The case.

It’s 9 o’clock at night. You are asked to review a 45 year old male on the ward for uncontrolled pain. He has a history of Crohn’s disease and is 24 hours post-laparotomy for small bowel resection & stoma formation. He is nil by mouth…

His current pain regime includes;

• Paracetamol 1g q6h
• Morphine PCA [2mg with 5min lockout] – 280mg used in prior 24 hours.
• Ketamine infusion [8mg/hr]
• Tramadol 100mg IV q6h
• Ketorolac 10mg IM q6h
• Bilateral surgically placed pre-peritoneal catheters with ropivocaine infusions (the left one ‘fell out’ 2 hours ago)….

On examination he is tachycardia and a little clammy. He has diffuse tenderness across the abdomen (L>>R) with percussion tenderness to the LLQ.

What are your thoughts ??

What can we offer this guy...?

A more thorough look...

What happened to our patient ??

The case.

64 year old female who is day 1 post elective left total-knee replacement. She has a past medical history of osteoarthritis, bipolar disorder and depression for which she takes quetiapine, lithium and paracetamol. You are asked to see her on the ward for optimization of her pain management with a concern that she “just isn’t quite right” with confusion & new onset of word finding difficulties.

Her current pain regime consists of

• Paracetamol 1g q6h
• Fentanyl PCA (10mcg q5min)
• Ibuprofen 400mg q8h

She did receive two doses of tramadol the day before….

On examination she has an altered mental state with disorientation to time and place. At times she speaks in absolute gibberish. Of concern is her symmetrical hyperreflexia and inducible lower limb clonus ….

What are your concerns ?

What investigations are you going to order ??

The results...

The diagnosis...?

More about Lithium...

Chronic Lithium Toxicity...

Progress & Follow-up...

References.

A 24 year old male rugby player presents to your ED with a severely painful, swollen left hand which occurred during a tackle and subsequent ruck.

These are his x-rays….

What about the lateral ??

What's going on here ??

The Anatomy...

The Injury...

References.

the case.

A 34 year old insulin-dependent diabetic male presents to your ED following a “collapse” stating he thinks he has had a seizure. He has had hypoglycaemic seizures previously. He lost his glucometer 3 or 4 weeks ago and has been guessing his sugars and corresponding insulin doses by ‘how he feels’…

He has severe bilateral shoulder & upper thoracic pain. Any attempt to move, touch or examine either shoulder results in unbearable pain (plus a stream of four-letter expletives).

As part of his evaluation you get the following x-rays….

Interpretation:

What would you do?:

The CT report:

Posterior Shoulder Dislocations.

The Follow-up...

References.

the case.

a 19 year old female arrives to your resuscitation bay following a high-speed rollover MVA where she was the restrained passenger.

• she has a clinically fractured mandible with some oropharyngeal bleeding, but a GCS of 15. she is able to use a yankauer-sucker and intermittently suction her own mouth.  you are happy with her airway for now
• she is tachycardia at 125/min, and had a transient episode of hypotension (systolic of 85 mmHg) which resolved without intervention.
  • with some analgesia her pulse settles to 110/min.
• her abdomen is exquisitely tender on the left side and she has a positive seat-belt sign.
  • she has free fluid on FAST exam (LUQ)
• she has midline spinal tenderness in the upper lumbar region…

A joint decision with the Trauma surgeons is made; and we head to radiology for a pan-CT. This revealed the following…

• Mandible fracture.
• Splenic laceration
• and this….

http://www.youtube.com/watch?v=9B1YMOr9LK0

What does the scan demonstrate...?

What's a Chance-fracture...?

Why is this injury so significant...?

So what happened next...??

References.

The Case.

A young boy is bought to your ED with an obviously swollen painful left arm after a slip and fall…

These are his xrays…

Describe this injury...

Supracondylar Fracture - Tell me more...

An approach to the Paediatric elbow X-ray...

Adapted from wikimedia.org

Left is normal. Right is obviously not...

What not to miss...

Management in the ED...

References.

the case.

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.

I am now 6 weeks into my 6 month anaesthetic secondment. There have been some interesting challenges settling into the new job but I am largely enjoying my time perfecting basic airway manoeuvers, laryngoscopy and playing with some brilliant airway toys (McGrath video laryngoscopes, the AirTraq, intubating LMAs etc). I thought I’d share with you a case (from Anaesthetic week 2) that presenting some multifaceted challenges & several points of reflection …

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.

Welcome to WordPress. This is your first post. Edit or delete it, then start blogging!

The case.

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 **

The case.

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.

the case.

