Friday, 20 April 2007

Wow What A Case!!!!

This anonymised case concerns a middle-aged male patient who presented to another hospital with a five day history of:

  • Pleuritic chest pain
  • Cough
  • Fever
The pleuritic chest pain was associated with breathing and was sharp in nature. In did not occur on moving. There was no central cardiac chest pain of ischaemic origin. The pain was also described to be in his back but it was not tearing in nature.

The cough was non-productive and intermittent.

The fever was low grade in its characteristic. He denied rigors and sweats.

The patient had been initially seen five days previously at our ER department and it had been considered that he had pleurisy and he was given acetaminophen and allowed home. However, these symptoms got worse and the patient was seen at the outpatients with the new symptom of Haematuria which was non-painful with there being no urological symptoms.

On examination she was stable but appeared in pain.

Pulse was 90/min, JVP was raised, BP normotensive but there was a drop of approximately 10mmHg in blood pressure during respiration. Temp 38 degrees and RR was 14/min. Sats 89% on room air.

Lymph nodes were not paplable.

The patient had dullness at both bases. With the patient sat forwards there was a loud sharp murmur in the tricuspid area on Inspiration which disappeared on Expiration. On lying flat, there were some audible crackles over the lower left parasternal border.

Whereas the initial chest Xray had been normal, then second one, just a few days later, revealed bilateral mild effusions and a globular heart. Her initial ECG when performed in the ER was normal, but the second revealed 1mm ST elevation in V5 and V6 with no reciprocal changes and no ST saddling or P-R depression. The voltage was also reduced.

Bloods revealed a raised white cell count, CRP 3o, slightly raised bilirubin but normal AST and ALT. ALP was slightly raised but no isoenzyme was taken. The haemoglobin was within normal limits. Renal function was normal. CK and CK-MB were not raised.

The suspected diagnosis was an acute pericarditis.

A cardiac echo was performed which revealed a rim of pericardial fluid with there being no RV collapse. There was no evidence of a vegetation either.

CT scan was performed which revealed the same pericardial effusion plus bibasal pleural effusions.

It was suggested that the effusions should be examined and the fluid obtained was yellow 'straw' coloured but slightly turbid. The white cell count was >3,000 and the pH 7.3. The sample was sent for Rheumatoid factor, culture, LDH, Glucose and TB examination.

Possible causes of acute pericarditis include:

Drugs and Toxins
  • procainamide
  • hydralazine
  • phenytoin
  • isoniazid
(Produce a Lupus-Like Syndrome)

  • Viral: Echovirus, Coxsackie
  • Bacterial: Streptococcus spp (particularly pneumococcus), Staphylococcus, Mycoplasma, TB, Haemophilus
  • Fungus: Histoplasmosis, candida, aspergillus, coccidioides
  • Recent cardiac surgery / intervention e.g PTCA
  • Post-AMI
  • Dressler's Syndrome
  • Post-Radiation therapy
  • SLE, RA, MCTD, systemic scleorsis
  • Infiltrative neoplastic diseases e.g. primary or secondary tumors
  • Lymphoma /Leukaemia
  • Uraemia, Hypothyroidism

Well, this is a very interesting case as the patient had clearly developed a percarditis and a rapidly enlarging effusion with signs of tamponade e.g. drop in BP and raised JVP. The murmur on sitting which disappeared on lying may be due to haemodynamic changes with venous flow changes. The typical scratching pericardial rub is also usually found with the patient sitting forwards BUT it is classically heard on Expiration not Inspiration.

The rapidly enlarging pericardial effusion with ensuing tamponade should prompt for the patient to be considered for pericardiocentesis. In this case, the pericardial effusion stopped enlarging and thus far, he has avoided requiring this procedure.

In respect of the haematuria and raised bilirubin level of which both direct and indirect bilirubin were raised, may be consistent with an intravascular haemolysis although typically the indirect level is raised.

Consideration should be given to Mycoplasma as the cause, as this can produce Cold Haemagglutinins which can produce such manifestations of haematuria. However, patients tend to develop a low grade anaemia which this patient did not have. Moreover, one should not rule out infective endocarditis here either.

Due to the rapidity of her symptoms, TB was considered unlikely, but it was still tested for.

There were two considerations here:

  • Pain relief
  • Anti-microbial therapy
This patient had been taking long-term aspirin although she had no cardiovascular history. One concern was of a haemopericardium from a haemorrhagic pericarditis. The usual therapy for pericarditic pain is NSAID therapy, but all anticoagulants should be avoided if there a rapidly enlarging pericardial effusion.

Hence, one suggestion was to use opioid pain relief instead. However, haemorrhagic transformation of pericardial effusion is a theoretical risk. The patient did eventually receive NSAID therapy.

Secondly, despite the vast majority of cases of acute pericarditis revealing a viral origin, it still needed to be considered as a bacterial cause especially as the pleural fluid contained such a high amount of white cells.

Hence, it was suggested adding a third generation cephalosporin (Ceftriaxone) which would cover the vast majority of organisms explained above plus continuing the clarithromycin to cover mycoplasma.

Blood cultures revealed Gram Positive Cocci and later identified as a fully sensitive streptococcus pneumoniae organism.

