin stops further ketoacid production & generates bicarbonate.
  * No clinical benefit from bicarbonate administration.
       - May cause paradoxical CNS acidosis.
  * Consider bicarbonate use in;
       - severe acidosis (pH < 6.9) w/ decreased cardiac contractility 
         & vasodilatation 
       - life threatening hyperkalaemia.

Cerebral Oedema:

• * Responsible for 60-90% of all DKA-related deaths.
  * Incidence ~ 0.5-0.9% of DKA cases.
  * Mortality ~ 21-24%.
  
  * Risk Factors:
       - younger age / New onset diabetes / longer duration of symptoms
       - greater hypocapnia (adjusted for severity of acidosis)
       - more severe acidosis
       - increased serum urea
       - bicarbonate therapy (to correct acidosis)
       - greater volumes of fluid given in first 4 hours
       - attenuated rise in serum sodium concentration (despite therapy)
       - administration of insulin in first hour of fluid therapy
  
  * Signs & Symptoms:
       - Headache / progressive bradycardia or hypertension
       - Altered neurological status
            ~ restlessness
            ~ irritability
            ~ drowsiness
            ~ incontinence 
       - Focal neurological signs (eg. cranial nerve palsies)
       - Decreased oxygen saturations.
  
  * Treatment:
       - Elevate head of bed
       - Reduce IV fluids to 1/3 the rate
       - Mannitol:
            ~ 0.5-1.0 grams/kg over 20 minutes.
            ~ repeat if no response in 30-120 minutes.
       - Hypertonic (3%) saline.
            ~ an alternative to mannitol
            ~ 5-10mL/kg over 30 minutes.
       - Intubation. Avoid aggressive hyperventilation.
       - CNS imaging (CT-Brain); 
            ~ confirming diagnosis/assessing for alternate diagnoses.

Reference.

1. Wolfsdorf, J. et al. Diabetic ketoacidosis in children and adolescents with diabetes. Pediatric Diabetes. 2009. 10 Suppl 12: 118–133.

It’s night shift & you’ve received handover of an entire department. You plug on and start chipping away at the waiting-list that doesn’t seem ever get any shorter….

At 3am your nursing staff alert you to an 11 year old female who just isn’t getting any better. She was admitted under Paediatrics on the evening shift with 24 hours of vomiting (no diarrhoea) & had failed her trial of fluid. Whilst she is waiting for a paediatric ward bed she has continued to vomit a further 8-10 times and is complaining of severe epigastric pain. She had used up all her available antiemetics and analgesics on her medication chart…

She looks miserable, crying in pain and clutching at her abdomen. She is slightly tachycardic (otherwise normal observations). Her abdomen is non-distended but exquisitely tender with percussion tenderness and rebound. She has reduced bowels sounds. There is a scar in her RIF indicating a previous open appendicectomy ( ~18 months earlier).

You review her bloods (WCC 16, otherwise unremarkable) and her urinalysis is normal.

Despite further boluses of morphine, she continues to vomit and complain of severe pain….so, you order an abdominal xray.

What’s going on here ?
What are you going to do now ??

Upon reviewing my film, my immediate concerns was of a closed-loop obstruction. On further questioning, the young patient had not opened her bowels for 2 days, and had not passed flatus for at least 24 hours. Our surgical registrar agreed to review the patient….

Paediatric Bowel Obstruction.

The symptoms are generally non-specific with irritability, persistent vomiting, abdominal pain and distention. There are many different causes and pathological processes behind paediatric bowel obstruction. They include the following….

Congenital Causes.

• atresia (duodenum, jejunum, oesophagus)
• pyloric stenosis
• meconium ileus
• aganglionic megacolon
• malrotation
• constriction bands
• intraabdominal hernias

Intussusceptions.

• Ages 3 months – 6 years.
• Requires a lead point (only found in 2-8% of cases)
  • Viral illness / gastroenteritis / rotavirus –> lymphoid tissue swelling.
  • Meckel’s
  • Peutz-Jaghers Syndrome

Incarcerated Hernias.

• Umbilical – very common. rarely incarcerate.
• Inguinal – very common. 10x more common in boys. more common in prematurity.
• Femoral – rare in children. females >> males.

Malrotation with midgut volvulus.

• 1 in 500 infants.
• Error of rotation around the SMA axis.

Postoperative Adhesions.

