Red fright or green light? | A child with fever

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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.

 

3kg baby replaced by 3kg of urine

Urine replaces baby
3.2 L of urine replaces 3.2kg of baby. 

I’m going to have a withdrawal bleed once I leave O&G’s hormonal fuelled adventures behind. It has been a mix of the high (on entanox) and the low (lying placenta). I’m no longer scared of the concept of pregnancy (even if the BNF seems to be – “no evidence of harm but what the hell – manufacturers advise avoid”). I’m glad I did it, but I’m more glad it’s over.

That said, it just wouldn’t be O&G without one last not-normal-fluid-out-an-orifice scenario to work through. Towards the end of the placement, I noticed several women who had normal vaginal deliveries developed urinary retention. Post op C section retention is nothing new; pretty much any major surgery has this risk. However, I was unaware of how frequent retention is post vaginal delivery, and how best to recognise/manage it.

Before we dive in, there’s a little analogy I find helpful. I used to think urinary retention must be absolute i.e. if the patient is passing something, it can’t be retention. I now think of it more like faecal impaction than full-on bowel obstruction. Just like you can have some overflow with faecal impaction, you can pass little overflow-y voids with retention. If the voiding volume is small and/or there’s voiding difficulty and/or suprapubic pain and/or there’s a high residual, treat it as potential retention even if there is some urine output.

A woman has a normal delivery. There was a second degree tear which was sututred. She had difficulty passing urine post delivery, passing 50ml then 60 ml in 6 hours post delivery. She complains of lower abdominal pain. She is a little tachycardic. The team assume she is dry and give her 3.5L orally over the next 24 hours. The urine output does not pick up, and her observations remain the same.

Our super SHO (not me) does a thorough examination discovers that there is suprapubic tenderness combined with the urge to pass urine. The patient feels really uncomfortable. A urinary catheter is passed. It drains 3.2L.

How did this happen?

During pregnancy (especially the third trimester), the bladder tone decreases and bladder capacity enlarges. Before she gives birth, the pressure of the gravid uterus compressing the bladder helps maintain voiding pressure. After delivery, the bladder expands and intravesical pressure drops. In 1.7-17.9% of women who have a vaginal delivery, this leads to retention.

So it’s kinda normal then. When do I worry about it? 

It can take up to 6 hours after a normal delivery for bladder sensation to return to normal (more if an epidural was used). If a woman has not passed urine within 4 hours after delivery despite adequate fluid intake, she should be given every opportunity to pass urine naturally. This means controlling pain, keeping her mobile, giving her privacy and perhaps trying a warm bath. If it reaches 6 hours, it’s time to catheterise.

But this woman passed a little. Does that count?

One void less than 200ml could still be consistent with retention (especially if accompanied with voiding symptoms such as suprapubic pain, poor stream, leaking/passing urine without the urge etc.)

OK, so now that we catheterised her, she had a residual of 3.2L. How you gonna deal with that?

There is no formal guideline. A ‘normal’ adult bladder distends up to 400-600ml. Distension beyond this volume should be uncomfortable. The fact it drained 3.2L means her bladder has been significantly distended.

That said, immediately post partum the bladder is naturally a little distended.

The urge to pass urine starts at around 150-250ml. If there’s a post-void residual of more than 150ml, it suggests a voiding issue.

You didn’t answer my question.

Fine. I found several approaches used by different midwife units. Nottingham’s guidelines specifically talk about how variable the guidelines from various units are. One approach for symptomatic retention that I found intuitive was from a New Zealand. With some slight modification to fit in with what I generally saw being done in the UK, we’ve got the following plan for overt (i.e. symptomatic) retention:

Once the 6 hour deadline has elapsed, you re-catheterise the patient. If there’s a small residual (<150ml) it’s fine – it’s not retention (maybe she was a bit dry). If it’s medium (150-700ml) keep it in for 24 hours and repeat the TWOC then. If it’s big (past 700ml), keep it in for 48 hours. This gives more time for the bladder to be unfull and hence hopefully return to its normal size.

On the second TWOC, if she does a good void (>200ml) within 6 hours, you check the residual. If the residual is less than 150ml, it’s all good. If it’s bigger, or she doesn’t do a good void in the new 6 hour deadline, then she failed the second TWOC which usually means a 7 day in dwelling catheter before a re TWOC. Another approach is intermittent self catheterisation.

