Adult Emergency Medicine: February 2015

Thursday 26 February 2015

FAST

I think I make FAST scanning more complicated than it needs to be. Four views - lungs are in eFAST, not FAST...although CEM has them on their checklist.

RUQ - Pouch of Rutherford-Morrison

- Start just anterior to the mid-axillary line, angled slightly backwards.
- Slide the probe towards the head to get a view of the diaphragm
- Look for pleural fluid - a jet black triange just above the diaphragm
- Ask the patient to take a deep breath if possible, particularly if rib shadows obscure the area of interest.

LUQ - Spleno-renal angle
- Posterior-axillary line at about the 6th to 9th intercostal space
- To get rid of rib shadows, and to get a better view of the spleen, slide the probe towarsd the hed and rotate it very slightly clockwise, producing an intercostal oblique view, so that the spleen (not the kidney) is seen.

Pelvic - Pouch of Douglas in females, rectovesical pouch in male
Fluid will collect here.
Place the probe on the pubic bone and note a bone shadow. Slide slightly towards the head to get a good longitudinal pelvic view.
Full bladder will be triangular in shape.
In a female, the body of the uterus sits in the intraperitoneal space just posterior to the bladder (Figure 19), so free fluid will be seen just posterior to the uterus. This space is often called the pouch of Douglas and sometimes just small amounts can be detected

Cardiac
Subxiphoid view - probe laid almost flat and angled towards the head. Apply probe pressure to indent the epigastrium

Pitfalls
Perinephric fat, especially in obese patients, may be misinterpreted as intraperitoneal free fluid. Consider comparison views between each kidney.
Free fluid isn’t always blood; consider ascites, fluid related to a ruptured ovarian cyst, ruptured bladder or peritoneal dialysis.

90% sensitive and 99% specific for traumatic haemoperitoneum

References
Emergency Ultrasound Made Easy
http://www.trauma.org/index.php/main/article/214/
http://www.sonoguide.com/FAST.html
CEM Website

Monday 16 February 2015

Carbon Monoxide

I thought I knew about Carbon Monoxide poisoning, and then I went to an (R)CEM day - and learnt a whole lot more about it.

Numbers
4,000 attend ED with CO
200 hospitalised

50 die each year

Pathophysiology

CO binds to haemoglobin with an affinity of approximately 220 times that of oxygen. CO shifts the oxygen dissociation curve to the left. It also binds to myoglobin and mitochondrial cytochrome oxidase, impairing ATP production. Somehow it also binds to platelets so that nitric oxide gets released.

CO binds to fetal haemoglobin and shifts the already left-shifted fetal oxyhaemoglobin dissociation curve further to the left. The half-life of CO in the fetus is longer than in the Mum.

CO is produced continuously in the body as a by-product of haem breakdown. This leads to a normal baseline COHb concentration of about 0.5%. In pregnancy and haemolytic anaemias this can rise towards 5%.

Animal research – dogs given COHb 65-70%. They died.

2/3 of blood removed, and replaced with already poisoned blood - they were fine. They were then injected with CO, and were also fine.

- Cigarette smoking leads to COHb concentrations of up to about 12% in heavy smokers

Non-smokers living away from urban areas have carboxyhaemoglobin concentrations of between 0.4% and 1.0%.

In an urban or industrial setting, concentrations of up to 5% may be considered normal.

- Methylene chloride (dichloromethane), which is found in some paint strippers and sprays. Once in the liver, is converted to carbon monoxide. Methylene chloride is stored in body tissues and released gradually.

- Electric fires, fires, wood burning stoves, barbeques, shesha pipes gas - anything.

Clinical Presentation

With prolonged exposure her symptoms could lead to hypotension, seizures, cerebral oedema, metabolic acidosis and respiratory failure.