• Responsible for 3-8% of intestinal obstructions in infants/children.
• Incidence lower after laparoscopic procedures than after laparotomy.

Annular Pancreas.

• Rare congenital anomaly
• Pancreatic tissue fully encircles the 2nd part of duodenum (leaving a non-distensible ring and a functional stenosis).

the conclusion.

The surgical registrar is agreeable with suspicion of bowel obstruction & the patient is consented for a diagnostic laparotomy. As the patient rolls off to theatre, I go home to bed….

My phone beeps midway through the day and I receive the following picture in an MMS.

Following surgical release, her bowel immediately reperfused & remained viable. She is discharged home 4 days later without complication…

my thoughts…

In the ED, we are often faced with a never-ending ‘To-Do’ list and are asked to meet time-lines for decisions and dispositions that seem to be getting shorter & shorter…

For me, this case is a reminder that if your patient:

1. isn’t following the expected path of the proposed diagnosis
2. isn’t getting better with the therapy instituted to date.

Take a step back and start from scratch, reviewing the case from the very beginning…

A 36 year old male presents through your sub-acute area with increasing facial pain & swelling. He reports a simple trip and fall 18 hours earlier (no alcohol on board, recalls all events), where his right cheek struck a concrete step. He had no LOC at the time, and has no historical features concerning for intracranial injury.

He is worried today as the swelling ‘just keeps getting worse’.

On examination he has obvious marked right zygomatic/maxillary swelling and ecchymoses. His cranial nerves are ok (particularly extra-occular movements and facial sensation). When you palpate his facial bones, for find something unexpected which leads you to expediting his CT scan….

What has happened here ?
What other injuries may have been sustained ??
What do you do next ???

Interpretation & Progress.

This CT demonstrates a comminuted, depressed maxillary fracture involving the orbital floor and lateral orbital wall (a ‘blow-out’ type fracture), with extension into the maxillary alveolar process.

The most striking feature of this CT-series is the abundance of subcutaneous emphysema, and of particular concern to me was the extent to which it had traveled (to contralateral carotid sheath, SCM & masseter, submandibular space & of most concern to me, the retropharyngeal space at the level of the epiglottis).

Whilst a bony injury of this magnitude requires little further ED work-up & can usually be referred to your Plastics/Maxillofacial surgeons as an outpatient, the amount of soft-tissue air in this case made us reluctant to simply discharge him home.

Subcutaneous emphysema in the setting of facial and neck trauma raises the suspicion & should prompt the consideration of an aero-digestive injury. Our patient in this case had a single isolated blow to the right cheek & no evidence of anterior neck injury (and gave excellent recollection of the events). He had no dysphagia, dysphonia or neck pain, but did report a recent runny nose. Regardless, we elected to pursue this further by asking our ENT colleagues to review him.

In short, he was admitted for observation & commenced on IV antibiotics. The ENT registrar performed a nasendoscopy in the ED revealing a macroscopically normal airway to the level of the cords. He was discharged home 48 hours later with no further sequelae from his injury.

Orbital Fractures.

The most common simple fracture of the orbit is the ‘blow-out’ fracture of the orbital floor.

Assessment:
* Bony fragments & orbital contents can sag/herniate into the maxillary sinus.

* Enophthalmos vs Exophthalmos (more likely to occur with medial wall involvement)

* Assess for diplopia & EOM (particular inferior rectus function)

* Pic courtesy of Otolaryngology Houston

* Pic courtesy of Zygomatic Complex & Nasal Injury

* Retrobulbar haematomas (or malignant orbital emphysema) can create an ocular compartment syndrome leading to blindness from acute ischaemic optic neuropathy. (Suggested by exophthalmos, reduced visual acuity & increased IOPs).

Management.

• Non-displaced or minimally displaced fractures can be handled as an outpatient with definitive repair delayed by up to 7 days.
• Antibiotics are required for open fractures and fractures that violate sinuses. Amoxicillin-clavulanate is sufficient.
• Lateral canthotomy is required for suspected or confirmed retrobulbar haematomas.
  • Check out Broome Docs 7th Podcast for more information…

Lastly; avoid sneezing and don’t blow your nose !!

This cane force air from the sinuses into soft tissues...

As it turns out, our man had a simple case of man-flu just prior to his injury and in the 12 hours prior to his ED arrival had been vigorously blowing his nose in attempt to clear his nostrils !!