Acute Bacterial Pericarditis is the likely diagnosis here although a Purulent Pericarditis had not been confirmed as a pericardiocentesis has not been performed. For that diagnosis a pericardial effusion should either be macroscopically or microscopically purulent. However, some infections such as viral and bacterial, particularly Mycoplasma hominis, do not produce a purulent effusion (UptoDate 15.1)

Infectious aetiologies resulting in a purulent pericarditis include pneumonia, endocarditis or even meningitis.

Ultimately, if this patient's pericardial effusion had failed to improve and / or her clinical condition worsens, then she would have needed a formal pericardiocentesis which has the advantage of being both therapeutic and diagnostic.

Typically, analysis of fluid in purulent pericarditis shows cells ranging from 6,000 to 250,000 per microL, low glucose of <35mg/dl style="font-weight: bold; font-style: italic;">UpToDate 15.1)

Antibiotic regimens depend on local resistance levels, the immunocompetency of the patient and whether the patient has developed the problem in the community or in hospital.

Most regimens include either a 3rd or 4th Generation cephalosporins and Vancomycin needs to be considered in view of the problems of MRSA in this era and this was later recommended in this patient.

Non- infectious aetiologies can also present with a purulent pericardial effusion such as malignancy, uraemia and recent surgery.

Finally, a transthoracic echocardiogram may miss an endocarditis and hence, a trans-oesophageal echo which has a higher yield would be advisable.

However, the modified Duke's Criteria does not require for a vegetation to be present to make the diagnosis of endocarditis, but please refer to my earlier blog on endocarditis for those details.

For a fuller explanation please see UpToDate 15.1.

The patient made an uneventful recovery and was left with a mild pericardial rub and no chest pain.

Monday, 16 April 2007

Rheumatological Case- V. Interesting

I have a very interesting rheumatological patient to tell you about.

Firstly, as always, the patient has been anonymised to safe guard confidentiality.

The patient was a middle-aged female and who presented to another hospital with a history of muscle pain in the proximal lower limbs, some upper limb-shoulder discomfort and pain in the occipital-neck area. The patient also had a low grade fever. The patient complained of no eye problem, no temporal tenderness, no jaw or tongue claudication (symptoms for Giant Cell Arteritis). The patient had no symptoms suggestive of infection. Patient had a normal appetite but had complained of some weight loss. There was no complaint of changes in bowel habit.

The was no joint pain or swelling. No skin rashes. No respiratory symptoms.

The patient had no other significant history and was taking no regular medications.
The patient had occasional alcohol and cigarettes.

Physical examination revealed a low-grade fever. Vital signs were otherwise normal. Eyes revealed a slight purple discolouration to the upper eye-lids.

The was no lymphadenopathy and cardiovascular, respiratory and abdominal examinations were normal.

Occipital tenderness was present one week previously but only seemed to be a problem when the fever was present. There was no temporal artery tenderness.

Neurological examination revealed proximal muscle wasting, some lower limb muscle discomfort on palpation. Power and Reflexes were maintained.

Clinical Impression from history and examination:

  • Polymalgia Rheumatica (PMR)
  • Possible Dermatomyositis

However, ESR >100 and CK was low NOT RAISED. Auto-antibody tests were all NORMAL although anti-JO-1 antibody is still awaited.

In view of the history, physical and blood results, the diagnosis is very likely to be PMR.

However, infection needed to be ruled out. CXR was normal. Urine examination was normal. Blood cultures were normal.

Cardiac ECHO was normal. CT scan of abdomen was again normal.

Despite this data, the doctors were advised to start antibiotic therapy with there being no evidence of a bacterial infection and a negative infection screen.

Following this therapy, steroids were advised to be commenced.

It was considered that this diagnosis was PMR in view of the history, symptoms, ESR >100 and with a negative auto-antibody and infection screen.

The concern here was the occipital pain experienced by this patient. This could represent Giant Cell Arteritis which has a significant overlap association with PMR (approx 25-30%). Patients with GCA are at risk of visual loss and arterial infarcts and need to be treated on an expedited basis with steroids and aspirin. Usually, an arterial biopsy is taken to confirm the diagnosis but even if the biopsy appears normal the diagnosis of GCA cannot be excluded as vessel changes can be multifocal.

Patients with PMR typically experience proximal muscles pain and weakness, but on physical examination, the power appears almost normal. The CK is normal although the ALP may be raised due to peri-portal inflammation. The ESR is usually high but even normal ESR can be consistent with PMR.

Dermatomyositis on the other hand can present with weakness, wasting but the CK is high as is anti-Jo-1 antibody. Other manifestations include purple skin changes around the eyes, on the dorsum of the fingers, elbows etc and are Heliotrope as so named. Patients may also have fibrotic lung changes and there is an association with malignancy (10% in patients aged >40yrs) although this is disputed. Such malignancy tends to be gastrointestinal in origin.

In this case, it was advised that the steroids be started on an expedited basis and one would have hopefully seen a response with 48 hours.

Steroids usually need to be continued for about 2 years and they are slowly tapered over that time mindful of the patient's symptoms and ESR.

This patient's blood sugars would also need to be monitored as steroids can induced Type2 Diabetes mellitus due to their multiple blood glucose elevating effects and insulin resistance.

In the long term this patient would have needed to have bone density scanning to look for osteoporosis with the treatment there being once weekly alendronate (fosamax).

Consideration should have been given to using a Proton Pump Inhibitor to reduce the risk of upper gastrointestinal bleeding especially as the patient would have been potentially taking several problematic gastric agents in the future including steroids, aspirin and fosamax.