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.

Guess what!

Guess what first! I will tell you the story later.

Lactate 17.66 mmol/l [0.65 2.45]

Alkaline Phosphatase 150 IU/L [30 115 ]
Albumin 32 g/l [35 50]
Calcium 2.55 mmol/l [2.20 2.60]
Phosphate 3.56 mmol/l [0.80 1.45]
Corrected Calcium 2.77 mmol/l [2.20 2.60 ]
Total Protein 75 g/l [64 83]
Globulin 44 g/l [21 39]

C-Reactive Protein <10.0 mg/l [0 10.0]

TROPONIN I (Random) 0.04 ug/l [0 0.08]

Sodium 136 mmol/l [135 145]
Potassium 4.8 mmol/l [3.5- 5.0]
Chloride 100 mmol/l [98 107]
Urea 7.5 mmol/l [2.5 7]
Creatinine 155 umol/l [70 120]

ABG
pH 6.78 [7.35 -7.45]
pCO2 13.2 kPa [4.7- 6.0]
pO2 10.7 kPa [11 -14.5]
Base Excess -22.0 mmol/l [-3.0 3]
Hb Fract Sat 78.9 %
Hb Oxygen Sat 79.8 % [91.9 98.5]

Magnesium replacement

This regimen is what we use at work. I don't take any responsibility if something went wrong. It is only clinical judgement and local protocol.

For rapid replacement (ICU setting) , 5g of Mg in 250 ml of 0.9% NaCl in 2 hours (Cardiac monitor/Telemetry required)

For slow infusion (ward), 3 gm in 0.9% NaCl 250 ml in 6 hours.

 

 

Related article1

Related article2

 

Cause of weight loss

74 year old man admitted with weight loss, Nausea and vomiting, Rt hip pain.

He has been under investigation for weight loss of 18 kg in last 3 months.

Back ground history showed

  1. COPD on Inhalers for many years
  2. Ex smolers (stopped 16 yeras)
  3. MI 1999 4.planned for total hip replacement by ortho.

On examination, he appeared well and alert apart from a thin body with scaphoid abdomen. Neuro, CVS, Resp and abdo exams nil significant. No leg oedema.

Recent OGD and Colonoscopy showed nothing.

FBC and U&E normal

CA 199 and CA 125 borderline high

T4 (15.5)normal and TSH (0.18) slightly low.

Sputum AFB pending.

We requested for CT (abd and thorax) Any comment?

Update: 10/12/2009:

Gouty arthritis to Care pathway

This 79 yr old man admitted with feeling unwell and knee pains.A&E saw and got orthopedic doctor to have a look, suggesting that less likey septic arthritis. But joint aspiration done and awaiting MC&S.

Referred to medics. ( It was me)

Background history showed

  • COPD on LTOT under respiratory physician
  • CKD stage 4,
  • LVF under cardiologist
  • Gout

We got rhuematologist to see him.Hight Uric acid on repeat blood test. Colchisine started. Paracetamol and Codeine were regular analgesics.

Pain settling in next a couple of days. Joint aspiration came back as negative culture. we start Phyiso and Occupational input for discharge.

But during the last weekend, he got a sudden onset abdo pain and vomiting. I was asked to see.

Family was around. He looked miserable. Holding sick bowl in which foul smelling fluid.

Amphetamine overdose

This young chap in his early 20s came in with Amphetamine overdose. He also took unknown excess amount of C-codymol tablets.

He looked anxious. CK came back as 44,567.

We did supportive measures , including hydration.

Repeat blood next day showed CK 16,880. Phosphate low.

I will add updates

 

Quinolones and Epilepsy

Not particularly drug interaction, Quinolones reduce the seizure threaddshold. we came acoss pateints presenting with fit after Ciprofloxacin was started.

It is also reported that quinolones associated with tendon rupture. especially Archille's

 

Choking

It was 11:45 PM. I was called some one had been chesty and vomiting.

I arrived at 11.50 PM. At first glace, I thought she was lying on her left side and sleeping. But when I tried to wake her up, no response at all. The nurse was around.

I asked her if she is for resus. Answer was yes. The crush team arrived by mid night.

I ran through the note. 78f admitted with symptomatic anaemia, still under investigation. Past medical history shows hypothyroid and hypertenstion only.

Blood 2 units was given previously. No previously episodes of vomiting.

Only on that night, she was not well with chesty and vomiting.

We commenced CPR. It was PEA. ECG monitor showed VT. We followed Resus guide lines while establishing IV access and taking blood gas, U&E, FBC. BM was 7.

After 6 minutes, rhythm changed to VF which was shokable. After 3x shocks, rehythm changed to VT again.