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…

The Case.

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 ???

The Case.

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.

The Case.

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

The Case.

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.

The Case.

This patient has been in your ED for over 24 hours waiting for a CCU bed. He presented with vomiting and syncope, but acquired left sided rib fractures during his collapse. He has been comfortable for most of the day on nasal-prong oxygen and a morphine PCA.

You are asked to see him as he has sudden worsening of his left-sided chest pain. He has become clammy and hypoxic.

This is what you see….

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

Flail Chest

Defined as segmental fractures (two or more locations on the same rib) of three or more adjacent ribs, resulting in an unstable chest wall. It is one of the most serious chest wall injuries due to its common association with pulmonary contusion and, along with massive haemothorax, tension & open pneumothorax, should be suspected and diagnosed during the primary survey of trauma victims.

The hallmark of this condition is the paradoxical inward movement of the affected chest wall during spontaneous inspiration.

The physiology of respiration is adversely affected by the flail chest in a number of ways;

• Greatly increased work of breathing
• Worsening hypoxia secondary to the underlying developing pulmonary contusion
• Muscular splinting due to pain
• Atelectasis secondary to poor ventilatory effort
• Decreased cardiac output.

Clinical Features & Diagnosis.

Usually diagnosed on physical examination by paradoxical chest wall motion. Pain, tenderness, crepitus or subcutaneous emphysema may also assist in localising the lesion. This may be incredibly difficult to see if the patient is already intubated and receiving positive-pressure ventilation at the time of examination.

A flail segment may be seen on CXR, however CT is more sensitive & provide information regarding the extent of underlying pulmonary contusion and other associated injuries.

* Sometimes they're obvious...

Management.

The patient with a flail chest should be treated as though a pulmonary contusion exists. The outcome of a flail chest injury is directly related to the underlying and associated injuries.

• Supplemental Oxygen.

• Close observation for respiratory decompensation.

• Chest Physiotherapy.

• Cautious fluid management.

• Analgesia.
  • multimodal (paracetamol, NSAIDS, opiates)
  • PCA
  • intercostal nerve blocks
  • high segmental epidurals (never seen these…)

• Respiratory Support
  (obvious problems such as haemopneumothorax or exacerbation of pain should be treated prior to instituting positive pressure ventilation).

• CPAP / BiPAP
  • for awake & cooperative patients
  • may avoid intubation
• Intubation & mechanical ventilation
  • demand-based ventilation (pressure-support) is most beneficial.
  • severe cases may need to proceed to high-frequency oscillation

Indications for early ventilatory support:
* Shock
* Severe head injury
* Comorbid pulmonary disease
* ≥ 8 rib fractures
* Age > 65 years.

• Surgery 
  • Controversial !!!
  • involves fixation of rib or sternal fractures
  • often reserved for when thoracotomy is undertaken to manage other injuries.

The Result.

Upon reviewing his PCA, there is a 3-fold discrepancy between dose-demands and delivery & it is clear that he is under-analgesed. He receives two boluses of IV Fentanyl and additional face-mask oxygen.

Bed-side USS excluded a new pneumothorax and an ABG shows a moderate oxygen requirement. His repeat CXR demonstrates a more confluent lower basal consolidation (?contusion or atelectasis).

He is admitted to HDU for observation, but avoids the need for positive-pressure ventilation following good pain control.

The Case.

64 year old male attends your ED with a complaint for 3 months of progressive weakness, however over the past 7 days he has had multiples falls secondary to his ‘legs just completely giving way’.  You note on the hospital records that he has a history of alcoholism (150-250 grams per day). After a long & drawn out discussion (think, blood from a stone) in an attempt to elaborate his history, you gain the knowledge that …

1. he has had some chronic worsening, low back pain
2. he has not eaten a proper meal for over a week (and no alcohol in that time either)
3. he has lost a ‘decent amount of weight’, but cannot objectify it any further.

He has no known past medical history & takes no regular medications.

He looks crook. Pale, diaphoretic and clammy. Tachycardic (@120/min) and hypertensive (165/110 mmHg). He is afebrile however. No murmurs, chest clear. Tender hepatomegaly. No midline back pain. Normal power, sensation and reflexes to both legs (with good peripheral pulses).

Here is his venous blood gas and accompanying chemistry….

What are your thoughts ?
Differential diagnoses ??
What are you going to do next ???

My Interpretation.

