Category Archives: Emergency medicine

Legal Highs

Legal highs now illegal! 

=“New psychoactive substances” – no penalty for possession. Generally multiple substances taken simultaneously. Previously sold as herbal incense or “bath salts”. Now online “party pills” etc. Packaging can remain the same but product changed. Mostly from China. 

Drug deaths in Scotland 3x higher than in UK as a whole, and higher than any other EU country. Since NPS are unidentifiable and typically multiple substances taken, it is hard to attribute specific deaths. 72% male. Synthetic Cannabinoids, cathinones (stimulant), phenethylamines (hallucinogenic), benzodiazepines. Can be smoked or ingested.

Toxbase has nicknames, but examples are Black mamba, Exodus, Damnation. 

Cannabinoids can cause tachycardia, long QT and hypokalaemia. For agitation avoid medication if possible else midazolam. Generally 6 hour effect. 

Cathinones snorted or injected as well. Euphoria, intense positive emotion. Dyspnoea, palpitations. Narrow complex arrhythmia. Trismus. Acidosis. Hyperpyrexia. Effects up to 24 hours. Check CK, coagulation, LFTs. 

To treat acidosis, treat everything else! Then phone Toxbase!

Phenylethylamines stimulant as above plus hallucinations. Coronary ischaemia, organ failure. 

Synthetic benzodiazepines tend to have pseudoscientific names. Flumazenil not used as risk of other drugs emerging to cause seizures etc. 

See Serotonin toxicity syndrome for hyperpyrexia, increased muscular activity, autonomic instability.

Meningococcal disease

Gram negative diplococci, causing meningitis and septicaemia. Sometimes bone/joint infection. Neisseria (not meningitidis) responsible for ophthalmia neonatorum.

Main serogroups:

  • A – responsible for epidemics of meningitis across “Meningitis belt” of Sub-Saharan Africa, until Men A monovalent vaccine introduced in 2010 (still epidemics, but due to other serotypes). Hajj also triggers outbreaks.
  • B – 4 component vaccine introduced in 2015 to deal with B being the most common cause of invasive meningococcal disease since introduction of MenC vaccine. Based on vaccine developed for New Zealand epidemic.
  • C – used to be most common cause of invasive meningococcal disease in UK until vaccine introduced. So successful that early dose was dropped from routine schedule, although later resurgence in older children and young people, so teenage booster and university catch up programme introduced.

Clinically, notorious for rapidly evolving, often fatal septicaemia with non blanching rash and limb ischaemia. Curiously, meningococcal meningitis, on the other hand, is the most benign of the various causes of bacterial meningitis. Can be mixed picture, ranging from a few petechial spots only with an otherwise typical meningitis presentation, or else meningococcal septicaemia with neck stiffness, where presence of meningitis is actually a good prognostic sign.

Exquisitely sensitive to antibiotics. Meningitis epidemics in Africa treated with single IM dose ceftriaxone!!! Nasal carriage is the reason for spread, so prophylaxis for close contacts important.

BTS/SIGN/NICE Asthma guidance

Latest revision 2025. See also asthma.

Diagnosis is about probability – high probability is recurrent episodes of cough, wheeze, breathlessness, chest tightness plus documented wheeze, atopic history, documented variable PEF or FEV1. Isolated episodic cough is not sufficient. Episodes typically triggered by viral infections, cold air, exertion, laughter or emotion. Start treatment, “typically” 6 weeks inhaled corticosteroids (ICS). If good response to treatment, then diagnosis is confirmed.

Diagnostic algorithm for asthma

If intermediate probability then spirometry with reversibility is preferred initial test for children old enough to do it (Grade D recommendation). If spirometry normal, then do challenge tests and/or Fractional exhaled nitric oxide (FeNO) measurement. For younger children, watchful waiting or trial of treatment [colour code suggests this is appropriate from age 1, but no advice given for under 1…].

FeNO has reasonable positive predictive value, but false positives in allergic rhinitis, rhinovirus and dietary nitrates, plus overlap in values between asthmatics and normal population (especially children).

Red flags –

  • Focal chest signs
  • Abnormal voice or cry
  • Failure to thrive
  • Vomiting
  • Wet/productive cough
  • Nasal polyps

Management

Self management education, written personalized plan. Assess control – consider using Asthma Control Test (ACT) questionnaire or similar.

Assess risk of future attacks. Co-morbid atopic conditions, younger age, obesity, and exposure to environmental tobacco smoke are markers of increased risk (some of these strongly socioeconomically linked, of course).

Ask specifically about medication use and assess prescriptions. Explore attitudes to medication as well as practical barriers to adherence.

