Admission reason

A 67 year old man presented with increased sleepiness.  3 days prior to the admission, he collapsed in the garden, witnessed by daughter. He attended A&E and he was discharged on the same day with head injury advice. Since then, he had been on increased sleepiness even in day times. Wife stated that he fell into sleep while talking.

He stated that he had a 6 month history of headahce, for which he had been seen by neurologist for headache with once a month follow-ups. Imagings had been done. Diagnosis was not conclusive. It was suggested  ?Trigeminal neuralgia.

So I put the presenting complaints as

1.    Headache for 6/12
2.    Increased sleepiness for 3/7

My consultant was not convinced my statement. He wrote down in his post take ward round section “admitted with increased sleepiness”

It is true. In fact patient did not come to hospital for headache, but for sleeping issue. His headache has been already under the management of neurologist even though recent issue could be related with previous issues. This consultant is very particular. His documentation is awesome. (He has got a unique hand writing style as well)

What a coincidence! Next day, A&E middle grade doctor referred me a young lady with toothache. It was found out that she took 10 grams of Paracetamol in 20 hours prior to admission. Toxic base suggested that paracetamol more than 150mg/kg in 24 hour is toxic level in non-high risk group. Her figure is 166 mg/kg. A&E happily started parvolex. Interestingly,  no management plan for toothache until she was moved to medical assessment unit. Of  course, they just forgot the reason of admission. I prescribed regular codeine and co-amoxiclav. We had to organize urgent dental appointment.

The same thing happened fortnight ago. A young chap was found out paracetamol overdose by A&E, following ear ache. Parvolex was started. When I saw the patient in medical assessment unit, he was in an agony of pain. His ear had full of pus. We had to transfer him to ENT hospital straight away.

Yes, reason of admission is very important. We must not forget to act it.

Symptomatic anaemia or/and Pulmonary Embolism

During my recent on-call, a 33 year-old-lady was admitted with a 2 hour history of sudden onset central chest pain started while she was in bed. No shortness of breath and no other respiratory symptoms. No palpitation. It was revealed that she had been easy to get tired in last 4 weeks. She gave 10/28 rather heavy menstrual history. Not investigated for that before.

She is a normally fit and well beauty therapist. Apart from previous ectopic pregnancy, nil significant medical issues in the past. She is not on any medication and no know drug allergy.

She is a mother of a son. Life long non-smoker and she drinks a couple of glasses of wine in the weekends. Family history was nil significant.

On examination, she looked well. Mildly pale. Apyrexia, normotensive. Pulse was 78. Cardiovascular, respiratory, abdominal examinations were unremarkable. No calf muscle swelling. No pedal oedema.

CXR:NAD, ECG NSR.
Admission blood tests showed Hb7. Low MCV and MCH. Otherwise, normal U&E and LFT.

My impression:

1.    Chest pain secondary to anaemia
2.    Hypochromic microcytic anaemia secondary to menorrhagia

So my initial management was

•    Iron study
•    Blood film
•    12 hr Trop to rule out ACS
•    Not for blood transfusion for the time being
•    If iron low, for iron replacement
•    If iron normal, Hb electrophoresis and haematology referral
•    Gynae referral for menorrhagia

My time was over and I went home.

2 days later,  I found her on the hospital push chair and the porter was bringing her to the CT department. That made me surprised.
So I did check her note when I had time.

I found out that she was discharged later on the day of admission with iron tablet. But someone checked repeat Hb which was 6.5 (Admission Hb 7). So she was called back for blood transfusion. In view of on-going chest pain even after discharge, CT PA was requested, which came back bilateral PE. What are the risk factors? I can not find it. Maybe a coagulation disorder.

Gynae team also reviewed her and requested USS Pelvis which showed fibroid in the uterus, explaining the cause of menorrhagia.
She had been on loading dose of Warfarin and therapeutic Clexane while waiting for target INR.

