Red fright or green light? | A child with fever

babysimple-01-01

A 14 month year old boy has a fever for the past 4 days. The fever peaked at 38.5°C as measured at home. The child has been irritable and clingy since arriving at the GPs, but has not shown any obvious pain. There is no photophobia, neck stiffness or rash. There has been a non-productive cough for two days, which is worse at night. There is no history suggesting stridor, respiratory distress or wheeze. He has had a runny nose over this time. He is tolerating food and drink, although he is eating less than normal. He sometimes vomits after eating. There have been no changes to his bowel habits and he is producing about 6 wet nappies a day.

Examination is difficult. He cries at the slightest intrusion of his personal space by anyone other than his mother. His temperature is 37.2, although mum tells you he just had calpol about thirty minutes ago. His pulse is 120. There is subcostal and intercostal recession when he is crying, but none when the crying settles. His respiratory rate when he is settled is 40. His saturations are 96% on air. The anterior fontanelle is neither bulging nor sunken.

An ENT examination is almost impossible. You eventually find it to be normal. There is no rash top to toe. His chest sounds clear. His abdomen is soft.

You go to write up your findings to give yourself time to think whilst mum dresses the child. You have not found the source for the fever. You look at the PMH – he was a preterm baby at 34/40 weeks but has been generally well since. His development has been fine. All his vaccinations have been up to date. He is an only child, and no household contacts have been unwell.

But it’s only a ‘fever’ of 37.2 – that’s not significant

You only have a snapshot of the child’s temperature. You cannot discount the parental concerns about fever over the past four days based on a one-off reading just now. NICE state:

“Reported parental perception of a fever should be considered valid and taken seriously by healthcare professionals”

Then it’s a feverish child with no source! Admit, admit!

There are basically two things that mean a feverish child may need admission –a) suspicion of a serious bacterial infection or b) not coping with the illness itself e.g. dehydration, first ever/complex febrile convulsion, respiratory distress etc.

Regarding a) – the majority (>80-90%) of fevers in children will be self-limiting viral infections.

Regarding b) – the majority of children will cope absolutely fine with a febrile illness.

Our task is to identify the minority who have a problem with a) or b) for further assessment. We should advise the remainder to self-care at home with safety netting. Sometimes you cannot quite 100% pin down the source; this in itself does not necessarily require an urgent assessment.

How do you interpret the fever in light of the fact that the child took calpol?

It does not matter. The height of the fever in a child over 6 months does not predict a serious bacterial infection, nor does it tell you how the child is coping with the illness. The height of the fever is therefore not going to alter your management plan.

In infants less than 3 months, a fever greater than 38°C should be seen urgently by a paediatrician (red flag in NICE guidelines).

In infants between 3 and 6 months, a fever greater than 39°C is an amber flag in NICE guidelines.

Isn’t it great that NICE guidelines are perfect! We don’t have to think, just use the table!

The traffic light system is helpful. It does not replace clinical judgment. This reflects the fact it is difficult (?impossible) to create a rigid scoring system for something as complex and nuanced as assessing a feverish children. The most common bacterial infection the traffic light system misses is a UTI – in fact, about one fifth of the time a child with a UTI will score green. There has been a suggestion to add urinalysis to the NICE traffic light assessment of the feverish child (http://www.bmj.com/content/346/bmj.f866). However, there are also some who feel that this study considered only the traffic light system in isolation, without considering the NICE guideline’s holistically. The purpose of the traffic light system was not to diagnose but to help with the initial triage of feverish children. (http://www.bmj.com/content/348/bmj.g2056/rr/691345)

So what is this magical table?

Have a look: traffic light system for identifying risk of serious illness

The main thing to emphasise is that NICE states that if the child appears unwell to you, refer urgently. Your clinical gestalt is valuable, no matter your level of experience with children ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458229/).

What happened in this case?

