Elderly Females and UTIs

UTI in elderly patients is a relatively easy diagnosis to make especially with urine analysis and urine culture providing the best clues.

Often, elderly patients present with fever and no urinary symptoms or they may present with just new or worsening confusion.

Obvious causes include long term Foley catheter usage and faecal incontinence causing contamination of the genital tract.

Atrophic female genitalia and with advancing age are other risk factors especially as the female urethra is shorter compared to the male.

Bacteriuria in the elderly is very common and may also be asymptomatic.

When a patient presents with recurrent UTI then further investigation may be warranted.

Patients in hospital or care homes may be infected by medical staff due to poor hygiene or other infectious patients in close proximity.

The infection may be due to a multi-drug resistant bacteria that was not effectively treated previously or the patient has been auto-infected in some way.

Of course, in younger patients, UTI can be precipitated from sexual intercourse. Also remember, elderly patients may also still be sexually active!

Other more unusual things to consider include fistula between bladder and bowel which might be due to malignancy, inflammatory bowel disease, diverticular disease as examples, which leads to direct faecal contamination of the urine.

Questions to ask include: Is your urine dark brown and cloudy? Faeces in the urine. Are there bubbles in your urinary stream on passing urine ? (not just bubbles in the toilet); this is pneumaturia and signifies gas from the bowel escaping into the urine.

The other questions of urinary frequency, nocturia, suprapubic discomfort, dysuria, haematuria, sexual activity and bowel symptoms should also be asked.

With the problem of re-infection, one question to ask the female patient is how they clean themselves following defecation. Females may put themselves at risk of faecal contamination of their genitourinary tract if they clean their anus from posterior to anterior i.e. downwards and forwards between their legs rather than away from the genitourinary tract (inferior to superior direction) i.e. from below upwards and behind them.

As mentioned, the female genital tract is anatomically more at risk of infection as the urethra is shorter than that of the male and it is more exposed to potential contamination.

Recently, on advising a junior doctor of this line of quite intimate questioning for a patient with her second severe UTI, I was met with a look of astoundment from the doctor that this question should be asked at all.

However, when he did ask the question, it was soon determined that the patient was indeed contaminating her genitourinary tract with faeces when finishing defecation and hence, she was auto-infecting herself causing recurrent UTI.

I appreciate that this questioning is delicate and perhaps embarrassing for both doctor and patient, but if established as the cause of the recurrent UTI, then the patient can be advised on how to avoid such problem in the future. Please consider!

Finally and perhaps most importantly, it should be noted that Foley catheters should only be introduced if the patient actually needs a catheter and not for aiding the nurses by reducing their workload. Remember, nursing care also includes patient toileting and if you as doctors are pressurised into inserting a catheter as the nurse is too busy to toilet the patient, then you may be putting your patient at risk of developing a UTI. If the patient does have a catheter, it should be removed as soon as possible and when practicably possible.

Also, hospitals and care homes should have appropriate Infection Control procedures whereby patients with severe infections e.g. pseudomonas, MRSA, are moved to areas where they pose less danger to other patients. That may mean putting patients in single rooms until the infection is cleared.

Infection control staff also advise medical staff on proper hygiene such as hand washing, disinfection and how to manage outbreaks and their importance in the hospital and community setting cannot be taken for granted.

Please let me know your opinions !!!

Influenza and Asthma!

This week was supposed to be my Winter Holiday, and my family and I had arranged to go travelling in Japan.

However, my whole family developed an Influenzal-like illness thereby putting an end to any travelling !

My son saw a doctor who diagnosed an infective viral exacerbation of asthma and gave him nebulised beta agonist and theophylline powder and my wife was told something like-- 'don't use the inhaler' (albuterol beta-agonist metred dose inhaler from the USA)......without being given any explanation why she should stop.....

This left me confused as it was against all the UK medical training and evidence I had come to know.

I am not a paediatrician, but this did not sound at all right to me, so I have investigated further.

So, on checking UpToDate for childhood asthma, it confirmed that Mild Acute Asthma should firstly be treated with beta-stimulant either via a nebuliser or metered inhaler via a spacer (as was done) and following this, an inhaled steroid should be provided too.

In the UK British Thoracic Society November 2005 guidance for asthma (some 98 pages !!), no where in the acute guidance does Theophylline feature apart from when all else fails in severe acute asthma !!

In fact, moderate to severe asthma suggests substituting inhaled corticosteroid for intravenous steroid, adding ipratropium, and failing that, to give intravenous magnesium or iv beta stimulant (salbutamol / albuterol).

As for adults with acute asthma, theophylline does not show any more improvement in acute asthma than the combined use of beta-stimulant, ipratropium and steroid administration.

I have heard of cases where patients at local clinics have been given iv aminophylline as a primary treatment in acute asthma and then sent to our hospital when they should have been given a beta-stimulant nebuliser and steroids. This kind of therapy is clearly against the current evidence base.