Not for routine house dust mite avoidance measures. Avoid smoking and second hand smoke.

Weight loss (including dietary and exercise programmes) for overweight and obese. Breathing exercise programmes can be offered as an adjuvant to pharmacological treatment for adults.

Treatment

ICS are recommended preventer. An asthma attack in the previous 2 years, symptoms 3 days a week, or using reliever 3 days a week, or waking 1 night a week are indications. Give twice daily at least until good control established.

Start at dose appropriate for the severity of the disease. In mild to moderate asthma, no benefit in starting at high dose and weaning. In children, “reasonable” starting dose is Very Low (100mcg twice daily of Clenil or equivalent).

5yrs and over, if add-on is required then choice between inhaled long acting beta agonist (LABA) or leukotriene receptor antagonist (LTRA). Only then increase dose of ICS from very low (100mcg Clenil or equivalent twice daily) to low (200mcg twice daily).

For exercise induced symptoms, generally just a sign that inadequate control! But if otherwise well controlled then give inhaled short acting beta agonist immediately prior to exercise. Then choice between LRTA, LABA, cromoglicate or theophylline.

Acute Severe Asthma

Levels of acute asthma attacks in children
  • Sats under 92%
  • PEF 33-50% of best or predicted
  • Can’t complete sentences in one breath, or too breathless to feed
  • HR >140 (under 5), >125 (over 5)
  • RR>40 (under 5), >30 (over 5)

Life threatening defined as:

  • PEF <33%
  • Exhaustion, poor resp effort [tautology?]
  • Hypotension
  • Cyanosis
  • Silent chest
  • Confusion

Treat –

  • Oxygen
  • MDI plus spacer if mild/moderate
  • If refractory to beta agonist, add ipratropium 250mcg mixed into beta agonist [same dose for everyone]
  • “Consider adding 150mg magnesium sulphate to each neb in first hour if symptoms started <6hrs and presenting with sats <92%” = 0.3ml of 50% MgSO4
  • Give oral steroids early, dose by age.

Second line treatment –

  • Consider single IV bolus of salbutamol (15mcg/kg over 10mins). For bolus dilute to 50mcg/ml with saline/glucose. For infusion, dilute to 200mcg/ml
  • Consider aminophylline for severe asthma unresponsive to maximal doses of bronchodilators and steroids. Loading dose slow injection over 20 mins! Then dilute to 1mg/ml with saline
  • Consider IV MgSO4 40mg/kg over 20 mins – dilute to 10% in saline or glucose.

Systematic review of IV Magnesium in children (2018) – pulmonary function improved, hospitalization and further treatment decreased. MAGNETIC trial of Magnesium nebs did not show a clinically significant improvement in mean asthma severity scores in children with acute severe asthma. But better Asthma Severity Score at 1 hour where saturations <92% at presentation and those with preceding symptoms lasting less than 6 hours [Lancet 2013]. 2022 Metanalysis found no benefit but varying protocols and populations.

Seizures

Seizures, fits, funny turns, convulsions, attacks…  None of these really has a medical meaning.  Convulsion suggests rhythmic motor activity, but that’s about it.  The implication of most of these is that there is excessive abnormal, involuntary muscle contraction, usually bilateral.  But more broadly, some involuntary, usually sudden and self terminating episode of abnormal (or at least non-purposeful) activity and/or impaired awareness. Can be sustained or interrupted.

Nottingham RCPCH approved guideline distinguishes:

  • Febrile?
  • Already on anti-epileptic medication?  Consider checking levels, or at least storing sample.
  • Predisposing conditions? eg neurodevelopmental problem, brain injury/surgery.
  • Neonate or young infant? Some additional possibilities eg hypoxic ischaemic encephalopathy (HIE), Fifth day fits, drug withdrawal (neonatal abstinence syndrome), pyridoxine dependent epilepsy.

Most commonly Febrile convulsions ie age related, benign.  Beware complex (multiple seizures in same illness, focal features, prolonged >15 mins) and any abnormal findings eg neck stiffness, bulging fontanelle, prolonged illness, abnormal cognition before/after.

Important differentials are:

  • meningitis
  • encephalitis
  • shaken baby (non-accidental injury)
  • brain tumour/haemorrhage, hydrocephalus
  • ingestion (deliberate or accidental)
  • metabolic (low glucose, calcium/magnesium, low/high sodium)

May represent first evidence of epilepsy.

Accidental Adrenaline self-injection

eg with Epipen or Emerade.

Causes vasoconstriction with potential for gangrene.