• Metabolic acidosis with respiratory compensation
  • HAGMA
  • Expected CO2 = 29 ± 2 mmHg
    • Actual CO2 = 24, therefore concomitant Respiratory Alkalosis.
• Lactic Acidosis ?cause
  • ?Sepsis (source unclear)
  • Osmolar Gap = normal.
  • Paracetamol / Salicylates / Ethanol = negative.
  • Medications / Drugs unlikely (he’s not taking any).

This fella was covered with broad spectrum antibiotics, given reasonable volumes of crystalloid and loaded with thiamine. His CXR, urine, CT-Abdomen (with spinal reconstruction) and CT-Brain were all unremarkable, so was admitted as a lactic acidosis (cause unknown), presumptive sepsis (source unclear) and likely alcoholic liver disease (low PLTs, tender RUQ). Click HERE to see his gradually resolving lactate (over the course of 6-7 litres of fluid).

Lactic Acidosis.

The Brief Biochemistry.

Lactic acid is derived from the metabolism of pyruvic acid (catalysed by lactate dehydrogenase & involving NADH & NAD+). Lactic acid is rapidly buffered (by extracellular HCO3) resulting in the generation of lactate. Lactate itself is metabolised back to pyruvate (largely by the liver, and a little by the kidney), which is then converted to CO2 & water or glucose.

The Types & Causes.

Type A.

• Associated with clinical evidence of poor tissue perfusion or oxygenation of blood (eg. hypotension, hypovolaemia, hypoxaemia, cardiac failure or sepsis).
• Overproduction.
  • Sepsis, sepsis, sepsis…
• Underutilisation:
  • Liver disease
  • Inhibition of gluconeogenesis
  • Thiamine deficiency
  • Uncoupled oxidative phosphorylation.

Type B.

• No clinical evidence of hypoperfusion.
• Three subtypes.
  • B1 = associated with systemic disease
    • Renal & hepatic failure
    • Diabetes
    • Malignancy
  • B2 = drugs & toxins
    • Metformin
    • Alcohols
    • Iron
    • Isoniazid
    • Salicylates
  • B3 = inborn errors of metabolism.

Personally, I find Cliff Reid’s LACTATES mnemonic much more helpful ….

L = Liver & Lung disease
A = Accelerated Glycolysis (adrenaline, salbutamol)
C = Congenital Disorders
T = Thiamine Deficiency
A = Anaerobic Metabolism
T = Toxic & Drug Effects 
E = Extracellular Movement in Alkalosis
S = Sepsis

* http://resusme.em.extrememember.com/some-causes-of-a-raised-lactate/

The Case.

A 28 year old female presents to your ED at 2am. She left the hospital 12 hours earlier with her newborn first child who is now 2 and half days old. Her main complaint is that of profound lethargy, fatigue, severe worsening bifrontal headache and breathlessness.

She is normally fit and well, takes no regular medications & has no significant past medical history. Her pregnancy was uneventful, but her delivery (at 39 weeks) was slightly hair-raising with foetal distress & decelerations due to an obstructive labour (requiring a ventouse).

She looks lethargic and is laying quietly in bed, but is speaking in full sentences. Her observations are within normal limits, but her BP catches your eye at 154/89. Her cardiorespiratory exam is unremarkable (specifically, her chest is clear, there are no murmurs & I cannot see a JVP). Her belly is soft with a palpable uterus, midway between  umbilicus & pubic symphysis. She has no peripheral oedema. Her GCS is 15 with reactive pupils and normal cranial nerves. She has impressively brisk reflexes (you don’t need your tendon hammer) and her power/tone/sensation appear symmetrical & normal.

Her bloods are completely normal! (FBC, LFTs, PLTs, even the CRP) !!

Now what ??

I was stumped & my differentials were far & wide. I basically documented the following…

• Headache, hypertension, pregnancy…
  • ?Post-Partum Pre-Eclampsia
• Weakness, lethargy, dyspnoea…
  • ?Peri-partum Cardiomyopathy
• Headache (recent pregnancy)
  • Cerebral venous sinus thrombosis
• Was she just depressed ???

The Continuation.

She is admitted under Obstetrics for “observation” and by morning was receiving hydralazine & labetalol after her BP climbed to the 190-220mmHg systolic range, with ongoing severe headache. 

CT-Brain w/ contrast ruled out cerebral sinus thrombosis & an MRI showed no sign of hypertensive encephalopathy (PRES).

Her LFTs, PLTS & Hb remained normal during her admission.

Pre-Eclampsia

Hypertension occurs in ~6-8% of all pregnancies.