A 25 year old registered nurse presents to her GP with a 6 day history of abnormal vision, which she noticed whilst checking her blind-spot when driving. This has been accompanied by painful extraocular movements & the sensation that her right eyelid was drooping. She has had a recent viral URTI & has been quite stressed at work with a pending presentation and upcoming exams….

She has been referred to your ED today (by the Ophthalmologist) with the following visual field examination

** hence the "droopy eyelid" **

On examination, her pupils are equal & reactive directly, but there is a positive Marcus-Gunn reflex on the right side. VA 6/5 on (L) & 6/18 on (R). Normal EOM, but reports pain in the right eye with lateral gaze (“like a tight cord pulling”).

She is holding a letter from the Ophthalmologist which states, “please start treatment!”

What’s the diagnosis ?
What are we treating & why ??

Optic Neuritis

The most common cause of unilateral painful vision loss in a young adult, typically, in patients ranging from 15-45 years.

It is the initial presentation in ~ 20% of cases of multiple sclerosis (an illness which is much more prevalent at high latitudes).

Clinical Features.

Patients are typically otherwise young & healthy. There may be a history of preceding viral illness. There is a female preponderance (3:1).

Symptoms:

• Painless loss of vision
  • hours to days
  • subtle vs profound
• Ocular pain (w/ eye movement)
• Reduced visual acuity (ranging from minimal loss to no light perception), colour & contrast vision
• Usually unilateral, though can be bilateral

Signs:

• Relative Afferent Pupillary Defect (RAPD) = Marcus-Gunn pupil
• Decreased colour vision > visual acuity
• ? Patchy visual field defects
• ? Swollen optic discs

Aetiologies / Differential Diagnoses.

Corticosteroid-responsive optic neuropathies.

• SLE, Sarcoidosis
• Behcet syndrome (vasculitis w/ oral & genital ulceration + uveitis)
• Autoimmune or chronic-relapsing inflammatory optic neuritis
• Neuromyelitis optica (ON associated with myelitis)

Other inflammatory conditions.

• Post-infectious, post-vaccination
• Acute disseminated encephalomyelitis (ADEM)

Compressive optic neuropathies.

• Primary tumours (gliomas, meningiomas, pituitary, craniopharyngioma)
• Metastases
• Aneurysms

Ischaemic optic neuropathies.

• Anterior / Posterior ischaemic optic neuropathy
• Giant cell arteritis
• Diabetic papillopathy

Infective conditions.

• TB, Syphilis, Bartonella (cat-scratch disease), Lyme disease
• Viral (measles, mumps, zoster, varicella, EBV)
• Cryptococcus, Toxoplasmosis
• Periorbital cellulitis / sinusitis.

Toxic / Nutritional neuropathies.

• B12 deficiency, ethanol/methanol, heavy-metals.

Investigations.

In a typical case of optic neuritis, without any clinical signs & symptoms of a systemic disease the yield from diagnostic tests is extremely low.

• MRI
  • An important prognosticator !!
  • Normal @ baseline = 25% risk of MS
    • 16% @ 5 years
    • 22% @ 10 years
  • One or more lesions = 75% risk of MS.

   

** an MRI demonstrating plaques from an unrelated patient with ADEM **

• CSF
  • The presence of oligoclonal bands correlates with later development of MS.
  • Those with oligoclonal bands usually have abnormal MRIs (therefore CSF sampling is unnecessary).
  • Reserve lumbar puncture for atypical presentations.

The Natural History.

Visual acuity reaches its poorest within 1 week, then will slowly improve over the next several weeks.

Spontaneous visual improvement should occur in >90% of patients within 2-3 weeks.

• 93% have VA of > 6/12 @ 1 year.
• 70% have VA of > 6/6 @ 1 year.

Progression to MS.

• 30% of patients presenting with acute optic neuritis develop multiple sclerosis within 5 years.
• 50% of clinically isolated optic neuritis go on to develop a second MS-defining episode by 15 years.

Treatment.

The role of steroids (predominately IV methylprednisolone) remains somewhat controversial.

• Initial studies (following 3 days of IV therapy) showed a reduced rate of MS development over 2 years of follow up.
• Subsequent review of the same cohort at 5 years post-treatment revealed no significant difference in the rate of development of MS.

RCT data on high-dose oral methylprednisolone vs placebo showed improved recovery at 1 & 3 weeks of followup, but no effect at 8 weeks (or in subsequent attack frequency).