If the volume for the first TWOC is bloody ridiculous like 3.2L, go straight for re-TWOC in 7 days.

Covert retention (post voiding residual >150ml without symptoms) is nicely covered by the same New Zealand guidelines. It seemed similar to what I see in the UK.

How is it going to resolve?

Postpartum retention is usually a short-term problem that resolves over weeks. It can lead to a persistent hypotonic bladder if poorly managed.

Unsweetened vomit

Pregnant women vomit a lot. I don’t just mean morning sickness. Pregnancy can result in altered taste and smell, which means certain foods and smells make them feel violently sick. Although most cases of pregnancy induced vomiting get better after 20 weeks, there are some unlucky ladies who feel sick every single day until the birth of their you-are-lucky-you-look-cute-otherwise-I’d-bloody little bundle of joy.

A lady in her mid 30s was admitted at 39/40 with persistent vomiting. It had been going for two days and she was vomiting nearly every hour. There was no change in bowel habits. There was upper abdominal tightening that occurred with the vomiting, but no other abdominal pain. No one else was affected at home and she had not been travelling or eating unusual foods. She had no vertigo or hearing problems. She had a throbbing headache of about 5/10 severity, especially on being upright. There were no visual symptoms or other neurology.

She was unable to keep anything down, including fluids, for the past 24 hours.

On examination she was dehydrated, with dry mucous membranes. Her urine showed 5+ ketones. Her observations were stable. Her urine was dark, but the output was adequate. There was no abdominal tenderness.

During the admission, she was persistently hypoglycemic. Her BMs were around 3-3.5 despite 5% dextrose being used as rehydrating fluid.

There was no PMH of anything, and no access she could have had to antidiabetic medications/insulin.

Her U&Es, lactate, TFTs, LFTs and calcium were all normal.

Would it be reasonable to attribute her low glucose to 36 hours fasting in the absence of any other medical problems?

I’m thinking no. Here’s why:

  • The body responds to low glucose by first switching off insulin and increasing glucagon production. This has the effect of increasing gluconeogenesis and glycogenolysis in the liver.
  • Catecholamines are also released as the glucose continues to drop. Biochemically, this causes glycogenolysis in the liver and muscle and gluconeogenesis in the liver and kidney. Clinically, this produces the cathecholamine excess symptoms – sweats, tremors, tachycardia and a sense of hunger (and anxiety).
  • Finally, growth hormone is stimulated (which stimulate lipolysis) as well as ACTH (which increases lipolysis and muscle breakdown).
  • If glucose continues to stay low, the patient may develop neuroglycopenic symptoms (dizziness, inappropriate behaviour, poor concentration, confusion, blurred vision, stroke-like symptoms and eventually coma/death). The body prioritises glucose for the brain. If the body can’t supply the brain with glucose, this means something is failing in a big way.

So, in a patient with an otherwise intact endocrine system, a healthy liver and a decent glycogen store, fasting alone will rarely produce hypoglycemia. Hypoglycemia from malnutrition usually occurs when at least one of those three things are out e.g. Addison’s disease, liver disease or prolonged malnutrition depleting the glycogen stores.

What else could cause hypoglycaemia?

Hypoglycemia causes can be split into fasting (occurring at least 6 hours after a meal) and non-fasting. I’m just going to focus on the fasting ones for today.

The fasting hypoglycemias can be split into those with an appropriately low insulin level and those with an inappropriately high insulin level.

Appropriately low insulin

Alcohol – independent of any effect on liver function, alcohol inhibits hepatic gluconeogenesis

Endocrine – usually a problem in the CRH-ACTH-cortistol axis, but also rarely growth hormone deficiencies.

Liver disease – loss of gluconeogenesis ability and/or inability to store glycogen

Renal disease – the kidney does do some gluconeogenesis, but not as much as the liver. The most common clinical application of this is end stage diabetic nephropathy reducing kidney function and therefore a decrease in the insulin/antidiabetic dose requirements.

Sepsis – can lead to impaired gluconeogenesis. However, more commonly hypergylcemia. One of the SIRS criteria is actually raised glucose in a non diabetic.

Pregnancy – the foetus takes priority over resources. Mum’s stores are depleted. This leaves her at risk of hypoglycaemia.