Definitions:

• Gestational hypertension (new BP > 140/90 mmHg) occurs during pregnancy (>20 weeks gestation) and resolves in the postpartum period (within 3 months of delivery).
• Preeclampsia is gestational hypertension plus proteinuria (>300mg in 24 hours or 1+ protein on 2 separate urinalyses within 4-6 hours).
  • Regarded as severe if in the presence of multiorgan involvement.
• Eclampsia is the occurrence of seizures in a patient with signs of preeclampsia.

Pre-eclampsia is the commonest medical complication of pregnancy & is associated with substantial morbidity and mortality for both mother and baby. It is a multisystem disorder of unknown aetiology that is unique to human pregnancy and is characterised by an abnormal vascular response that is associated with increased systemic vascular resistance, enhanced platelet aggregation, activation of the coagulation system, and endothelial-cell dysfunction.

Risk factors for the development of preeclampsia include; advanced maternal age, previous preeclampsia, obesity, multiple pregnancies, preexisting thrombophilia (Factor V Leiden, Protein C or S deficiency, homocysteinaemia etc) & limited exposure to father’s sperm.

Complications:

• CNS
  • Eclampsia (seizures)
  • Cerebral haemorrhage or oedema
  • Cortical blindness
  • Retinal oedema
  • Retinal blindness / ischaemia

• Renal
  • Cortical or tubular necrosis

• Respiratory
  • Laryngeal oedema
  • Pulmonary oedema

• Liver
  • Jaundice
  • HELLP syndrome
    • Haemolysis
    • Elevated LFTs
    • Low PLTs
  • Hepatic haemorrhage or rupture

• Haematological
  • Disseminated intravascular coagulopathy
  • Microangiopathic haemolysis

• Placenta
  • Infarct or abruption

• Foetus
  • Preterm delivery
  • Intrauterine growth retardation
  • Hypoxia / neurological sequelae
  • Periterm death

Clinical Features:

• Severe hypertension (systolic > 160mmHg or diastolic > 110 mmHg)
• Persistent &/or severe headache
• New epigastric pain & tenderness
• Vomiting
• Visual disturbances (blurred vision, photophobia, diplopia, scotomata & cortical blindness)
• Hyperreflexia (brisk deep tendon reflexes)
• Oliguria
• Dyspnoea or retrosternal chest pain
• New swelling to hands, face or feet.

Investigations:

• Raised serum creatinine
• Thrombocytopenia (PLTs < 100)
• Evidence of haemolysis (elevated Bilirubin or low haptoglobins)
• Haemoconcentration
• Deranged LFTs (2x upper limit of normal)
• Urinalysis: 1+ protein, >300mg / 24hours.
• CT-Brain: ?intracerebral haemorrhage (patchy haemorrhages & micro-infarcts can occur) ?sinus thrombosis

Management:

The textbook answer lies with adequate and proper prenatal care & monitoring, including identification of women at high risk, early detection by the recognition of clinical signs and symptoms, and progression of the condition to severe state.

Whilst the only definitive ‘cure’ is delivery (which is always appropriate for the mother), it might not be best for a very premature foetus. The decision between delivery and expectant management depends on fetal gestational age, foetal status and severity of maternal condition at time of assessment.

From an Emergency Department perspective, it involves early identification of the disease with prompt referral to Obstetrics.

** Figure taken from Lancet 2005; 365: 785–99 **

For the ED doc, it is important to know the following;

• Suspect & find evidence of end-organ dysfunction
• Control blood pressure (aim diastolic BP <105 mmHg)
  • Methyldopa & CCBs for long term therapy
  • Hydralazine (5-10mg IV q20min)
  • Labetalol & Nimodipine also appropriate
  • Avoid beta-blockers (esp. Atenolol), ACEi & ARBs.
• Control seizures
  • Magnesium sulfate:
    • 4-6 grams loading, then 2g/hr infusion
    • Observe for respiratory depression & loss of reflexes (calcium gluconate is an appropriate treatment)
    • Halves the risk of eclampsia
• Avoid diuretics & hyperosmolar agents, as well as limit IV fluids.
• Early referral for delivery planning

Post-Partum Preeclampsia

Preeclampsia is generally cured by delivery of the placenta, however in some women the disease process can worsen during the first 48 hours following delivery. Delayed postpartum preeclampsia can be defined as signs and symptoms of the disease leading to readmission more than two days but less than six weeks after delivery. These presentations are usually atypical and these women might be at risk for pulmonary oedema, renal failure, HELLP syndrome, postpartum eclampsia and stroke and therefore warrant close observation & followup.

One particular study (retrospectively following 152 patients with delayed post-partum preeclampsia) demonstrated ~63% had no antecedent diagnosis of hypertensive disease. 14.5% went on to develop eclampsia. The most common presenting complaint was headache (69.1%)

For your general presentation of post-partum headache, I would strongly recommend this paper for a concise straightforward approach.

