What would be recommended first line pharmacological treatment for this patient?

This patient has nodal osteoarthritis (OA). This is a condition of synovial joints characterized by focal areas of damage to the articular cartilage and remodelling of underlying bone. OA affects up to 20% of the population who are greater than 60yrs of age. The main symptoms of OA include pain and immobility. In the photos graphs you can see classical Heberden's nodes in her DIP joints. Similar nodes at the PIP joints are termed Bouchard's nodes. The CMC joint in the hand is also commonly involved in nodal OA. Interestingly this lady has OA of the hip - hence the walking stick.

In most cases paracetamol is an effective and relatively safe treatment for patients with mild-moderate OA pain. NSAIDs have been proven to be effective in reducing OA pain but they do carry risks such as gastric ulceration; adverse renal effects and precipitating relapse of heart failure. Up to 1.5% of NSAID users per year develop serious upper GI complications such as a major bleed or perforation. More patients die of NSAID related upper GI bleeds, ulceration and perforations per year in the UK than RTA related deaths. There is conflicting evidence that topical NSAIDS have long term benefit, if any in OA. DMARDS have no place in the treatment of OA.

What is the initial treatment priority?

Patients with DKA, tend to be significantly dehydrated due to osmotic diuresis, and reduced fluid intake. In adults this is usually at least 3.5 to 7 litres.

A treatment plan for DKA would typically be:

• Check blood gas, capillary glucose, U+E, blood glucose, FBP.
   
• Give IV Normal 0.9% Saline - at rate of 15 to 30 mL/kg per hour for first two hours, then at reduced rate. Be careful in children, as rapid rehydration can increase the risk of cerebral oedema.
   
• Give typically 10 units actrapid insulin subcutaneously (although the subcutaneously route may absorb poorly if patient shut-down), followed by infusion at a rate of 2 to 6 units per hour.
   
• Monitor potassium and capillary blood glucose - depending on U+E, typically starting KCl+ at 20 mmol per hour at in second hour.
   
• Change to IV dextrose when capillary blood glucose falls, and continue with insulin infusion. The aim is to correct acidosis by flushing out the ketones, not just to correct the blood sugars.

What is the commonest cause of large hepatosplenomegaly in UK/Ireland?

Hepatosplenomegaly is enlargement of both the spleen and liver. Causes include:

(i) Haematological disease - Myeloproliferative disease, Leukaemia, Lymphoma, Pernicious anaemia, Sickle cell anaemia, Thalassaemia.

(ii) Acute Infection - Acute viral hepatitis, Infectious mononucleosis, Cytomegalovirus.

(iii) Chronic liver disease (including Chronic alcohol abuse, Chronic active hepatitis, NASH, Amyloidosis, Acromegaly, Systemic lupus erythematosus), with portal hypertension. In the early stages, cirrhosis can cause liver to enlarge, and indeed alcoholic hepatitis can produce tender hepatomegaly, but later as more scar tissue replaces normal tissue, the liver shrinks.

Which of the following fluid regimes would be most appropriate?

Often colloid (eg. Gelofusion or Voluven) is recommended as it stays in blood vessels longer - but crystalloid (eg. Normal Saline) can be used.

The important thing is to give a small volume rapidly - this will not run through a drip counter (as drip-counter max rate is typical 999ml/hour) - whereas 250ml Normal Saline over 2 minutes = 7500ml/hour (although some suggest using a longer time of 10 minutes). A wide bore (16 or 14 gauge venflon) is needed. Measure the blood pressure before, during and 5 minues after this bolus.

If the pulse falls and BP rises this indicates the patient is hypovolaemic (absolute or relative) eg. from blood loss or sepsis, so more fluid should be given. It is also useful to note the duration of any BP rise.

(For more info see: Surgical Tutor - Fluid balance and: Student BMJ - Fluid challenge)

Causes of hypotension: (use mnemonic CPR):
  C = Capacitance - eg. volume loss from dehydration, diarrohoea, internal/external bleeding, burns.
  P = Pump failure - eg. MI, valve prolapse, tamponade, beta-blocker overdose.
  R = Resistance - eg. increased in PE, decreased in sepsis/SIRS as vasodilation.

What does this show?

The ECG has P-waves so is not Atrial Fibrillation (AF).

Is not First degree heart block as that would have long PR interval.

QRS's are narrow so is not VF nor VT.

Is not an Agonal rhythm which would be extreme ventricular bradiacardia, with wide flattened QRS.

It is Wolf-Parkinson-White (WPW), as has shortened PR interval (less than 3 squares < 120ms) and delta waves (slurred upstroke to the QRS indicating pre-excitation), as shown in diagram below. This delta wave is the classical feature. The QRS may be broad, and there can be secondary secondary ST and T wave changes. WPW is due to an accessory pathway between atria and ventricles. Patients present with SVT which may be due to AV re-entry tachycardia, pre-excited AF, or pre-excited atrial flutter. In symptomatic patients, the ideal treatment is to use radio frequency catheter ablation to destroy the accessory pathway.

WPW showing shortened PR and delta wave.

A good illustration of normal, and Wolff-Parkinson-White Syndrome accessory path-way.

(For more info see ECG links on Links page on www.medicalfinals.co.uk.)