Rare stuff – inborn errors of metabolism.

Inappropriately high insulin

Diabetic meds – by far the commonest. The body can’t ‘switch off’ insulin that is pushed into it. Insulin secretagogues can also cause hypogylcemia. A clinical possibility: An elderly diabetic patient with decreasing renal function has been on a sulfonylurea for ages. The sulfonylurea has reduced clearance because of the reducing renal function, so the patient ends up developing hypoglycaemia.

Insulinoma – classic MRCP case. A prolonged fast for 72 hours is the key test. Normally insulin should switch off. However, if the patient is hypogylcemia with a high insulin level (and raised C peptide to show it was endogenous insulin) then you are a diagnostic machine for spotting an insulinoma.

Bottom line: My patient probably had depleted glycogen stores from her baby which meant when she got into a fasting state, she didn’t have the reserves.

The four types of dizziness in clinical medicine

Dizziness

A 24 year old woman with a positive pregnancy test is seen in the EPAU with three days of lower abdominal pain. A transvaginal ultrasound shows she is 5 weeks pregnant, but ‘cannot rule out ectopic pregnancy’.

The patient is informed of the symptoms of ectopic pregnancy to look out for.

On mentioning ‘feeling faint’ as a red flag, she mentions episodes of room spinning for the past three days. She also feels light headed and ‘about to pass out’.

These episodes last less than a minute at a time and are provoked by head movements. There is no vomiting. She has no tinnitus or hearing problems. She has no double vision, speech problems, weakness or numbness.

On examination, her eye movements are conjugate and there is no nystagmus. A Dix-Hallpike manoeuvre is done to confirm the diagnosis.

This patient was treated as BPPV. However, she had also mentioned feeling light headed and feeling ‘about to pass out’. How should we sort these symptoms?

The official NICE CKS question for distinguishing vertigo from the other types of dizziness is “When you have dizzy spells, do you feel light-headed or do you see the world spin around you as if you had just got off a playground roundabout?”

For me, dizziness falls into one of four species (vertigo, disequilibrium, presyncope and lightheadedness) in about 80% of cases. Then there’s the 20% who complain of multiple types at once e.g. “It does feel like the room is spinning and I’m also about to fall over and pass out”. I decided to find out how best to distinguish these types, as well as think about the key questions that lead you to the differential for each of the subtypes.

True vertigo

Vertigo

False sense of movement. Like when you get off a merry go round.

Top questions: Is it central or peripheral?

The traditional table as found at Initial Evaluation of Vertigo:

Type Peripheral Central
Nystagmus Combined horizontal and torsional;inhibited by fixation of eyes onto object;fades after a few days; does not change direction with gaze to either side Purely vertical, horizontal, or torsional;not inhibited by fixation of eyes onto object; may last weeks to months;may change direction with gaze towards fast phase of nystagmus
Imbalance Mild to moderate; able to walk Severe; unable to stand still or walk
Nausea, vomiting May be severe Varies
Hearing loss, tinnitus Common Rare
Nonauditory neurologic symptoms Rare Common
Latency following provocative diagnostic maneuver Longer (up to 20 seconds) Shorter (up to 5 seconds)

GP Online’s quick answer: Do a head impulse test. If positive, this points to a peripheral cause. If normal, this points to central (or psychogenic) vertigo.

But how do I do a head impulse test?

Main differentials:

Central – stroke/TIA, MS, vestibular schwanoma. Can also be part of migraine.

Peripheral – – 93% of all primary care cases of vertigo are one of BPPV (last seconds to minutes), Meniere’s (lasts hours, with fullness in the ear, hearing loss and tinnitus) or vestibular neuronitis (starts bad then gets better over days to weeks). A perilymphatic fistula can also occur after head injury or surgery.

Disequilibrium

Disequilibrium

Off balance, wobbly. Like being on a moving ship.

Your eyes, vestibular system and peripheral nerves all provide input to the cerebellum to keep you balanced. In elderly patients these inputs gradually decline, leading to disequilibrium. Having musculoskeletal problems and being on antihypertensives doesn’t help. Disequilibrium can also happen in younger patients with significant neurological / vestibular disorders.

These patients feel much more balanced when they have something to hold on to e.g. furniture, as this provides them with another source of proprioception.

