Wednesday, 7 March 2007

Quiz No 2

Today is a quiz. I have included a short history and physical with some nice pictures for you to interpret. There are no formal blood results for you to rely on.

This patient presented with a sudden onset of cough and dyspnoea.

Patient remained breathless for 4 days before presenting to hospital.

There was no sputum produced and no haemoptysis.

Patient complained of a dull chest ache when coughing. There was no acute / sharp chest pain.

The patient had a previous history of angina pectoris and rheumatoid arthritis.

Daily medications included: Prednisolone, amlodipine, ISDN, ranitidine.

Patient was a non-smoker.

There was no history of DVT /PE.

On examination:

Temperature of 39.1, pulse 120 regular, RR= 25/min, SpO2 95% on 5 L O2, BP 120/80.

Drowsy consciousness but able to answer questions

Dry tongue and decreased skin turgor

Aortic ejection systolic murmur and tachycardia.

Dullness to percussion at left base and coarse breath sounds. No crackles.

Abdomen within normal limits.

Right lower limb very warm more than left. No evidence of calf muscle tenderness / dilated veins / redness / pain. Mild oedema bilaterally but equal in amount.

Blood Gas: Hypoxaemia SpO2 70mmHg (room air), pH 7.46, HCO3 22, pCO2 30

Chest Xray

CT scan

Question 1: Give two possible diagnoses that may coexist.

Question 2: What does the CXR show?

Question 3: What does the CT scan show?

Question 4: What other two important blood tests would you do to separate the two diagnoses?

Question 5: What treatments would you start empirically in this acutely in this patient?

Please send me your answers and they will be moderated and published.

Answers in one week from today !!

Tuesday, 6 March 2007

Clot versus Bleeding-- The Dilema

This is a great case! I hope you find this interesting. As usual, it has been anonymised.

A male patient of 55 had recently been on a short holiday to Hokaido and had been well during that time.

On coming back to central Japan, he was feeling unwell with a sore throat and was diagnosed with influenza. Unfortunately, he fell over sustained a contusion to the right knee leading to severe bruising and a swollen, painful knee.

He was bed bound for two days and slept most of the time.

On the night of admission, the patient got up from bed and he was seen to slowly slump to the floor with a loss of consciousness for 1 minute. The patient's right arm was seen to move erratically for up to 20 seconds similar to a seizure. There was no tongue biting and no urinary incontinence. The patient awoke after a few minutes and his consciousness was clear.

On arrival to hospital, the patient was noticed to have low oxygen saturations.

Examination revealed mild fever 37.8, pulse 70 min and regular, BP120/80 (lying), RR 24/min. SpO2 was 80%, Patient was over weight.

Red throat.

CVS- JVP- not raised. Sounds 1 + 2 normal. No mumurs.

RESP- mild right sided crackles that mostly cleared on coughing.

ABDO: Within normal limits.


Right Lower Limb: Swollen, severely bruised. Right patella was painful and easy to move. There was a mild patella tap consistent with a probable intra-articular bleed.

The left leg was normal.

ABG: revealed normal pH but severe Hypoxaemia (PaO2: 52mmHg).

CXR: Nothing focal. No pneumonia or other obvious lung pathology.


Bloods: Slight neutrophilia and raised CRP.

Knee Xray: No obvious fracture seen.

CT head: NAD

In view of the collapse, and profound hypoxaemia with the history of leg injury and immobilisation plus an overweight body habitus, Pulmonary Embolism was suspected.

A Spiral CT was performed which showed thrombus in the right and left pulmonary vessels. A perfusion scinitigraphic scan was performed which showed multiple small perfusion defects consistent with small PEs seen on the spiral CT.

Doppler scans of the lower limbs showed no evidence of thrombus.

Echocardiogram revealed a relatively normal pulmonary artery pressure of 26mmHg but the Right Ventricle was slightly distended with 1st degree Tricuspid Regurgitation. Ejection fraction was 68%.

Hence, the physicians had made the great diagnosis of PE.

The patient was eventually commenced on heparin treatment by his physicians.

The patient's limb remained unchanged and the heparin was successful.

An excellent comment I received from a senior doctor suggested that in such cases heparin should always be commenced even if the patient's limb becomes compromised whilst treating PE to save the patient's life.

That is a tough decision to take for any doctor and is the balance between treating the patient but also trying to do no harm to your patient.

Do you agree with this approach?

What would you do in such a situation?

Without your comments other doctors or students are unable to learn so please give your opinion on this blog.

Monday, 5 March 2007


Todays comment is in respect of seizures.

There are many, many causes of seizures and when a patient presents in a post-ictal state with there being little or no history available, it becomes the physicians responsibility to hunt for the cause.

For example, we recently had a case of a 65yr old diabetic female who presented with a new history of seizures. As always, this case has been anonymised.

She had been previously well.

She was diabetic, with an old MI and had been a smoker in the past.

She was taking anti-hypertensive agents, atorvastatin and aspirin.

She had three seizures and was treated with a phenytoin infusion which halted the seizure activity.

Blood pressure on admission was 199/95

The patient had apparently not bit her tongue nor had any incontinence.

When examined by a senior doctor, the patient the following day, GCS was 15/15.

Pupils equal and reactive to light. The patient was complaining of a severe bitemporal headache and neck pain. It was painful flexing the neck forwards.

The patient had clearly bitten her tongue and she had dry faeces on her legs suggestive of faecal incontinence.

Cranial nerve examination was normal apart from chronic diplopia that predated this event.

Tone was normal throughout the lower limbs.

Pronator drift was absent.

Power and reflexes were normal throughout.

Babinskis were negative.

Kernig's Test produced BACK PAIN but the patient had had a lumbar puncture the night before.

All bloods were negative and CRP was 0.01

CXR was normal.

CT and MRI had been considered non-diagnostic, but when I reviewed the scan I noticed a very small intracerebral haemorrhage that was very easily missed. There was no SAH visible.

However from the above, it was clear that this patient being a diabetic with hypertension and on aspirin succumbed to an intracerebral haemorrhage resulting in recurrent acute generalised seizures.

In view of the positive meningeal signs it was of concern to me that there may have been subarachnoid extension of bleeding.

On the other hand, the neck pain and headache may have been due to his severe seizure activity and the lower back ache may have been related to the previous traumatic lumbar procedure.

The patient had her aspirin stopped and under went a CT angiogram which revealed no SAH and the patient was referred for a neurosurgical opinion.

However, the only way to truly rule out an SAH is to perform a repeat lumbar puncture to look for xanthochromia.

The above case is an excellent example of a common cause of seizures.

Always consider the back ground previous medical history and always look at the drugs as these may cause or complicate seizures.

In her case, being diabetic on insulin could have resulted in an hypoglycaemic seizure; being an ex-smoker could have caused lung cancer, cerebral metastases and secondary seizures. Being hypertensive and taking aspirin can result in intracerebral bleeding and secondary seizures as in this case. Taking anti-hypertensive agents such as thiazide or loop diuretic agents can result in hyponatraemia and seizures.

The history is of prime importance if it can be elicited from friends or family.

Please let me know your comments.