4.3% of 1758 patients presenting to 4 EDs had raised COHb levels

Unsuspected positive cases 3.5%:

COPD 7.5%

Headache 6.3%

Flu-like 4.3%

Chest pain 3.3%

Seizures 2.1%

More Severe Symptoms:

The appearance of intoxication or a personality change

Impaired mini mental-state examination

Vertigo and ataxia

Breathlessness and tachycardia

Chest pain (due to angina or myocardial infarction)

Loss of consciousness

Seizure or multiple seizures

Abnormal neurological signs including blindness, deafness, and extrapyramidal effects.

High risk features include chest pain, history of unconsciousness, any continuing neurological symptoms or signs (especially cerebellar features) and pregnancy due to the effects on the foetus

Chronic Presentation

Chronic fatigue

Emotional distress

Memory deficits

Difficulty concentrating

Sleep disturbances

Vertigo

Neuropathy

Paraesthesias

Recurrent infection

Polycythaemia

Abdominal pain

Diarrhoea

Clinical Assessment

Neuro exam: including tests of coordination and balance, MMSE, short term memory for chronic.

Cherry red skin is only seen in severe poisoning, with levels >20.

Investigations

CO reading taken from a breath analyzer - lactose intolerant patients have raised H2 in their expired breath which can interfere with the readings.

Venous blood should be taken into anti-coagulant and sent to the laboratory.

Treatment

Administration of oxygen speeds the elimination of CO from the body. Without therapy, the elimination half life of CO is 4-6 hours. Administration of high flow oxygen by a tight fitting mask at normal atmospheric pressure reduces half life to approximately 76 mins.

Get your NIV out – you just need the seal and the flow rates of O2 high enough to maintain 100% oxygen. Even manually holding a BVM over them with a good seal does the job.

There is debate about the added value provided by hyperbaric oxygen. A COHb concentration of >20% should be an indication to consider hyperbaric oxygen especially if has any other symptoms:

Loss of consciousness at any stage

Neurological signs other than headache

Myocardial ischaemia/arrhythmia diagnosed by ECG

The patient is pregnant

If metabolic acidosis persists despite correction of hypoxia and adequate fluid resuscitation consider correction with intravenous sodium bicarbonate.

I wrote a powerpoint presentation on this - ages ago - feel free to use and adjust...

References

http://www.enlightenme.org/the-curriculum-zone/node/11057

http://www.enlightenme.org/learning-zone/its-been-gas

http://www.enlightenme.org/learning-zone/heating-it%E2%80%99s-not-just-bills-giving-you-headache%E2%80%A6

http://learning.bmj.com/learning/module-intro/acute-carbon-monoxide-poisoning-diagnosis-management.html?moduleId=10011945&searchTerm=%E2%80%9Ccarbon%20monoxide%E2%80%9D&page=1&locale=en_GB

http://emergencymedicineireland.com/2012/10/smoke-without-fire/?ut

Toxbase

Tuesday 10 February 2015

Cyanide

There was a chemical incident declared once because the pre-hospital team could smell almonds- they thought cyanide could be involved. Turns out someone had been baking...

Cyanide is released by the incomplete combustion of nitrogen-containing materials, and metabolised from amygdalin. Amygdalin can be found in the pits of many fruits, such as apricots and papayas and raw nuts.

Cyanide is a colourless gas with a bitter almond smell, detectable by only 40% of people.

http://www.christem.com/storage/cyanide%20mechanism

CN blocks cellular respiration by blocking the cytochromes. Affected cells convert to anaerobic metabolism, and a lactic acidosis results. The CNS and the heart are most sensitive.

Symptoms

#fcem #toxicology #FOAMed #revision Features of cyanide toxicity. pic.twitter.com/1UYxjDrIPI
— Kirsty Challen (@KirstyChallen) July 15, 2014

Symptoms after exposure to high vapor concentrations may include the following:
Transient hyperpnea and hypertension 15 seconds after inhalation
Loss of consciousness in 30 seconds
Respiratory arrest in 3-5 minutes
Bradycardia, hypotension, and cardiac arrest within 5-8 minutes of exposure

Symptoms after exposure to lower vapor concentrations or after ingestion or liquid exposure may include the following:
Feelings of apprehension or anxiety
Vertigo
Nausea, with or without vomiting
Muscular trembling
Loss of consciousness
Headache
Dyspnea

Patients exposed to cyanogen chloride experience severe eye and mucous membrane irritation.Low-dose exposure results in rhinorrhea, bronchorrhea, and lacrimation. Inhalational exposure results in dyspnea, cough, and chest discomfort. Onset of symptoms after exposure to nitriles (acetonitrile and/or propionitrile) may be significantly delayed.