References. 

• Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition
• Paul Young’s Intensive Care Mind Maps - “Hypertensive Emergencies in Pregnancy”
• Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet 2005; 365: 785–99
• Duley L, Meher S, Abalos E. Management of pre-eclampsia. BMJ. 2006 Feb 25;332(7539):463-8.
• Al-Safi Z et al. Delayed postpartum preeclampsia and eclampsia: demographics, clinical course, and complications. Obstet Gynecol. 2011 Nov;118(5):1102-7.
• Stella CL et al. Postpartum headache: is your work-up complete? Am J Obstet Gynecol. 2007 Apr;196(4):318.e1-7.
• Sibai BM. Etiology and management of postpartum hypertension-preeclampsia. Am J Obstet Gynecol. 2012 Jun;206(6):470-5. Epub 2011 Sep 16.
• UpToDate.com – “Preeclampsia: Clinical features and diagnosis”

23 year old female is bought to ED by her family after an intentional overdose of ~ 100 ‘diet tablets’ which she ingested 1.5-2 hours earlier.

She is agitated, anxious, tremulous and profoundly diaphoretic.
P 170. BP 123/70. Sats 100%. RR 32. Temp 36.8*C.
Patent airway. Chest clear. Soft, non-tender abdomen.
Pupils 4mm (equal & reactive).
Normal tone & power in all 4 limbs.
5-6 beats of inducible clonus at the ankles.

BSL 13.1
ECG. Sinus tachycardia @ 170/min (confirmed by increasing paper-speed to 50mm/sec).
VBG.

What do you think she took ?

As it turns out, she consumed 100 of these….

Essentially we were dealing with an acute caffeine toxicity…..

• 100 tablets of 100mg Caffeine = 10 grams
• ~ 140mg/kg of Caffeine.

methylxanthine toxicity…

The Pharmacology.

Methylxanthines are purine derivatives that are structurally related to adenosine. They have an extremely narrow therapeutic index & adverse effects can occur even at therapeutic doses. Theophylline, caffeine & theobromine are the major members of this group.

Caffeine is the most commonly used psychoactive drug in the world; however has been used medically for apnoea of prematurity, analgesic adjuncts, appetite suppression (for weight loss) and diuresis.

• ~100% of the oral dose is bioavailable.
• Peak oral absorption is in 30-60min (delayed in overdose)
• Volume of distribution is low (0.6L/kg)…

Whilst theophylline’s use continues to decline, I consider this an important toxicity to be aware of. Caffeine’s metabolism occurs by biotransformation via P-450 pathways. Its primary metabolite is theobromine (… chocolate), via 1-demethylation however also forms theophylline via 7-demethylation. As a result, theophylline concentrations are measurable following caffeine ingestion and overdose.

• At increased concentrations (overdose) methylxanthines switch to zero-order kinetics (ie. a fixed amount of drug is eliminated per unit of time).

Multiple toxic mechanisms have been proposed for methylxanthines including competitive antagonism of adenosine, altered intracellular calcium transport & inhibition of phosphodiesterase, leading to elevated intracellular cAMP concentrations.

Undesirable effects of caffeine can appear after ingestion of as little as 50mg, however more significant toxicity appears after ingestions of up to 15-30 mg/kg. Fatal doses of caffeine have ranged from 5 to 50 grams (lethal dose estimated to be 100-200 mg/kg).

• Standard cup of coffee = ~ 80-100mg caffeine
• Guarana containing energy drinks = more caffeine…

Clinical Features.

Early manifestations include anxiety, tremor, nausea & vomiting and tachycardia.

Severe poisoning is associated with:

• Cardiac Dysrhythmias 
  • SVTs / AF or flutter / ventricular tachycardia
  • [stimulation of B-adrenergic receptors]
• Refractory Hypotension
• Seizures& myoclonus
  • [secondary to adenosine antagonism - adenosine normally inhibits CNS excitatory neurotransmitter release]
• Metabolic abnormalities
  • Hypokalaemia (severe, refractory)
  • Hypophosphataemia, hypomagnesaemia.
  • Hyperglycaemia
  • Metabolic Acidosis (usu. lactate).
  • Rhabdomyolysis / myotoxicity

Management. 

Resuscitation (ABCs).