It’s a fever of unknown source. There are some suggestions of a viral source (runny nose, non productive cough) but nothing definitive. There is no way you can predict what will happen in 4, 8 or 24 hours. The mother was told to contact us if the child remained clingy/crying frequently at home. Given the child had green flags at the time of assessment, and the mother knew when to come back or when to go to A&E, the child could be watched at home with appropriate safety nets.

Cool. Alternating paracetamol and tepid sponging then to keep T < 38.

NO! That is so 2008. You treat fever only so the child doesn’t feel distressed. You do not give antipyretics to target a temperature.

And you only give ibuprofen or paracetamol (at least initially). Alternating doses leads to frequent dosing errors. If the fever is not controlled with either agent alone, and the child is distressed, then maybe you could alternate them – but ask the parents to keep a written record of what they have given and when. And forget tepid sponging. Just dress the child in clothes which are appropriate for the room temperature.

Any specific advice for the parents?

NICE CKS mentions the following:

 

  • Look for signs of dehydration including poor urine output, dry mouth, sunken anterior fontanelle (usually closed by 18 months), absence of tears, sunken eyes, and poor overall appearance).
  • Offer regular fluids (if breastfeeding, continue this as normal) and encourage a higher intake if signs of dehydration develop.
  • Dress the child appropriately for their surroundings, with the aim of preventing overheating or shivering.
  • Avoid using tepid sponging (using cool water) to cool the child.
  • Check the child regularly, including during the night (how often depends on the situation).
  • Keep the child away from nursery or school while the fever persists, and notify the nursery or school of the illness.
  • Advise parents and carers to seek medical help if:
    • The child is getting dehydrated.
    • The child has a fit.
    • The child develops a non-blanching rash.
    • The fever lasts longer than 5 days.
    • The child is becoming more unwell.
    • They are distressed or concerned that they are unable to look after the child.

 

Advertisements

Rare presentation of a rare condition (which is a common presentation of a common exam condition)

In some ways, our job consists of making the colourful spectrum of real life medicine fit the black and white confines of the hospital protocol or the textbook definitions. Though the presentation of this next case was as black and white as it gets, the way it was dressed up to the AMU could lead you up the wrong path. As you go down the case you will get more clues; see how early you can figure it out.

A 59 year old man originally from Eastern Europe had felt tired for the past 3 months. He had seen his GP, who discovered a normocytic anaemia (Hb 7.4) with a normal WCC and platelets. (The patient’s haematinics were normal, making a mixed iron/folate/B12 deficiency unlikely. His reticulocyte count and kidney function were also normal.)

The patient reported no source of bleeding, including normal bowel habits. He had no skin or joint symptoms. He felt there was no change to his appetite, but did notice about 5 kg of weight loss over this time. There was no fever, but yes, there were occasional drenching night sweats.

PMH revealed rheumatic fever as a child, which left him with a systolic murmur of some sort that the GP was unable to classify further.

He took no regular medications.

Apart from this he was normally a fit and well builder. He had been unable to go to work in the past month because of the tiredness. He lives with his wife. Social history was otherwise unremarkable.

On examination, his obs were Pulse 105, BP 134/90, RR 16, Sats 99% on air and T 37.8. The clerking FY1 noted this:

Splinter Haemorrhage
Splinter Haemorrhage

On palpation there was splenomegaly.

On auscultation there was a loud pansystolic murmur radiating to the axilla.

Bloods confirmed a normocytic anaemia with a WCC of 10.1 and a CRP of 53. His U&Es, LFTs and Coagulation were all normal.

A urine dipstick showed haematuria (+++).

A transthoracic echo showed a mitral valve oscillating vegetation, with severe mitral regurgitation and normal LVEF.

Three sets of blood cultures returned two days later which all grew strep viridans sensitive to benzylpenicillin.

What is actually going on in IE?