The main place for aminophylline is in chronic respiratory conditions such as childhood chronic asthma, COPD or in patients who are unable to use an inhaler or have poor compliance.

In such cases of chronic asthma, there is evidence that combined with beta-stimulant and steroid, there is better control of asthma symptoms. Here again though, it should not be given in place of beta-agonist or inhaled corticosteroids but rather compliments their beneficial effects. In this setting, aminophylline can allow the reduction of steroid dose and frequency of beta-stimulant use (UpToDate 15.1)

I appreciate that the Japanese Guidelines advocate aminophylline as a second line agent but as far as I am aware, they have not been updated recently.

Aminophylline is a cheap drug and has alot of physiological effects such as bronchodilatation, anti-inflammatory effects and anti-chemotaxic effects against eosinophils, but obtaining therapeutic levels may be problematic and patients already on oral preparations or who drink coffee can develop toxicity which includes: tachycardia, tremor, seizure (<1%),> In such patients, IV preparations should be avoided to prevent such toxicity.

The treatment of acute asthma in the UK and USA is certainly different compared to what I have seen in Japan.

The UK Guidance can be viewed here: http://www.brit-thoracic.org.uk/iqs/sid.08626940972447923509053/
Guidelinessince%201997_asthma_html (PLEASE CUT AND PASTE TO GO TO THE SITE)

The UK guidelines only institute IV aminophylline in the acute setting when nothing else works and patients are in intensive care (adults) or Pediatric ICU (PICU) but certainly not in place of other measures mentioned above.

Please consider before using this drug.

Do you have extensive experience in the use of this drug and agree or disagree with the above blog? If so, please leave a reply as this is an open forum (albeit moderated) and your opinions would be helpful for other junior doctors to learn.

Types of Chest Pain

Whenever I teach a doctor for the first time and the history is about pain, I always ask various questions about the pain to which I get looks of bewilderment because surely pain is just pain, right???????........Wrong.

There are many different types of pain.

Let me take an example about chest pain. I was recently told a short history about a patient with GI bleeding and chest pain.

The doctor had failed to elicit any further history of the pain.

Questions that should have been asked included:

• What type of pain? Severe, crushing, squeezing chest pain (cardiac) [Like an Elephant sitting on your chest] or severe ripping/tearing pain going through to the back (dissection), sharp and/or worse on inspiration or moving (pleuritic), superficial or deep pain (superficial may be from skin / muscle or bone).

• Does the pain radiate any where? To the neck / jaw / arms (cardiac), to the back (dissection), to the abdomen (inferior ischaemia / MI / dissection). Is the pain worse on lying flat and better sitting forwards? (Pericarditic pain).
  

• Did the patient suddenly become acutely breathless with chest pain? (Pulmonary Embolism / Pneumothorax / Dissection / Massive AMI).

• Did the pain come on gradually or suddenly? Gradual pain may be associated with infection / malignancy / unstable angina / chronic and progressive dissection / pleurisy / myositis / shingles. Acute onset pain must always be taken seriously and may signify an MI, PE, Dissection.

• How severe was the pain? Try to use the Pain Scale, with 1 being minimal pain and 10 being the most severe pain imaginable and 5 somewhere in between. Of course, one person's perception of pain is different to that of another person and so the pain score needs to be individualised. This is useful to use as a guide to assess the severity of the complaint.

• Was the pain continuous or intermittent? Ischaemic pain may reach a crescendo of severity before continuing or subsiding. Pleuritic pain is by definition not continuous as it tends to occur during deep inspiration and gets easier on expiration. Did the pain come on or get worse with exertion?

• Did anything make the pain better or worse? Do you have a Nitro Spray? If so, did it make the pain better.

• Did the patient lose consciousness with the pain? PE, Dissection, Aortic stenosis and severe ischaemia, Massive MI.

• Was the patient vomiting with this chest pain and have a grey look and sweaty? Very cardiac sounding but of course can occur with dissection or any cause of shock. The 'grey look' and sweatiness are due to catecholamine output. The vomiting tends to occur with MI but this is not a good discriminator.

Other causes of chest pain include a oesophageal spasm type pain which is sometimes indistinguishable from cardiac chest pain. This pain also improves with nitrate or calcium antagonist but a patient will tend to have a normal ECG during such episodes.

Gastro-esophageal Reflux Disease (GERD) may cause a retrosternal, rising, burning type pain and an acid sensation at the back of the throat. Worst cases can cause vomiting. Patients will also suffer from flatulence.

Spontaneous rupture of the oesophagus can cause worsening chest pain (from mediastinitis) and patients may develop swollen upper chest and neck from surgical emphysema of air beneath the skin. Hence a history of patients eating when the pain started maybe important.

Also, sometimes, chest pain is mistaken as abdominal pain especially in the epigastric area and hence, disorders such as peptic ulceration, cholecystitis, pancreatitis, sub-phrenic abscess etc also need to be considered when thinking of pain in the chest.