• Severe overdoses should be managed in an acute resus area, with complete cardiorespiratory monitoring
• Immediate life threats include;
  • hypotension
    • IV fluid boluses, occasionally vasopressor are required
  • seizures
    • benzodiazepines
    • no role for phenytoin…
  • dysrhythmias
    • sedation often helps
    • beta-blockers (esmolol or metoprolol)
    • adenosine & verapamil also effective
  • electrolyte disturbances
    • esp. K+ replacement
    • check a CK level

Decontamination.

• Activated charcoal is indicated even if presentation is delayed
• Aggressive control of vomiting

Enhanced elimination.

• Haemodialysis is the definitive life-saving intervention in severe poisoning (and achieves good clinical outcomes if started early)
• Multiple-dose activated charcoal can also be helpful (for the generated theophylline, not caffeine itself).

Remember, when in doubt – get a hold of your Poisons Centre or Toxicologist. 

The Outcome.

Our young patient was treated initially with IV fluid boluses (2L N.Saline), potassium replacement and aliquots of IV midazolam. The benzos worked a treat. Patient settled and heart rate slowed to the 110-120 mark. At the two hour mark, her acidosis was improving (lactate down to 4.2 mmol/L).

We were advised to by our Toxicology service to take a theophylline level (to use as an indicator for possible need of dialysis). Her’s was normal.

She spent the night in the ICU and was well enough the following morning to be referred to the Psychiatry team.

References.

1. Murray L, Daly F, Little M & Cadogan M. Toxicology Handbook. 2nd Edition. Elsevier 2011.
2. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Edition.
3. Shannon M, Borron SW, Burns M. Haddad and Winchester’s Clinical Management of Poisoning and Drug overdose 4th ed.
4. Schmidt A, Karlson-Stiber C. Caffeine poisoning and lactate rise: an overlooked toxic effect? Acta Anaesthesiol Scand. 2008 Aug;52(7):1012-4. Epub 2008 May 20.
5. Wrenn KD, Oschner I. Rhabdomyolysis induced by a caffeine overdose. Ann Emerg Med. 1989 Jan;18(1):94-7.
6. Holstege CP et al. Massive caffeine overdose requiring vasopressin infusion and hemodialysis. J Toxicol Clin Toxicol. 2003;41(7):1003-7.

Of interest, I did stumble across this great rant whilst doing some reading….

The Case.

A 46 year old restrained passenger in a high-speed MVA rolls into the resus bay. She is intubated & sedated [easily ventilated & oxygenated, no evidence of chest trauma], persistently tachycardic @ 160/min with a systolic BP of 90mmHg & has a very postive FAST exam….

She spends less than 15 minutes in your ED (extra IV access, blood transfusion continued, limbs splinted) before heading for a trauma laparotomy. She has a liver laceration (repaired) and capsular haematoma, complete bladder rupture (repaired) and splenic haematoma (managed conservatively). Post-op she goes via radiology for a ‘pan-scan’….

Her post-operative ICU stay is a rocky one, marked by ongoing transfusion, coagulopathy and persistent tachycardia (still around 160 beats per minute). Some 6 hours later with her haemoglobin & INR stable, she remained tachycardic at 150-60 (still sinus) & has developed a temperature of 38.6*C.

What are your thoughts ??

Some clever-duck in the ICU ordered the following which seemed to put it all in perspective…

The causes for thyrotoxicosis include…

• Graves Disease (toxic diffuse goiter)
• Toxic Multinodular Goiter
• Toxic Adenoma (single hot nodule)
• Factitious Thyrotoxicosis (too much thyroxine…)
• Thyroiditis (Hashimoto’s, de Quervain’s, post-partum, amiodarone-induced)
• Iodine-induced hyperthyroidism (amiodarone & contrast-media)
• Metastatic Follicular Thyroid Carcinoma
• TSH-producing tumours

In the case of our patient it was assumed to be…..

post-contrast thyrotoxicosis.

Iodine-induced thyrotoxicosis was first described when iodine supplementation was introduced to areas of endemic iodine deficiency. In the First World, it is most commonly iatrogenic following administration of intravenous contrast as well as amiodarone (which contains up to 75mg of iodine per 200mg tablet). [Note, the recommended daily intake of iodine is approximately 150 micrograms.]

Contrast Media & the Normal Thyroid.
Within 21 days of a large dose of contrast medium, normal subjects have no change in total T4 & a small decrease in free T4 & T3. There is also a small decrease (followed by rapid increase) in TSH, but it remains within normal limits.

Iodine-induced thyrotoxicosis is not a single aetiological entity and may occur in patients with a variety of underlying thyroid disorders (especially Grave’s & Multinodular Goiter, ie. a person with pre-existing autonomous thyroid tissue; not under the control of TSH). Those who are elderly, or live in an area of dietary iodine deficiency are more at risk.