We considered reversible causes 4H and 4T.

Courses

We are taking courses whenever we have a chance as a part of continuing medical education. At the same time, we need to feed our hobby, exploring and practising medicine.

You may already know this website.

http://www.mkupdate.co.uk/courses.php

There are loads of other websites for cousrsesIf you are interested, you may book in advance. 

 

 

 

Trop 1.5 in 2 hour time

Not exciting, but interesting to me

During last weekend oncall, 47M came in with 10 hr history of chest pain. Central chest pain, 8/10. radiated to lt shoulder.

PMHx: Nil significant, No DM, No HTN

FHx: 3 brother died of MI at the age of 47, 49, 52. Sister had heart attack, but she survived

SHx: never smoke, occasioanal drinker

Cholesterol: DK

O/e Still on pain 3-4/10 on GTN as A&E started

CVS: NAD

Resp: NAD

Abd: NAD

Legs: NAD

ECG: T flat in lateral leads, otherwise normal

CXR: NAD

Trop I on Adm (10hr) 0.05

Interestingly 12 hr Trop I came back as 1.5.

So he is for CCU and to continue with ACS protocol. He needs agniography / and angioplasty

 

2 Questions in my mind

1. Why Troponin I soared from 0.05 to 1.5 in 2 hr time, instead of gradually rose?

2. What would be the genetic association of the patient's condition?

Efalizumab Withdrawn From US Market

Efalizuman is a recombinant humanized monoclonal antibody that binds to CD11a. Because of its side effect, it is to be withdrawn from market in the USA. 

April 9, 2009 — Efalizumab (Raptiva, Genentech, Inc) is undergoing a voluntary, phased withdrawal in US markets because of a potential risk to patients of developing progressive multifocal leukoencephalopathy (PML). Source

When we dont need to offer Abx for IE prophylaxis?

Do not offer antibiotic prophylaxis against infective endocarditis:

– to people undergoing dental procedures
– to people undergoing non-dental procedures at the following sites:

 

  1. upper and lower gastrointestinal tract
  2. genitourinary tract; this includes urological, gynaecological and obstetric procedures,and childbirth
  3. upper and lower respiratory tract; this includes ear, nose and throat proceduresand bronchoscopy.

Do not offer chlorhexidine mouthwash as prophylaxis against infective endocarditis to people at risk undergoing dental procedures.

 

Quick NICE lines

Non accidental injury

Nearly ending up in trouble. It also happened in yesterday's oncall

A&E tried me to refer 86 yr old bed bound lady from nursing home cam in with ? elbow injury.

Once I heard 2 facts, 1. from nursing home 2. elbow injury, I was not so interested in that patient.

You know about nursing home. You know the reason why people need nursing home.

I was too tired at that time as I had been busy in last 10 hours with acute patients. My brain not working well. So i tried to refuse to accept patient as medical.

I am impressed. A&E staff grade is very expereience. She was upset when I tried to refuse. But she was patient and explained again.

86 yr,from Nursing home

demented,

bed bound,

not walking,

but 2 injuries on elbow and hip.......

 

Oh my god

what came to my mind is baby P

Fake arrest call, but saved the life

It happened in recent on-call.

80 yr old man brought in by ambulance with feeling unwell, confusion and collapes. Seen by A&E doctors in resus. ECG showed 5-6 p wave with 1 QRS.

I was referred. in 10 min, rapidly deteriotaed. BP went down to 80/50. GCS also going down. He needed emergency pacing, which is external pacing first, beofore sending to cath lab.

We did fast bleep to anaesthetist to come down. We did fast bleep to cardio reg to come down. 5 min wait while we started praparing to anaesthetise patient for external pacing . For some reason, nobody arrived apart from cardiology nurse who made ready for external pacing.

So we had to make arrest call. 2222. All crash team arrived in 2-3 mins, anaesthetist registrar, cardiology registrar and other on-call people.

BP picking up after a few minutes after external pacing.

For active treatment or for palliative care?

Last week, a 56 year old, known alcoholic liver disease and Stage 4 adenocarcinoma of lung, came in with confusion and abdominal discomfort. His lung cancer was diagnosed 10 months ago and he refused any active intervention. He has cirrhosis of liver with ascite. He had drain 1 month ago. He has a carer who is his friend living together. His brother was out of contact.

On admission, well conscious. No focal neurological deficit. Hb 9. LFT: Albumin 19.

Day 1, decided to drain. 6 hour drain according to hospital guide line. No evidence of infection in ascitic fluid.

Day 2 looks fine

Day 3, slightly less alert.