As the under review HPA guidelines on blood cultures states:

“IE is infection of the heart valves and/or other areas of the endocardium. It usually occurs at the site of a predisposing cardiac lesion or congenital defect where there is turbulent blood flow, encouraging endocardial damage and adhesion of platelets. A fibrin clot is deposited on the damaged endocardial surface and becomes colonised with organisms which have entered the bloodstream, so forming infected vegetation. Viable bacteria may be present deep within the vegetation as well as on the surface making antimicrobial treatment difficult.”

Why did this man get IE?

Intact valvular endothelium is normally quite resistant to colonisation. The rheumatic fever caused some degree of valve damage, which makes it easier for any bacteria that happens to be in the blood to make a camp there.

What bugs are most likely in this case?

According to the UK guidelines (2012), the most common causes of NVE in non-intravenous drug users are currently S. aureus (28%), coagulase-negative staphylococci (CoNS; 9%), streptococci (35%) and enterococci (11%); 9% are culture-negative.

The main times staph aureus dominates over streptococci is healthcare associated IE, IVDU associated IE and in the first year following a prosthetic valve placement. Staph aureus is the second most common cause of IE in prosthetic valves in the first year after coagulase negative staphylococci. In fact, the closer it is now to the time of the prosthetic valve placement, the more likely that any IE the patient is currently having on that valve is caused by coagulase negative staphloccoci.

How should cultures be taken?

According to the UK guidelines:

“In patients with a chronic or subacute presentation, three sets of optimally filled blood cultures should be taken from peripheral sites with ≥6 h between them prior to commencing antimicrobial therapy.”

It adds:

“There is no evidence to support the commonly perpetuated view that blood cultures should be taken from different sites. All skin surfaces are colonized by bacteria and adequate skin disinfection is key to reducing contamination. Taking blood cultures at different times is critical to identifying a constant bacteraemia, a hallmark of endocarditis.”

In practice, this means it would be 12 hours from your first suspicion of IE to giving your first set of IV antibiotics in a patient with a chronic or subacute presentation.

But the sepsis six! Each hour’s delay results in a 7.8% increase in mortality! What should I do if the patient is septic with IE?

According to the same guidelines:

“In patients with suspected IE and severe sepsis or septic shock at the time of presentation, two sets of optimally filled blood cultures should be taken at different times within 1 h prior to commencement of empirical therapy, to avoid undue delay in commencing empirical antimicrobial therapy.”

If you spoke to a sepsis champion, they would feel very uncomfortable about knowingly delaying giving antibiotics in any patient with severe sepsis or septic shock. In fact, the guidance from the sepsis world is to give fluids, oxygen and antibiotics ASAP and only take cultures before giving antibiotics if this would not delay giving antibiotics.

I’ll have to cross check what to do in this situation with a sepsis don.

What is the most common extracardiac manifestation of IE? 

Though this man had a splinter haemorrhage, this could be related to his occupation as a builder. The patient was unsure if this line in his nail was new or old. Splinter haemorrhages are a pretty rare feature of IE in the developed world, where the presentation is usually fairly early. Janeway lesions, Osler nodes and clubbing are all subacute signs, and are also quite rare in the developed world.

Cerebral complications are the most severe extracardiac complications of infective endocarditis, as well as the most frequent (occurring in 15 to 20% of patients). A haemorrhagic or ischaemic stroke may result. In other words, if a patient has an unexplained stroke, we may question whether or not there is underlying IE (after dealing with the stroke).

To TOE or not to TOE?

Same guidelines:

Role of TOE in IE
Role of TOE in IE

What should the first line antibiotics be whilst awaiting culture results in this case?

According to the same guidelines:

Empirical antibiotics in IE
Empirical antibiotics in IE

Note amoxicillin rather than the benzylpenicillin. Although you should follow your hospital policy, it seems that amoxicillin has better activity against enterococci, which cause 11% of native value IE. The newest versions of the BNF support this.  Fully sensitive streptococci might still be managed with benzylpenicillin.