There is little literature on the risk of iodine-induced hyperthyroidism, however one study of 788 patients (followed up post coronary angiography) demonstrated that only 3 showed features on hyperthyroidism at followup (< 0.3%).

There is one set of guidelines that I have discovered that I think would be helpful for patients we scan & discharge from the ED.

• Do not give contrast media to patients with manifestations of hyperthyroidism.
• Patients at risk (Grave’s, MNG etc) should have close follow-up (GP or Endocrinologist) & repeat TFTs following a contrast injection.
• Be cautious in performing contrast-CTs in patients undergoing therapy with radioactive iodine.
• Prophylaxis is unnecessary. 

The Outcome.

Our patient is commenced on an esmolol infusion & neomercazole. She had multiple further trips to the OT for ongoing repairs (pelvis stabilisation, femur #), & she has a total thyroidectomy a week following her accident.

References.

1. Kulstad CE, Carlson A. Contrast-induced thyrotoxicosis. Ann Emerg Med. 2004 Sep;44(3):281-2.
2. Pasimeni G et al. Refractory thyrotoxicosis induced by iodinated contrast agents treated with therapeutic plasma exchange. A case report. J Clin Apher. 2008;23(2):92-5.
3. van der Molen AJ et al. Effect of iodinated contrast media on thyroid function in adults. Eur Radiol. 2004 May;14(5):902-7. Epub 2004 Feb 28.
4. Hintze G et al. Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects. Eur J Endocrinol. 1999 Mar;140(3):264-7.
5. Beckers EA, Strack van Schijndel RJ, Weijmer MC. A contrast crisis. Lancet. 2000; 356:908.
6. Rosenʼs Emergency Medicine. Concepts and Clinical Approach. 7th Edition

Recently, a colleague of mine was wanting to perform a diagnostic tap on a patient with cough, fever and a CXR suggesting a left sided pleural effusion….

I was asked to perform a bedside USS to mark out the safest place to perform the pleural aspirate.

I percussed the chest to the dullest point and then slapped the ultrasound on (left posterior chest wall, longitudinal plane, just below tip of scapula).
This is what I saw…

Needless to say the needle was re-sheathed and the procedure aborted. I am convinced that if we were going by x-ray and clinical examination alone we would have created more problems for this guy.

What made a difference….

1. Turner JP, Dankoff J. Thoracic ultrasound. Emerg Med Clin North Am. 2012 May;30(2):451-73.
2. Ultrasound Podcast Episode 31 (Pneumothorax & Pleural Effusion) & Episode 32 (Pneumonia & ARDS)
3. Sonocloud

The Case.

An 11 year old boy is bought to ED by his mother on a busy weekday evening. Mum reports that he has been ‘a little bit off’ over the past 24 hours, in particular he’s not keeping down his food or fluids. She is also worried about his colour, stating ‘he looks a little pale and sweaty’.

You find him a little wheezy on auscultation, with room air saturations of 93%. Of concern is his pulse rate of greater than 150 per minute.

This is his ECG…

What’s your interpretation ?
What would you do next ??

For extra info, here’s his CXR.

My Interpretation:

Rate: 166 / min.
Rhythm: Sinus (p waves present)
Axis:
* Abnormal P-wave axis (negative in II, III, aVF + positive aVR & V1) ?retrograde P-waves
* QRS Axis – normal.
PR short ~80msec. Narrow complex QRS ~80-90msec. QTc ~ 440msec
LVH by voltage.
?delta waves (I, II, aVL)

DDx.

? Sinus tachycardia (with ectopic atrial pacemaker)
? Junctional tachycardia with retrograde atrial activation
?? Re-entry pathology (short PR)

The Case.

A sunny Saturday morning in Sydney and your 56 year old patient was just outside doing some gardening when they feel a rather sharp bite on their right hand (on webspace between thumb and index finger).

He arrives to the ED distressed and very anxious. His vitals signs are normal and he has localised pain only.

He then hands you this saying “this is the bugger that bit me !!”  …..

Where do you go from here ??

BIG BLACK SPIDER

A niche post for my East-Coast Australian colleagues….

In Australia, spiders are incredibly common & their bites occur more frequently than snakebites. Luckily for us, spider-bites are usually trivial and require no treatment. There are however two groups of spiders that can cause significant envenomation;

1. Red Back Spiders
2. Funnel Web Spiders

A Funnel Web Spider     
A Red Back Spider        

Funnel Web Spiders are arguably the most deadly spiders worldwide, but are confined to the eastern coast of Australia. Creating a diagnostic dilemma is the fact that the potentially lethal Funnel-Web looks very similar to other ‘big black spiders’  that can inhabit the same area. These include trap-door spiders and mouse-spiders.