75 year old male with fall

75 male, previously independent

Admitted with

fall while walking (tripped)

Neck pain

No loss of consciouness

BG: Prostate problem with normal PSA

Medication: Tamsulocin, Finasteride

Initial investigation:

FBC Normal, Urea 10, Creatinine 135,

XR (cervical spine): nil significant

Initial mamangment:

Bed rest

Neck collor

orthopaedic review after MRI spine

Analgesic

During first week:

Orthopeadic surgeon excluded any cervical spine injury

Renal function getting worse with Urea 14, Creatinine 220. (which is new for him as creatinine in 2 months ago was 112)

86 year old lady came in with back pain

86F, who lives on her own, normally mobile without any aid

PC: Back pain following a fall

mechanical fall

pain at lower back

felling weakness of lower limb

BG: Hypertension, Angina

Meidcations: ACE I, beta-blocker, Anti-angina, Aspirin

O/E

generally well.

CVS: Nil significant, but BP 90/50

Resp: NAD

Abd: NAD

CNS: AMT 9/10, no focal neurological deficit

Investivation:

Hb 10 with MCV normal, U&E normal, Calcium Normal

ECG: nil acute

CXR; slight cardiomegly, lungs clear

XR (Lumber): suggested fracture at T12 with minimal compression.

In flight Tuberculsis

Streptokinase installation

You know the indication for Streptokinase installation in patients with pleural effusion/ empyema.

 Here is our routine.

Once indicated,

Streptokinase 250,000 units mixed with Normal saline in 50 ml syringe (total volume 50 ml)

put into chest tube

Flush with 50 ml of Normal saline.

We do it 12 hoursly for 3 days

and then review

if the patient need ?surgical intervention or not

Pleurodesis step by step

it is a painful procedure. So enough analgesics and local analgesia required:

  • 5 mg Oramorph 30 mins before procedure
  • 20 ml of 2% Lignocaine 20 mins before
  • Flush with 20 ml of Normal saline
  • Wait 15 mins
  • put 2 g of Talc (rate is not to fast /not too slow.. for about 1 min time)
  • Flush with 20 ml of N.saline
  • Clamp for 2 hours
  • Unclamp and leave over night
  • Remove the chest drain next morning.

Issue in this procedure is pain control.

In some hospitals, they do not give oramorph.

Need to follow hospital/local guide line

yes, there is a slight variation.

Here is BTS (British thoracic society) guide line

Titofiban : Glycoprotein IIb/IIIa inhibitors

Glycoprotein IIb/IIIa inhibitors tirofiban

Indications


Patients with continuing chest pain who are considered at high risk and would benefit from early coronary revascularisation should receive glycoprotein IIb/IIIa inhibitors. Those with the following features are at particularly high risk of infarction or death:

• Recurrent ischaemia (symptoms) – ongoing ischaemic chest pain

• Recurrent ischaemia (ECG changes) – ST-segment depression- T-wave inversion

• Troponin I elevated > 0.4 ng/ml

Addenbrook Hospital Antibiotic guide line

Addenbrook's antibiotic guide line

DKA Guide line

DKA guide line

Methotrexate guidelines

Methotrexate guide lines

Insertion of a central venous catheter

About insertion of a central venous catheter

A central venous catheter, or central line, is a long hollow tube made of silicon rubber which is placed into one of the large veins in the body. One end of the line remains outside the body and can be used for injections. The other end is positioned inside a large vein, usually near to the heart. There are a number of veins into which the catheter can be placed; the most common being the axillary vein that lies just beneath the clavicle (collar bone) or the jugular vein that lies just above the clavicle at the base of the neck.

Insertion of a PICC

A peripherally inserted central catheter (PICC) is a long hollow tube that is inserted into one of the large veins your arm. One end of the tube sits in a vein (usually just above the heart) and the other end comes out from underneath the skin in your arm. The catheters are usually recommended for patients who need certain types of medicines or treatments that are irritant or damaging to smaller veins; or whom need injections over a long period of time. Insertion of the catheter requires a sterile operation, which is usually performed under local anaesthetic. More information on PICC’s is given in the further information section below.

Mental capacity and consent to treatment guidance for clinicians

1.1 Treatment without valid consent is potentially an assault. In most cases gaining valid consent is straight forward, as most patients are clearly able to understand the information presented.

 

1.2 Where this is not the case, there is a problem because nobody else, not even the next of kin, can give consent on behalf of an adult who lacks capacity (this is different for children).

 

1.3 It is important that all doctors have a clear understanding of the relevant issues relating to Capacity to Consent to treatment and how to assess the patient’s capacity to make decisions, especially in respect of consent to treatment. If you have any concerns about your ability to adequately assess capacity to consent you must involve a senior colleague

Antibiotics guide line

short antibiotic guide line

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