• No role in long-term visual outcome.

Treatment with oral prednisone alone increases risk of recurrent optic neuritis.

Meta-analysis data (from 12 RCTs) confirms that whilst high-dose IV methylprednisolone is effective in improving short-term visual recovery, there is no significant benefit in long-term outcome.

There are specific circumstances however, where corticosteroids should be offered:

• Monocular patients
• Severe bilateral visual loss
• Occupations requiring normal visual acuity

THE DOSE = 1 gram IV methylprednisolone for 3 days.

The Follow-up.

Well, there was concerns that she had features of bilateral optic disc swelling & that her visual field defect was now life altering (unable to drive, unable to work)…..

She is enrolled in ambulatory care for 3 days of IV methylprednisolone and over the next 2-3 weeks her visual acuity and fields improve significantly. Her MRI was normal.

She is now back behind the wheel, working in the ED & able to enjoy reading her partner’s blog @ thebluntdissection !!

Hi Ali !! Thanks for letting me share this.

References.

1. Eye Emergency Manual. An Illustrated Guide. NSW Department of Health. www.health.nsw.gov.au
2. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
3. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
4. Shams PN, Plant GT. Optic Neuritis: A Review. The International MS Journal. 2009; 16:82-89.
5. Guercio JR & Balcer LJ. Chapter 9.6 – Inflammatory Optic Neuropathies & Neuroretinitis. Yanoff & Duker: Ophthalmology. 3rd Edition.

A 38 year old male presents to your ED with left sided chest heaviness which radiates to his left shoulder & down the arm. He has associated dyspnoea, nausea & vomiting. He looks unwell.

He underwent a CT-Coronary Angiogram 4 months earlier showing a Calcium-Score of 450 !! (‘Extensive plaque burden’. 8x increase in Framingham predicted risk). However, a Sestamibi study performed at the same time showed no evidence of inducible ischaemia.

This is his ECG…

What’s your interpretation ?
Is it significant ??
Where do you go from here ???

my take…

• Sinus tachycardia at ~ 100bpm.
• Normal axis. Normal intervals.
• ~1.5mm STE in aVR, with widespread ST depression (V2-5, II, III, aVF).
• DDx. Left main ischaemia vs triple vessel disease !!

He was treated aggressively with aspirin, GTN infusion & heparin.
I elected to withhold clopidogrel (a decision backed by Cardiology).

As his pain settled the following ECGs are taken…

For me this case was all about…..

aVR

The right-ward facing unipolar lead.

Obtains information about the right, upper side of the heart including the right ventricular outflow tract and basal septum.

Why is it important ??

Toxicology (particularly Na-channel blockade), dysrhythmias (P-wave configuration, identification of AV dissociation etc.) & ischaemic chest pain ….

In the setting of cardiac ischaemia, ST-segment elevation in aVR can indicate left main coronary artery stenosis.

• Significant mortality (~70%)
• Medical therapy not helpful –> patients need cardiac catheterisation
• Other ECG features:
  • Concurrent STE in aVL
  • STE in aVR > STE in V1.
• The greater the ST-elevation, the greater the mortality !!

It may also indicate proximal LAD occlusion or triple-vessel disease.

A recent post by Dr Smith on aVR has bought to my attention this important paper…

An Early and Simple Predictor of Severe Left Main and/or Three-Vessel Disease in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome

Am J Cardiol. 2011 Feb 15;107(4):495-500

A 22 year old male is retrieved to ED after a nasty workplace accident where he was pinned between a truck and wayward forklift. He had sustained injuries to his head/face, upper thorax and perineum, however our most significant concern was regarding his right lower limb. He had a displaced, angulated compound femur fracture that required sedation and pre-hospital reduction. There were reports of significant bleeding at the scene.

No immediate interventions were required following his primary survey, but his right limb revealed a nasty tissue defect and open fracture (now splinted). There was no active blood loss, but his leg distal to the injury was pale and cold with no appreciable dorsalis pedis or posterior tibial pulses.

Here are his initial xrays….

As there was concerns regarding intraabdominal and pelvic injuries; he was taken to radiology for CT, including angiography of his lower limbs….

He went straight to theatre from radiology, and unfortunately underwent an above-knee amputation.