Presyncope

Presyncope

The prodrome to a vasovagal minus the actual loss of consciousness. This includes sweating, tunnelling of vision, palpitations, warmth, pallor and everything sounding distant. Much less likely to be caused by an arrhythmia than syncope (page 2649 of the ESC guidelines) but work up is generally the same.

Lightheadedness

Lightheadedness

Feeling generally disconnected from the environment. Everything may feel unreal. “Like I’m floating, doctor”. There may be some mild motion/balance problems on direct questioning, but these are not the main concern of the patient. This type of dizziness is associated with anxiety and hyperventilation/panic attacks.

Twelve fun facts about dizziness:

1. Dizziness is the fifth most common presenting complaint to primary care in the UK.

2. Vertigo is the commonest type of dizziness, and BPPV is the commonest cause of vertigo.

3. Vestibular sedatives (like prochlorperazine) do not have a role in BPPV. They may even delay central nervous compensation. The Epley manoeuvres are what you need (or alternative manoeuvres for patients with neck problems).

4. In contrast, vestibular neuronitis (peripheral vestibular nerve failure, usually triggered by a virus) or labyrinthitis (hearing symptoms as well) can benefit from short term use of a vestibular sedative. There is also a role for corticosteroids.

5. BPPV usually self resolves in 10 weeks.

6. New central vertigo will need MRI.

7. Headache is not a typical presenting complaint of anterior circulation ischaemic strokes. According to GP Online, about a third of patients with ischaemic posterior circulation strokes will have a headache, which is usually occipital. This means vertigo + new headache = potential stroke.

8. Vertigo brought on by loud noises is peripheral.

9. Meniere’s disease initially presents as episodes; eventually permanent damage occurs which could lead to deafness. This is why ENT input is advised in suspected cases.

10. Betahistine is only licensed for Meniere’s. It is not used for other causes of vertigo.

11. Vertigo going on for months with a normal MRI is most likely to be anxiety related.

12. All is not lost with persistent vertigo. It can respond to vestibular rehabilitation and physiotherapy.

Making an impact on impacted faeces

A 80 year old lady is admitted with abdominal distension and difficulty breathing. She is found to have ascites secondary to an ovarian malignancy.

Her ascites are drained. One day later her pain is much improved although she is constipated, so her opiods are stopped. She is started on macrogol (one sachet twice a day). Three days later senna (15mg at night) is added. Five days later she still complains of persistent constipation.

She is drinking about 1 litre a day and is generally immobile. She passes hard small stools every two to three days. She denies straining or PR blood. Her rectum is loaded with impacted faeces. Manual evacuation of the faeces removes three golf ball sized impacted faeces. The next day she passes only small watery stool.

You are called to review her. What is the most appropriate treatment for her constipation?

A suggested approach

How to convince a surgeon to accept a RIF pain referral

I just love gyane on call. A 43 year old woman is brought to A&E complaining of severe right iliac fossa pain for the past day. A pregnancy test is negative. The surgeons think it is a gyane problem. The gyane team think it is appendicitis.

How can you avoid bouncing the patient between the two teams?

In this first post, I’ll go through the features of appendicits that a gyane person could use to convince the surgeons to come take a look.

Appendicitis 

There are two approaches. If the history is classic, you go to theatre. If it’s not but feel there’s enough to make you suspicious (and you have time), you might consider imaging.

Classic presentation

The classic clinical presentation goes through five sequential stages over two to three days:

  1. Vague umbilical colicky pain that does not bother the patient enough to attend

    Stage 1: Non specific colicky abdo pain
    Stage 1: Non specific colicky abdo pain
  2. Anorexia, nausea and gentle vomiting

    Stage 2: Loss of appetite, nausea and mild vomiting
    Stage 2: Loss of appetite, nausea and mild vomiting
  3. Constant right iliac fossa pain that does bother the patient enough to attend (perionitic i.e. worse on coughing/moving, patient keeps still, guarding and rebound tenderness)

    Stage 3: Localisation of pain to RIF with peritonitis features
    Stage 3: Localisation of pain to RIF with peritonitis features
  4. Low grade fever (<38)

    Stage 4: Low grade fever
    Stage 4: Low grade fever
  5. Leucocytosis (12-15*10^9 cells per mm^3)
Stage 5: Leukocytosis
Stage 5: Leukocytosis

This classic history occurs in less than 50% of patients.

