Welcome

I struggled to find PEM resources for my CT3 year, despite the variety of excellent resources out there. I hope this website will help point you in the right direction. I'm not a PEM expert, but am following the guidance CEM have issued (in the form of a syllabus) to put together this page. This page is not endorsed by CEM, and any mistakes are mine.

Please comment with corrections, additions and further suggestions.

All the information here is collected from the internet, and it might be out of date or inaccurate, so please use your judgement and adhere to your hospital's protocols. If you do notice any errors or omissions please comment so we can put them right!

To navigate, decide whether you want to start with a PMP or a PAP. You can then select which PMP or PAP you want to look at. You will then be taken to the summary page for that PMP, with links expanded topic collections. If you know what topic you want to look at already, click on the link on the right hand side.
Showing posts with label PMP6. Show all posts
Showing posts with label PMP6. Show all posts

Friday, 14 February 2014

Reduced Consciousness in Children

The unconscious child has some specific causes which we have looked at in more detail. There are also some more general causes, covered thoroughly on enlightenme. There are some specific guidelines from Nottingham that are universally accepted.


History
- Clues to dehydration
- Consanguinous relationship should be sought.

Specific Examination
- The child should be examined to look for physical clues which may suggest an underlying metabolic problem, such as dysmorphism, hypotonia, failure to thrive and enlarged liver.
- Look for herpetic lesions
- Paediatric GCS


Investigations
- Blood gas: pH, pCO2, bicarbonate and lactate may provide useful information in cases of shock, sepsis, trauma, respiratory distress, or suspected acid-base imbalance.
- If sepsis suspected: urinalysis, full blood count: haemoglobin, white cell count and differential, and platelet count; blood culture (meningococcal pcr depending on clinical presentation), CRP.
http://adc.bmj.com/content/93/2/183.1.extract
- Metabolic-specific cases: Venous/arterial blood gas, glucose, urinary ketones, LFTs, serum ammonia, U+Es (consider if BM <2.6mmol/L)
- Overdose cases: Plasma, serum and urine to be saved for later analysis of specific agents e.g. opiates, tricyclics

Management
ABCDE
Consider trial of naloxone


High ammonia levels (>200micromol/L) are neurotoxic. Lower levels with a sodium benzoate infusion.

If meningitis is suspected, treating with steroids (dexamethasone 0.15 mg/kg prior to first dose of antibiotics) reduces profound hearing loss if the causative agent is Haemophilus influenza type B (HIB) and less so in cases of meningococcal or streptococcal infection.

Herpes simplex encephalitis should be suspected in a child with a decreased consciousness and focal neurological signs, fluctuating consciousness, contact with herpetic lesions.

DKA in Children

DKA = hyperglycaemia (BG >11 mmol/l) pH < 7.3 bicarbonate < 15 mmol/l
Any two of the three are needed to make the diagnosis. 

There is minimal information on DKA just in children, but plenty of information about DKA in general. 10 children a year die from DKA.  There is an excellent module from the BMJ about type 1 diabetes in children, DKA vs HONK on BMJ, a case  and a doctors.net module.


The pathogenesis of DKA is nicely illustrated by the Calgary Guide DKA can happen at any age, in type 1 and type 2 diabetes. It happens when the pancreas doesn't produce any insulin, so the body starts burning fatty acids instead, producing ketones. It is rare in Type 2 diabetes. Euglycaemic DKA is a recognised feature, but quite rare.

There is no cause for DKA identified in 40% of cases. It may rarely be precipitated by sepsis, and fever is not part of DKA. DKA is most commonly caused by a lack of insulin - non compliance, un - diagnosed diabetes, or concurrent illness. The "sick day rules" are nicely summarized on DFTB.

The commonest age for diabetes diagnosis is children between 10 and 14. The number of babies being diagnosed is increasing. There is another peak at around 40.