Try:

  • warm water immersion
  • local nitroglycerin paste
  • subcut infiltration with a mixture of 1.5mg of phentolamine, 1mL of 2% lidocaine (at site and along course of digital arteries)

[advised by National Poisons Information Service]

n=365 adrenaline injections to hand, 213 to digit.  No cases with clinically apparent systemic effects, only a few patients had ischemia. No patient was admitted or had surgery. [Annals of Emergency Medicine. 56(3):270-4, 2010 Sep. PMID: 20346537]

Paediatric Sepsis 6

Consider sepsis or septic shock if a child has a suspected or proven infection and has at least 2 of the following:

  • Core temperature <36°C or >38.5°C
  • Inappropriate tachycardia (according to local criteria or advanced paediatric life support guidance)
  • Altered mental state (e.g., sleepiness, irritability, lethargy, floppiness, decreased conscious level)
  • Reduced peripheral perfusion or prolonged capillary refill.

If in doubt, seek an experienced opinion!

Within 1 hour of presentation, sepsis should be treated with:

  • Supplemental oxygen
  • IV (or IO) access – within 5 minutes of presentation – and blood tests including blood cultures, blood glucose,  and blood gas.
    • FBC, serum lactate, and CRP should also be ordered for baseline assessment.
    • Low blood glucose should be treated
  • IV or IO antibiotics should be given with broad-spectrum cover as per local policies.
  • Fluid resuscitation should be considered – aim to restore normal circulating volume and physiological parameters. Isotonic fluid (20 mL/kg) should be titrated over 5 minutes and repeated as necessary.
    • Beware fluid overload – look for crepitations and hepatomegaly.
  • Experienced senior clinicians or specialists should be involved and consulted early.
  • Inotropes should be considered early if normal physiological parameters are not restored after giving ≥40 mL/kg of fluids. It is important to note that adrenaline (epinephrine) or dopamine may be given via peripheral IV or IO access.

UK Sepsis Trust have Red Flag screening & action tool –

Start Sepsis6 pathway if ONE red flag:

  • objective change in behaviour or mental state
  • Unrousable or won’t stay awake
  • Looks very ill to HCP
  • Sats under 90% or new need for oxygen
  • Severe tachypnoea
  • Severe tachycardia
  • Bradycardia
  • Not passed urine in last 18h
  • Mottled, ashen or blue skin, lips or tongue
  • Non-blanching rash

Otherwise, any amber flags:

  • Behaving abnormally, not wanting to play
  • Significantly decreased activity/parental concern
  • Sats under 90^% or moderate tachypnoea
  • Moderate tachycardia
  • CRT >=3secs
  • Reduced urine output
  • leg pain
  • Cold feet/hands
  • Immunocompromise

If 2 then do bloods, consider if just 1.  Review by ST4 within 1 hour.

If lactate >2 then start Sepsis6

Diabetic Ketoacidosis

DKA – BSPED guidance 2021.

The potentially serious acute complication of diabetes.  In the absence of adequate insulin, glucose levels start to rise in the blood, spilling over the threshold for kidney resorption and causing a diuresis.  Metabolism switches to ketone bodies, causing acidosis.

Presents with weight loss, tiredness, vomiting, heavy breathing (Kussmaul), reduced consciousness.  Diabetes symptoms of course, if first presentation, which might just be new wetting, or unusually heavy nappies.  Can be confused with pneumonia, or appendicitis! Often missed diagnosis.  In 2020 Lanarkshire audit, half had seen GPs at least once before diagnosis, with many having had bloods done rather than BM, or being asked to hand in urine the next day… 40% had BM done by family member!

Traditionally 15-17% of new presentations of diabetes are DKA, but with pandemic went up to 66%

ISPAD def DKA = Bicarbonate pH under 7.3 (H+50) PLUS ketones 3+ (blood or urine).

Beware can develop with normal glucose levels IN THOSE TAKING INSULIN.  Suspect if blood ketones above 3 in known diabetic, refer to hospital.  Between 0.5 and 3, follow sick day rules.

Mild (over 7.2 or 63) vs moderate (7.1-7.2 or 79) vs severe (79+) categories.  Treat as 5 vs 7 vs 10% dehydrated respectively.

All get 10ml/kg over 30 mins (assuming you start IV fluids) unless shocked (10/kg over 15 mins, repeat up to 40 then inotropes).

Maintenance fluids (0.9% NaCl with 20mmol KCl per 500ml bag) as per traditional formula (Holliday-Segar method) – 100ml/kg/d for under 10kg; 50ml/kg/d additionally for each kilo between 10-20kg; 20ml/kg/d for each kilo above that.