Of all the features, the two which really increase the chances of appendicitis are right iliac fossa pain and a migratory history.

There are scoring systems such as the Alvadaro score. However clinical judgement may be superior, especially for more senior clinicians.

Examination tips: Rebound tenderness can be a bit mean if the patient is clearly in pain. Ask the patient to cough and if pain is localised to the right iliac fossa, then this is a good sign.

Is a PR exam helpful? Probably not, especially in the presence of a convincing history and examination. (That said, tenderness on the right side on PR may lead to suspicion of a pelvic appendix so may be worth doing if there is an atypical presentation or if other diagnoses are being considered).

Tests pretty much everyone gets: Urine dipstick (including pregnancy in females), FBC, CRP, U&E.

What to do: If you have a classic history and examination, go to theatre. Go directly to theatre. Do not pass radiology. Do not fill out a CT Abdo request.

Non classic presentation

Who typically presents atypically?

The young, the old and the pregnant. Important atypical presentations include acute confusional state (elderly) and right upper quadrant pain (pregnancy).

What types of appendices present atypically?

Retrocaecal appendix – more right loin pain, less right iliac fossa pain

Pelvic appendix – like a UTI with urinary frequency, suprapubic tenderness and even pyuria/haematuria.

Tenderness on the right side in a PR (or PV) examination is supportive of a pelvic appendix.

What to do: If you have a not quite classic history and examination, think through the differential. If the patient is not acutely unwell, it may be worth organising some imaging (often CT Abdo/Pelvis or a TVUSS gynae scan) to support the diagnosis or look for other causes.

Next week: How to convince a gynaecologist to accept RIF pain

Using the CRP on inpatients

“Stay in till tomorrow to recheck the CRP. If it goes down to less than 100 he goes home.”

“It’s day 2 post op. The CRP is 167 from 67 the day before. Is that normal or do we look for a possible infection?”

“Giant cell arteritis? Use ESR, CRP is useless.”

I decided to read up on the CRP, focusing on bits that would help make sense of the clinical situations above.

1. The half life of CRP is 18-19 hours.

“Stay in till tomorrow to recheck the CRP. If it goes down to less than 100 he goes home.”

This half life is remarkably constant no matter what else is going on, be it renal failure, liver failure, sepsis, polypharmacy etc. This means that the plasma level of CRP is dependent on how much was made and when.  It is only dependent on factors affecting its production, not its elimination.

Once the insult is removed, CRP should drop toward baseline. It should be normal within two or three days (which corresponds to 3-4 half lives i.e. 7/8th or 15/16th eliminated).

The CRP can therefore lag behind the clinical picture. If the patient is clinically well and has an identifiable insult that has recovered in the last 48 hours, you do not necessarily need to wait for the CRP to come down to ‘prove’ the patient has recovered.

2. CRP levels usually peaks at about 48 hours after the insult.

“It’s day 2 post op. The CRP is 167 from 67 the day before. Is that normal or do we look for a possible infection?”

CRP production does not happen instantly at the time of the insult; it is delayed by at least 2 hours, and really kicks in at around 6 hours. This means that the CRP would normally rise between day 1 and day 2 post op for example.

3. The CRP goes up with most causes of inflammation.

“Giant cell arteritis? Use ESR, CRP is useless”

CRP is made pretty much exclusively by the liver as part of the acute phase response. The acute phase response includes a protein synthesis strategy change by the liver following activation of the innate immune system by something nasty – an infection, autoimmune disease, burns, trauma or maybe a neoplasm. A raised CRP is very sensitive for ‘some inflammation somewhere’ but very unhelpful for determining the aetiology.

The most famous exception is SLE, where CRP often stays normal whilst the disease flares. Interestingly, the SLE patient still mounts a CRP rise in response to infection. This means that measuring CRP during a suspected flare can help distinguish between an autoimmune flare or an infection.

A normal ESR is seen in 8-22.5% of cases of giant cell arteritis. In contrast, an elevated CRP is thought to be near 100% sensitive for the condition. You can have an elevated CRP with a normal ESR in GCA. However, it is ESR rather than CRP that is used in the diagnostic criteria for GCA.