Clinical Features
Polyuria, polydipsia. Abdominal pain, vomiting or drowsiness. 
In secondary enuresis (bedwetting in children who have been dry) always think ?DKA.
Associated with coeliac disease, thyroid disease and vitiligo.
Low CO2 levels seen on capnography can help diagnose DKA!

Investigations
- Blood gas
- U+Es
- Near patient ketones if available (superior to urine ketones)

- VBG to assess degree of acidosis
- As indicated - leucocytosis is common in DKA and does not necessarily indicate sepsis
- CXR, throat swab, blood culture, urinalysis, culture and sensitivity etc as indicated
- Elevated anion gap (to 25-35 mmol/L) - anion gap: Na+ - (Cl-+HCO3-) >15 mmol/L
- U+Es 2 hours after resuscitation begun, then 4 hourly

Treatment
Circulation:
- Assess degree of dehydration. There is an excellent calculator from BSPED that lets you put in the patient's weight, estimated dehydration, and fluid given already - then calculates remaining fluid needed.

- Fluid resuscitation only if clinically shocked to maximum of 30ml/kg
- Requirement = maintenance + deficit - fluid already given
- Deficit = % dehydration x body weight
- Use NaCl + 20mmol KCl in 500ml. If BM <14mmol/L add glucose to the fluid. (After 12 hours, if Na stable or increasing - change to 500ml bags of 0.45% saline/5% dex/ 20mmol KCl)

Insulin
- Insulin only after IV fluids have been running for at least an hour.
- Weight based insulin dosing at 0.1units/kg/hour- once you know the potassium as supplementation likely.
- Bicarbonate is rarely necessary but might help improve cardiac contractility in severe shock. Consider bicarb in profoundly acidotic children only.
- May continue normal long acting insulin (eg. glargine). Stop s/c insulin pumps.
- Phosphate levels are always low, but there is no evidence in adults or children that replacement has any clinical benefit and phosphate administration may lead to hypocalcaemia.


Cerebral Oedema
Complicates about 1% of cases of DKA in children and is lethal in 20% to 50% of victims

Signs and Symptoms
- Headache, irritability, slowing pulse, rising blood pressure, reducing conscious level
- Papilloedema is a late sign.

Management
Inform senior staff
- Exclude hypoglycaemia as a possible cause of any behaviour change
- Hypertonic (2.7%) saline (5mls/kg over 5-10 mins) or Mannitol 0.5 – 1.0 g/kg stat (= 2.5 - 5 ml/kg Mannitol 20% over 20 minutes).
- restrict IV fluids to 1/2 maintenance and replace deficit over 72 rather than 48 hours
- Move to PICU and discuss with senior staff



Tuesday, 11 February 2014

Febrile Seizures

Paediatric blue call for a twitching hot tot - you either love them, or hate them. As most of the time the child is pretty much back to normal by the time they arrive in the ED, it's easy to get a bit blaze about Febrile Convulsions or Febrile Seizures.


Febrile seizures: Seizure accompanied by a fever in the absence of inter-cranial infection due to bacterial meningitis or viral encephalitis.

They happen in 3% of children, between 6 months and 3- 5 years of age. The peak incidence is 18 months. Only 6-15% of seizures occur after 4 years. They are normally brief, with a 30-40% risk of a further attack.
10% increased risk if child has first degree relative with febrile seizures
A febrile seizure is more likely the younger the child, the shorter the duration, lower the temp at seizure and family history.  1-2% lifetime risk of epilepsy, same as all kids - complex focal have 4-12% risk

Presentation
- Short duration (<15minutes)
- Single seizure
- Brief post-ictal period
- Fever identified
- Prolonged seizure (5 - 10min) more likely to have a recurrence.

Investigations
Minimal evaluation needed
Urinalysis may be indicated - UTI common cause
Lumbar Puncture - only if child is not well looking, fully immunised, presenting with a simple febrile seizure. It
For complex seizure, consider bacterial meningitis as a cause - it can be difficult to clinically rule it out.