Physical findings of cyanide exposure are generally nonspecific. They classically have cherry red skin.

Laboratory Investigations
- Normal arterial oxygen tension, high venous oxygen tension = decreased AV difference (<10%)
- High anion gap metabolic acidosis
- Raised lactate

Antidotes

#REBELReview 67 Cyanide Toxicity Treatment http://t.co/Fo3oz5PIN2 #FOAMed #FOAMtox #MedEd #ABIM #EMBoardReview #USMLE pic.twitter.com/j6FlhcmlKs
— Salim R. Rezaie (@srrezaie) June 1, 2014

To accompany episode # 1.. a fabulous #FOAMed visual representation of the mech of action of cyanide antidotes http://t.co/RxRCsTmnci
— FOAMcast (@FOAMpodcast) May 24, 2014

Minimal symptoms that resolve spontaneously need observation only.

Other Factors
- Oxygen
- Consider sodium bicarbonate if severe lactic acidosis
- Treat haemodynamic instability and cerebral oedema

@Lmellick video on smoke inhalation injury https://t.co/SbhSGXZWZX #FOAMed
— Jasmin Hamzic (@jasmin_hamzic) January 11, 2015

#EMSqoD A:Cyanide can be the toxic agent in smoke. http://t.co/r2Hu7eFs & http://t.co/Tt439mpi So use cyanokit, 50% increase in ROSC #FOAMed
— Dr. Howie Mell (@DrHowieMell) January 4, 2013

Cyanide poisoning: key facts #FOAMed #Toxicology #FCEM pic.twitter.com/LYGWeNf451
— Natalie May (@_NMay) July 9, 2013

References
http://blog.clinicalmonster.com/2015/02/em-ccm-carbon-monoxide-and-cyanide-poisoning/
https://umem.org/educational_pearls/2675/
http://www.enlightenme.org/knowledge-bank/cempaedia/industrial-chemical-incidents

Friday 6 February 2015

Inhalation

The CEM syllabus says knows the rarer causes of breathless-ness including "inhalational injury from chemical and physical irritants, foreign body inhalation". A search for that came up with cyanide poisoning and methaemoglobinaemia - so have written a bit about them too on further blog posts. I also think that carbon monoxide poisoning is important - blog post to follow.

History
The following key points should be taken in a focused history
Exactly what exposed to and how much (ie volume and concentration)?
What route?
What protective measures were taken?

What treatment was given?

PPE
Some chemicals do not cause secondary contamination e.g. chlorine.

Smoke Inhalation
- Monitor for 4-6 hours in the ED.
- Observe for longer if high risk items in their history:
History of closed-space exposure for longer than 10 minutes
Carbonaceous sputum production
Arterial PO2 less than 60 mm Hg
Metabolic acidosis
Carboxyhemoglobin levels above 15%
Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg
Bronchospasm
Odynophagia
Central facial burns
Pulmonary injury from smoke inhalation causes hyperinflation and atelectasis. Debris from cellular necrosis, inflammatory exudate, and shed epithelium combine with carbonaceous material to narrow airways that are already compromised by oedema. Reflex bronchoconstriction further worsens the obstruction.

Metals
Metal fume fever (MFF) is an acute disease induced by intense inhalation of metal oxides- mostly zinc. It is a self-limited syndrome characterized by fever, myalgias, headache, and nausea. Symptoms develop 4-12 hours after exposure and typically last several hours; severe cases generally resolve in 1-2 days. Observation is usually all that is necessary.

The exact pathology of MFF is not well understood but likely involves the deposition of fine metal particulates in the alveoli.