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.


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.