Management
As per departmental policy. Example from Manchester on the CEM website here.
If seizing, follow status epilepticus guidelines.
No evidence on duration of observation, although 24 hours has been suggested.

Advice
Normal seizure advice
Antipyretics do not prevent convulsions but may provide comfort. Diazepam also should not be used as prophylaxis.
 

Sunday, 26 January 2014

Hypoglycaemia in Children

As many of us treating children are first and foremost adult physicians, I suspect that hypoglycaemia in children is over treated. There are standard guidelines in EPLS and APLS - but these are generally associated with cardiac arrest rather than in isolation. Hospitals have produced their own guidelines, many of which are freely available on the intranet.

Hypoglycaemia = BM <2.6mmol/L

Signs and Symptoms
Autonomic features (warning signs):
    sweating, hunger, tingling around the mouth
    tremor, tachycardia, pallor, palpitations and anxiety.
    These warning signs may be lost in patients with repeated or prolonged hypoglycaemia.

Neurological features:
    Lethargy, tiredness, change in behaviour
    Headache, visual disturbance, slurred speech, dizziness.
    Altered level of conscious, coma, convulsions.

Causes of Hypoglycaemia
High sugar requirement
Excess insulin
Inborn errors of metabolism
Early manifestation of other serious disorders (sepsis, congenital heart disease, inter - cranial event).
Gastroenteritis  - (rare in children <5 so shouldn't be routinely analyzed at triage)
Ketotic hypoglycaemia - toddlers with lethargy or seizure following a prolonged fast. May be unresponsive in the morning.


Treatment
Bloods for analysis
Oral carbohydrate challenge - unless child too unwell for this. The BNF is fantastic at recommended non pharmacological treatments first. Don't give dextrogel/ glucogel - coke, lucozade, sugar cubes, jelly babies work a lot better. Most diabetics I know would do anything NOT to have glucogel as it tastes so disgusting! Even the BNF doesn't advise it!


Bolus of IV glucose:
      EPLS dose is 5-10ml/kg 10% dextrose and 2.5ml/kg in the newborn.
      APLS has changed to 2ml/kg.
If no IV access available, give IM glucagon   0.5mg < 8 years, 1mg >8 years
IV infusion of 10% dextrose at 6-8mg/kg/min) to maintain sugar >4mmol/L

Critical Blood samples 
Should only be taken during hypoglycaemia (BSL <2.6mmol/l)
  1. Glucose and lactate: fluoride oxalate tube
  2. Insulin, C-peptide, cortisol, growth hormone: plain tube on ice
  3. Ammonia: heparinized tube on ice
  4. Ketones and free fatty acids: fluoride oxalate (BLF) tube (1ml*)
    (Do also bedside test ketones)
  5. Amino acids, electrolytes: heparinised
  6. Acid-base: capillary sample
  7. Blood drops onto a Guthrie test card (for acyl-carnitine profile)
  8. Others if required e.g. Toxicology studies (Salicylates, ethanol, sulfonylurea )
  9. Urine for ketones, glucose, reducing substances, amino acids, organic acids and maybe toxicology. 
This is summarised on a lovely chart here:


And here's my summary card, lest I ever forget which tubes to fill! 
 

Seizures in Children


There's lots of information on seizures, and it can be hard to know the differences in management between children and adults. Most of the information says the same thing - just in different ways. There's a podcast from BMJ Learning and information from EMBasic. Nothing really covered generalised seizures in children, so I actually looked at a paper text book to get some information on seizures in children - the "Sunflower Book" as we called it at medical school! 


A seizure is defined as "a clinical event in which there is a sudden disturbance of neurological function caused by an abnormal or excessive neuronal discharge. Seizures may be epileptic or non-epileptic". 