Anyway, I am happy she looked comfortable. She has been in right direction. But clearly, we still need to find out the cause of PE. I wish she does have nasty malignant disease.

History of the classification of COPD

Classification of severity of airflow obstruction (when post-bronchodilator ratio of forced expiratory volume in one second (FEV1) to forced vital capacity (FVC) is <0.7)

The use of platelet transfusion

 

Here are the some recommendations of the use of platelet transfusion.

If you go to BCSH guidelines, you can get the full version.

 

Prophylaxis for surgery

Haematology guidelines

 

BCSH guidelines are here

GI bleed after recent NSTEMI

During my on-call time, a 88 yr old chap came in with 2 bouts of coffee ground vomiting, preceded by a feeling of indigestion.

His background showed

  • NSTEMI 4week ago with 12 hr Troponin 2.88
  • Angiography  2 weeks ago ( 3 vessel disease: only for medical management in view of co-mobidities)
  • 2 storkes (first 1998 with residual Lt weakness, 2nd 2008 with right weakness)
  • Multiple TIAs (last time 8 months ago)
  • Type 2 DM on Metformin
  • Ex-smoker (30 pack years)
  • Wheel chair bound

Medications

  • Asprin (has been for more than 10 years)
  • Clopedogrel (after NSTEMI)
  • Ramipril
  • Simvastatin
  • Metformin

On examination

Insulin regimens

In normal physiology, there is a basal insulin secretion regardless of eating. There is an extra rise of insulin after eating. So, in type 1 diatebes, patient needs base line insulin with or without eating. It is for the normal body metabolism.

 Next, we need to be familiar with type of insulin and names before prescribed. There are 2 main insulin production companies, which are Novo Nordisk and Eli Lilly.

Basically, the followings are the types of insulin we are commonly using at my work , despite a variety of preparations.

1980-1990 (R-DNA)

  • short acting :Actrapid, Humulin S
  • Intermedate and Long acting: Insulintard, Humulin I
  • combined: Mixtard 30

1990-2007 (Analogue)

  • Short acting: Humulog, Novorapd
  • Intermedate and long acting: Glargine, Levemir
  • Combined: Novomix 30, Humulog Mix 25

Hululog has more rapid action than Actrapid.

How to give:

ACS in Omeprazole

We saw many patients who came in with ACS, have been in Omeprazole for their stomach problem.

ACS protocol needs to start Aspirin and clopidogrel. Omeprazole significantly decreased clopidogrel inhibitory effect on platelet according to the evidence based medicine.

So we replace Omeprazole with Ranitidine.

Here is the related article on HeartWire.

Munich, Germany - A new study using platelet-aggregometry testing to assess the effects of different proton-pump inhibitors (PPIs) on platelet response to clopidogrel suggests that omeprazole might be alone in adversely interacting with the widely used antiplatelet therapy [1]. The study, published in the April 2009 issue of Thrombosis and Haemostasis, hints that other PPIs tested—pantoprazole and esomeprazole—might be a safer bet for minimizing gastrointestinal side effects and bleeding in patients requiring long-term clopidogrel treatment.........See more here
http://www.theheart.org/article/960023.do

How to diagnose PAF on take?

A&E referred me this 57 year old lorry driver presented with so called chest pain during my on-call hour.

I reviewed A&E notes, blood test results, ECG and CXR before seeing the patient. All routine blood tests were normal and admission Troponin was negative. ECG was normal sinus rhythm with no T/ST change. CXR unremarkable.

When I chatted with patient properly, it was not really a chest pain.

He expressed he never experienced such a strange feeling while watching tele. Patient described it as "Bang" "Bang" twice from his heart, followed by pounding heart. The attack last about 30 mintues.

At this point, I got a clue. So I asked the patient to tap the bed with his hand as he felt duing the episode. It was revealed that he tapped with vearying rates and varying intensity.

Interestingly, this patient has a knowledge how to feel his radial pulse. He said he felt his pulse that time,which was sometime fainting and sometime strong.

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