The following decision algorithm was created to help differentiate between these spiders, classifying them into three groups; 1. big black spiders (which includes the Funnel-Web) 2. Red Back Spiders and 3. all others (which are generally unlikely to cause significant effects).

**taken from NSW Health Guideline / adapted from Isbister & Sibbritt 2004 **

Clinical Features.

The bite is usually witnessed and very painful. Fang marks are often visible.

The Funnel Web produces a venom that contains potent neurotoxins which prevent inactivation of sodium-channels and lead to a massive increase in autonomic activity and neuromuscular excitation.

Systemic envenomation develops rapidly (30-120 mins) and features include:

• General (agitation, irritability, vomiting, headache and abdominal pain. Decrease LOC & coma can occur)
• Autonomic (Sweating, piloerection, lacrimation, salivation)
• CVS (Tachycardia, hypertension [alternatively hypotension & bradycardia can occur], pulmonary oedema.
• Neurological (muscle fasciculation [esp. tongue], oral tingling, muscle spasm & coma).

Consider the diagnosis in a young child who presents with sudden severe illness with inconsolable crying, salivation, vomiting & collapse.

It is important to note that other BBS’s do not cause significant CVS, autonomic and neurological features. An important DDx is that of Red Back envenomation, which is heralded by the triad of local pain, sweating & piloerection. Again, it does not cause coma, fascicultations or pulmonary oedema.

Evaluation & Management.

Prehospital / First Aid.

• Application of pressure immobilisation bandage

Hospital (General).

• Do not remove first aid until ready to treat
• Allocation to acute/resuscitation area capable of cardiorespiratory monitoring
  • Monitor closely, IV access (x2)
  • Bloods (FBC, Electrolytes, renal function, CK, Coags)
• Preparation for management of respiratory failure, hyper or hypotension, pulmonary oedema & coma.
• Relevant History:
  • Was spider seen? (description of spider)
  • ?multiple bites
  • Where (geographic place) and when (elapsed time)?
  • Timing of first aid
  • Details of symptoms
• There is no venom detection available for spider-bites.

Hospital (Specific).

• If there are any symptoms of systemic envenomation, give 2 vials of CSL Funnel Web Spider Antivenom IV.
• In severe envenomation with dyspnoea, APO or altered LOC, give 4 vials of CSL Funnel Web Spider Antivenom IV
• In cardiac arrest administration of undiluted antivenom via rapid IV push may be life saving (at least 4 vials should be given).
• Be prepared to give more !! 8 vials is a common dose.

Antivenom Therapy.

• Two vials is minimal dose
• Children require the same dose as adults.
• Further doses are often required and should be given until all significant symptoms and signs have resolved.
• TWO IV lines are recommended (one for antivenom, one for potential anaphylaxis treatment).
• No premedication is required.
• Start infusion very slowly & observe for reaction (aim to have dose in within 15-20mins).

The majority of cases will be less obvious, and the patient is well with no apparent envenomation. The following flow chart (taken from the NSW Health’s Snakebite  & Spiderbite Clinical Management Guidelines) demonstrates a guide to observing and evaluating the various presentations of big black spider bites !

An envenomed patient treated with antivenom can be discharged at 12 hours if clinically well, however its best to not discharge them at night.

Essentially, if the patient is asymptomatic and has no clinical evidence of envenoming, then observe them for a minimum of 6 hours after the removal of first aid.

This is exactly what happened to our avid weekend gardener. He went home at the 6 hour mark (via the store to buy some thick gardening gloves).

References.

1. Snakebite & Spiderbite Clinical Management Guidelines 2007 – NSW Health 
2. Isbister GK, Sibbritt D. Developing a decision tree algorithm for the diagnosis of suspected spider bites. Emerg Med Australas. 2004 Apr;16(2):161-6.
3. Isbister GK, Fan HW. Spider bite. Lancet. 2011 Dec 10;378(9808):2039-47. Epub 2011 Jul 15.
4. Isbister GK et al. Funnel-web spider bite: a systematic review of recorded clinical cases. Med J Aust. 2005 Apr 18;182(8):407-11.
5. Murray L, Daly F, Little M & Cadogan M. Toxicology Handbook. 2nd Edition. Elsevier 2011.
6. http://www.thepoisonreview.com/2010/01/22/killer-funnel-web-spiders-invade-sydney/