Hb 65, ESR 110. Differentials?

What ESR really measures

A 67 year old woman had an unexplained Hb of 65 g/L. The only previous Hb result was 103 g/L from over four years ago. She felt generally tired with achy muscles most of the day for the past few months. An ESR had been sent, and came back as 110.

Q. Arrgh! PMR! Myeloma! Anaemia of chronic (rheumatological disease) of some kind!

A. Possibly. But it’s still quite likely that the ESR is a result of the anaemia, which raises the Rate at which Erythrocyte Sedimentate (sedimentate is totally a word).

Q. Dammit. We can only use CRP in these situations reliably.

A. You could measure plasma viscosity directly instead of ESR. This is expensive and not done in the NHS generally, and anyway you don’t usually need to unless you are a rheumatologist. And if you are, you probably know more about the merits of CRP vs ESR vs PV than me so I’ll shut up.

Q. Is this your shortest post yet?

A. Yes.

Q. Why?

A. Because if you can’t get a reliable ESR result, it doesn’t matter. Most of the conditions which benefit from ESR over CRP can be reviewed by a rheumatologist later. The only emergency where an ESR changes management is GCA; if you suspect this in a patient with an unreliable ESR, you can discuss with an on-call rheumatologist or treat now and await the formal biopsy.


Anything intermittent in medicine is electrical

A lady in her late 50s with a background of metastatic colon cancer was referred by her GP with a Hb of 6.1 (MCV 89.8, WCC 20.9, Plt 117). This was noted because she had been complaining of worsening shortness of breath for the past week.

Her Hb the day before was 6.4, and her Hb 2 weeks ago was 11.6. She had had one previous transfusion when her Hb was restored from 5.3 to 9.4. Before and after that episode, she was generally around 10.5-12.

On arrival, she had a pulse of 130, a BP of 117/78 and was saturating 100% on air with a respiratory rate of 14. She had a temperature of 36.6.

I like to split the differential for shortness of breath according to the onset of symptoms. It would be very tempting to attribute the whole thing to anaemia, arrange a blood transfusion and leave it for the day team to follow up. I arranged for the transfusion to begin and then clerked her.

The shortness of breath was a gradual onset, and had been gradually progressing. Her shortness of breath had left her unable to walk more than 5m. This compares to a week ago, when she was able to walk around her supermarket with no problems.

She had intermittent chest pain, which was worse on inspiration. Shortness of breath, chest pain worse on inspiration, tachycardia and a PMH of metastatic cancer? I decided not to do any investigations into PE/DVT. This is either mad or brave. Here’s my thinking: The pain localised to her left lower ribs, directly over where the costochondral joints are. She was able to point to a specific point on her chest where the pain was. The pain lasted a maximum of 5 minutes, coming in waves when it was there. It occurred mostly in the morning on awakening. It was brought on by postural changes such as when getting out of bed and by overlying pressure. Between episodes, there was no pain at all. There was no cough, and no leg swelling/pain.

The other thing is that she was saturating at 100% on air, and still felt short of breath. This means that there is no problem getting oxygen from the atmosphere into the lungs, nor in getting oxygen from her lungs into her circulation. Of the causes of pleuritic chest pain, you would expect a pneumonia to affect the former, and a PE to affect the latter. The problem here was clearly quite different; there was not enough oxygen carrying capacity in her blood.

The shortness of breath was improved by lying flat, which counted against co-existing heart failure, which potentially could have been precipitated by anaemia. There were no infection pointers on history despite the raised WCC.

There was no history suggestive of GI, GU, PV, intracranial, intra-articular or other superficial bleeding.

She was generally quite an active lady for someone with metastatic cancer, and had no problems living with her husband in managing her ADLs. She was also a lifelong non smoker.

Her CVS, Resp and abdominal exam were all normal, except for the pulse of 130. Her mucous membranes were actually relatively moist, and she was talking comfortably in full sentences. There were no added noises in the chest, nor any swelling around the ankles/calves. There was no splenomegaly.

The question now became what caused the normocytic anaemia. Broadly, the causes can be split into a failure to make RBCs, or losing RBCs.

You fail to make RBCs either because the marrow is rubbish or because the marrow is not stimulated properly.

You lose RBCs in bleeding, hypersplenism and haemolysis. Haemolysis splits into congential and acquired. Acquired haemolysis splits into autoimmune and mechanical. I will make a diagram for all this at some stage.

I was struggling to come up with an adequate explanation for her acute episode of pretty severe normocytic anaemia. I decided the best plan would be to treat her anaemia, and then review what symptoms if any she had post transfusion. I went to see the consultant ready to defend the decision to avoid D-dimers or a chest xray in this case unless she does not respond to the transfusion.

I was relieved and heartened by the consultant agreeing with this. So many AMU clerkings get ‘routine’ chest xrays, and I do not understand this. If you are struggling to put something meaningful on the chest xray request card, surely that should be an indication to think twice about whether or not it is justified, not to make up that you heard crackles on the left base on examination as I have seen and been encouraged to do by several doctors.

As for the cause of the anaemia, the consultant asked me to link cancers in general to normocytic anaemia, going back to pathology. Having just tutored in the 6 hallmarks of cancer, I thought of tissue invasion and the bleeding risk. This was not was he was after. He asked me to think again about the metastatic nature of the cancer. It went to the bone, and then my eureka moment. The bone marrow. Any cancer causing lytic lesions in the bone could eventually invade the bone marrow itself.

As for the intermittent symptoms, my consultant told me he was not worried about PE or pneumonia.

“Only four things cause intermittent symptoms in medicine, and they are all electrical.”


“Yes, electrical. Seizures are electrical. Neurological pain is electrical. Arrythmias are electrical. Muscle spasms are electrical. Pretty much all intermittent symptoms are one of these four. ”

“What about colic?”

“That’s surgical.”

The more I thought about it, the more I agreed. There were some exceptions, like osteoarthritis pain being worse on exertion and then clearing, or calf claudication worse on exertion. I think this concept could be improved by adding the word ‘spontaneous’. This would exclude symptoms that clearly arise following a provoking factor. I am struggling to come up with an exception to the rule that all spontaneously intermittent symptoms in medicine are electrical in nature, and are one of a seizure, neurological pain, an arrhythmia or a muscle spasm.

Any ideas?