Whilst the decision making process was rather straight forward in this case, it did lead me to revisit the ED-based evaluation of suspected peripheral vascular injury….

peripheral vascular injury…

Typically these injuries are divided into blunt vs penetrating, however they generally result in a similar spectrum of vascular injuries (including laceration, transection, entrapment, avulsion, intimal tears/flaps, pseudoaneurysm, AV-fistulas, thrombosis & spasm).

Detection & treatment of vascular injuries must take place within the context of overall resuscitation of a patient. This also includes the control of active bleeding.

The assessment of peripheral vascular injury can be divided into three categories;

1. Hard findings
2. Soft findings
3. High-risk asymptomatic wounds (based on mechanism of injury).

Hard Findings of Vascular Injury.

• Pulsatile bleeding
• Loss of distal pulses
• Audible bruit or palpable thrill (indicative of AVF)
• Expanding or pulsatile haematoma
• Overt distal ischaemia (the 6 P’s)

The incidence of arterial injury is > 90% if any of these are present !! 
Surgical exploration is required.

Soft Findings of Vascular Injury.

• Palpable, but diminished pulse
• Isolated peripheral nerve injury (due to common proximity to vessels)
• History of severe haemorrhage in the field
• Unexplained hypotension
• Large, non-pulsatile haematoma
• ?delayed capillary refill (in combination with other signs).

 Up to 35% of patients with soft-signs will have positive angiographic findings !!

High-Risk Injuries.

• Proximity of wound to a neurovascular bundle (< 1cm)
  • Includes; axillary, brachial, common femoral & popliteal arteries.
• Bites from large dogs or other animals.
• Severely displaced fractures.
• Crush injuries.
• Major joint dislocations (especially knee).

Meticulous examination is required to look for the above hard & soft signs. Surprisingly, these are relatively dependable (Sensitivity 92%, Specificity 95%).

• False positive findings can occur in shock, preexisting vascular disease, arterial spasm or compression. (Occurs in ~ 10-27% of cases).
• False negative findings can result from pulse transmission through a soft clot, past an intimal flap or via collateral circulation. Distal pulses can persist in 6-42% of patients despite significant arterial injury.

Diagnostic investigations.

These must be tailored to the patient & their injury, and should never delay a definitive treatment to an obvious arterial injury (especially if the clock is approaching the all-important 6 hour warm ischaemia time).

Modalities include plain radiography, pulse-oximetry, hand-held Doppler, ultrasound (including colour-flow and duplex), CT & MRI. CT-angiography is now the most commonly used primary diagnostic study for the evaluation of penetrating lower extremity vascular injury.

The investigation that I wanted to focus on is Arterial-Pressure Index, as I feel it can be easily done at the bedside as an extension to your physical examination.

• Measured with a manual BP-cuff and hand-held Doppler, the systolic blood pressure is measured and compared between the injured and the contralateral unaffected limb.
• An API of < 0.90 increases the likelihood of vascular injury and should prompt further investigation (like CT-angiography).
  • Sensitivity 95% / Specificity 97%.
  • PPV 100%
  • NPV 95%
• API of 0.90-0.99 = observation for 24 hours with repeated examination.
• Normal examination and API = discharge home !!
  • If both normal = 100% negative predictive value.

Caution w/ API: Limited usefulness in deep arteries (profunda femoris, profunda brachii & peroneal arteries) which do not produce palpable pulses & with shot-gun wounds which often cause multiple small arterial injuries.

Summary.

• Hard signs = surgical exploration. No need for angiography unless there is an associated skeletal or shotgun injury.
• Patients (without hard signs) who have abnormal physical examination &/or API < 0.90 should have further evaluation to rule out vascular injury.
• Normal physical examination and API > 0.90 = Discharge home !!

References.

1. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
2. Levy BA et al. Screening for extermity arterial injury with the arterial pressure index. Am J Emerg Med. 2005 Sep;23(5):689-95.
3. Sadjadi J et al. Expedited treatment of lower extremity gunshot wounds. J Am Coll Surg. 2009 Dec;209(6):740-5.
   
4. Mills WJ, Barei DP, McNair P. The value of the ankle-brachial index for diagnosing arterial injury after knee dislocation: Prospective study. J Trauma  2004; 56:1261.
5. Fox, N et al. Evaluation and management of penetrating lower extremity arterial trauma: An Eastern Association for the Surgery of Trauma practice management guideline. J Trauma. 73(5):S315-S320.