There are lots of differential diagnoses for seizures, and a careful history will help you elucidate the true cause. 
Febrile Seizures - see later
Paroyxysmal Disorders - "funny turns"
Breath holding attacks - child cries, holds his breath, and goes blue. Sometimes children loose consciousness. Behaviour modification + distraction may help.
Reflex anoxic seizures - occur in infants or toddlers. May have a first degree relative with a history of faints. Commonest triggers are pain or discomfort - minor head trauma, cold food (ice-cream or cold drinks), fright or fever. Triggering event, then child becomes pale and falls to floor. May have a generalised tonic-clonic seizure. The episodes are due to cardiac asystole from vagal inhibition. Seizure is brief and the child rapidly recovers. Ocular compression under controlled conditions often leads to asystole and paroxysmal slow-wave discharge on the EEG.
Syncope- faint if in a hot or stuffy environment. Clonic movements may occur.
Migraine- paroysmal headache involving unsteadiness or light-headedness as well as visual or GI disturbance. These symptoms may occur without the headache.
Benign paroxysmal vertigo- recurrent episodes of vertigo, 1- several minutes + nystagmus, unsteadiness or falling.
Cardiac arrhythmia-  prolonged QT = rare
Tics, daydreaming, night terrors
Self-gratification- genital stimulation for comfort, rather than sexual gratification.
Pseudoseizures / fabricated / induced illness: eg adult injecting insulin
Paroxysmal movement disorders - well-circumscribed episodes, genetically determined, no loss of consciousness.

Epilepsy
Incidence 0.05% and prevalence 0.5%
There are lots of different types of epilepsy, depending on which part of the brain is affected. Not all epilepsy is tonic-clonic.
 - Frontal seizures - motor or premotor cortex. May lead to clonic movementsAsymmetrical tonic seizures can be seen, which may be bizarre and hyperkinetic.
- Temporal seizures- strange warming feelings. Lip-smacking, plucking at clothes, automatism.Consciousness can be impaired.
- Occipital seizures -distortion of vision
- Parietal lobe seizures - contralateral dysaesthesias or distorted body image

Epilepsy Syndromes
- West Syndrome - flexor spasms
- Lennox-Gastaut syndrome - drop attacks
- Childhood absence epilepsy

Take a full and careful history. You need to do a full and careful examination - to reassure the parents if nothing else. Most patients can be discharged with outpatient follow up and very careful advice:  cycling in traffic, swimming alone, deep baths, contraception + pregnancy and driving.

Status Epilepticus

The definition of status is, as always controversial. The "traditional" definition is a seizure that lasts 30minutes or more or clusters of seizures lasting for more than 30minutes with no recovery in between.

In 2008, the Neurocritical Care Society introduced a new definition for Status Epilepticus because (to quote boringEM)…
"- By 5 minutes a seizure is like the Energizer Bunny: it keeps going and going… and is unlikely to stop.
 - The brain is frying: 30 minutes (the old definition) was too long because neuronal injury/pharmacoresistance likely occurs WAYYYY before 30 min of continuous seizing."

"Status Epilepticus: Continuous seizure activity for greater than 5 minutes or the occurrence of sequential seizures over a similar period without recovery of consciousness between seizures"

It can be caused by:
 Febrile illness
 Infection (particularly meningoencephalitis)
 Trauma
 Metabolic derangements (including hypoglycaemia & electrolytes, eg. hyponatraemia)
 Medication change
 Drugs
 Idiopathic

Treatment
The NICE Guidelines have a very sensible summary of treatment that is very clear, although it doesn't mention PO/Buccal midazolam. The College of Emergency Medicine has some excellent local charts, including one from Manchester, that has lots of good information on it that is well presented.


Benzodiazepines are always the first, and second choice. We can give benzos by so many routes that we don't need to get stressed about gaining IV access. If we don't manage to gain IV access, paraldehyde is still in the paediatric guidelines. Unlike the adult guidelines, the paediatric guidelines are still very clear that we don't give phenytoin if the patient is already on phenytoin - maybe because we assume children are more likely to be compliant?