  • Calculate deficit as above. Subtract initial 10/kg bolus (but not shock boluses) and correct over 48hrs
  • ONLINE CALCULATOR (dka-calculator.co.uk) comes with disclaimer, gives fluid calculations but then prints out 16 pages which you don’t need! [KB]
  • Note SCOTSTAR has separate DKASupportDocument for those likely to need transfer

See graphic in BMJ 2016.

Complications

If acidosis not correcting, check cannula, check fluid calculations, consider sepsis.  Replace insulin syringe! Acidosis can also be caused by hyperchloraemia (hence Plasmalyte preferred at RHC – less chloride).

Risk of thromboembolism due to dehydration and immobility during recovery.

Cerebral oedema

25% mortality from cerebral oedema, 34% long term neurodisability.  Headache, irritability, agitation.  Posturing, focal neurology eg eye movements, pupil asymmetry.  Cushings triad – bradycardia, hypertension, breathing irregularity.

Hypertonic saline (2.7 or 3%, 2.5-5ml/kg over 10-15 mins) or mannitol (20%, 0.5-1g/kg over 15 mins), no preference.  

Switching

Stay on DKA pathway (and not transfer to subcutaneous insulin) until:

  • The patient has been reviewed by a Consultant, or paediatric diabetes team medical staff and
  • The patient has no evidence of dehydration has no nausea or vomiting for 6 hours, and
  • Has blood glucose less than 10mmol/l, and
  • The blood ketones have fallen below 0.9mmol/l

Cerebral oedema

Cytotoxic vs vasogenic (resistant to steroids) vs interstitial (obstruction eg meningitis – not steroids, ?osmotic) vs osmotic (CSF, ECF low osmo) vs hypertensive.

In DKA, there is a 25% mortality from cerebral oedema, 34% long term neurodisability. 

Presents with headache, irritability, agitation (which can be difficult when child is unwell with something else).  Then altered consciousness, posturing, focal neurology (check eye movements, pupils).  Classically Cushing’s triad: hypertension, bradycardia, irregular breathing pattern.

Clinical diagnosis really.  CT can show (better than MRI!).

Hypertonic saline (2.7 or 3%, 2.5-5ml/kg over 10-15 mins) or mannitol (20%, 0.5-1g/kg over 15 mins), some people prefer hypertonic saline but whatever is closest to hand!  Frusemide adjunctive.   

Consider Aciclovir if diagnosis unclear (in case herpes encephalitis – CT not great, LP can be non specific).

Brain protection = 30deg head up, midline position. Avoid hypotension. Avoid hypocapnia (intubate and ventilate if in doubt).

Hyponatraemia common – typically due to SIADH but treat any underlying cause, esp hypovolaemia.

Sudden Unexpected Death in Infancy (SUDI)

Or Cot death?  Or SIDS (Sudden infant death syndrome)?

It is well recognised that some babies go to sleep apparently healthy, and then don’t wake up in the morning.  Even after a full post mortem (PM) investigation, no cause is found.  This unexplained phenomenon however has some very well recognised features eg age 2-6 months, prematurity, maternal smoking, poor socio-economic conditions, prone sleeping.

SUDI was originally defined by CESDI (Confidential Enquiry into Stillbirths and Deaths in Infancy) as death between 7 and 365 days where unexpected and unexplained at autopsy, during an acute illness that was not recognised as life-threatening, due to an acute illness of less than 24 h duration in a previously healthy infant (or death after this if life had only been prolonged by intensive medical care); definition also includes deaths from a pre-existing occult condition, and deaths from any form of accident, trauma or poisoning.

I find SUDI most useful for describing the initial situation one may find oneself in, particularly from the point of view of bereavement, need for medical and police investigation.  Interestingly, many of the same risk factors pertain to both deaths unexplained (ie SIDS, or strict SUDI) and to accidental deaths (with the exception of prone sleeping).

SIDS is the ICD recognized term, so is what is generally put on a death certificate.  However pathologists vary in their use of the terminology, some will use “Unascertained” to mean SIDS, others will use SIDS but reserve Unascertained for cases where there are additional factors that somehow cast doubt on the diagnosis.

Similarly, overlying (smothering) as a cause of SUDI is often inferred from the history, but may be specified on the death certificate to differentiate from SIDS.

PM finds a cause in about a 1/3 of cases) eg

  • Infection
  • Cardiomyopathy, anomalies of coronaries
  • Ion channelopathies
  • Metabolic disorders eg MCAD

See also Prevention, and Sudden unexpected postnatal collapse.