Of course, other questions such as previous chest pain history e.g. AMI, angina should be questioned about, including Family History. Smoking history, diabetes, hypercholesterolaemia, history of dissection in the family / PE and DVT should also be asked.

In respect of the above, it is not fully comprehensive and is only a guide on the questioning with regards to emergency history taking of chest pain. It is impossible to cover all aspects of chest pain in this short blog.

However, in this case, the patient had ischaemic sounding chest pain and dizziness with tarry stool and haematemesis. It is likely that the profound haemorrhagic shock caused cardiac ischaemia and dizziness which promptly reversed on restoring the circulation with blood. ECG when patient was pain free was normal. There had not been an ECG when the patient had developed chest pain.

CK and Troponin T were normal. However, Troponin T takes time to rise and for current tests, this should be performed at about 6 hours and NOT on admission as the CK and Troponin are likely to be normal despite the patient sustaining myocardial damage.

If pain sounds atypical for chest pain or other serious pathologies then question about back problems as pain in the chest can occasionally be due to radiation from a spinal source to the anterior chest wall. Also, consider other diagnoses such as Syndrome X (ischaemic sounding chest pain but normal angiography studies, Prinzmentals (Variant) angina, Early Shingles (zoster) before the typical dermatomal rash forms. One should also asking about the patient's current mental health state, as sometimes patients with develop pain with no organic cause. Sometimes, in such cases, patients may be suffering depression and as such, this type of pain is termed psychosomatic or somatisation. However, this is a diagnosis by excluding the more serious causes FIRST.

UpToDate on PDAs

Today I want to talk about my special love (apart from my family of course !! :) ) .....PDAs.

As I have previously mentioned, PDAs are quite popular in Japan, but I consider that they are under utilised here to some degree.

I have discovered that UpToDate can now be used on the Palm based PDA platform such as the LifeDrive and Palm Treo handheld devices running Garnet OS 5.4.

Unfortunately, having tried to run the software on the Sony Clie TH55 (Palm OS 5.2) it does not work ! Hence, if you want to use UpToDate you need a newer type Palm.

Below are some photos of my old LifeDrive with UpToDate running. It is great!!




However, Palm based PDAs are going to become extinct in the future, or at least, that is what is being said in the PDA world, with Microsoft Windows Mobile 5 (Pocket PC) taking over with its multi-tasking capabilities.

However, although UpToDate also support the WM5 PPC PDAs and earlier versions, the software (which I have) does not run on a Japanese language WM5 PDA !!

In fact, after asking for support from UpToDate (which is excellent I might add) they mentioned that UpToDate for Pocket PC does not support 'Chinese Characters'.

So, if you have a Japanese Pocket PC, it would seem that at present, UpToDate will not run either.

My advice would be, if you want to use UpToDate on a PDA, either get a Palm running OS 5.4 or a PDA phone where UpToDate can be accessed via its site on the internet via the PDAs internet browser.

I think that UpToDate is a very good tool for physicians on the ward and now that it is in PDA format, it should become a highly useful tool for the physician who needs a second opinion !

Fever, Cough and Sputum

Here is another great case which has been anonymised to protect patient confidentiality.

Patient was admitted from Outpatients at another hospital with the following:

• Fever
• Cough with sputum
• Chest Pain
• Headache

The fever had come on after a few days of feeling unwell. The patient had recently suffered with influenza and had overcome that illness in February 07. The fever was constant at about 38 degrees. There were no associated rigors. The patient denied sweats except in the last few days leading up to admission.

The cough was a new problem and was productive of yellow / dark coloured sputum. There was no history of haemoptysis. No recent weight loss, or loss of appetite. The patient was a long-term smoker (20/day for 20 years). There was no history of asbestos or TB exposure.

The patient also suffered with left sided chest pain which was worse on coughing and deep breathing. It was described as Sharp and the part could not take a deep breath. The was no description of cardiac chest pain.

The headache only occurred on coughing and was temporal in origin. No eye symptoms and no neck pain or stiffness.

The patient denied earache or throat pain.

The patient denied any leg pain or swelling and there was no complaint of breathlessness.

Previous History included Atypical Angina (angiography was normal) and some asthma.

Drugs included some inhaler therapy for asthma but no angina treatment.

Family history included lung cancer in a near relative.

Social history - patient was married with two children and was in employment in the electronics industry.

The was a pet dog at home but the patient denied allergies to fur.

On further questioning, the was no history of foreign travel or travel to onsen.

On examination the patient looked well. The temp was still 38 degrees, pulse 80 regular, BP 120/70, Sats 94% on room air, RR= 16/min

There was no evidence of lymphadenopathy.

Cardiovascular, Respiratory and Abdominal examination were entirely normal except for pain when pressing on the patient's anterior left upper ribs.

Legs were described as normal.

Blood results were all normal except for a raised CRP of 15. WCC, Neutrophil % were normal.

Differential Diagnosis based on Hx and Physical

• Drugs-- N/A
• Infection--Bacterial post-influenzal pneumonia (staph aureas), pneumococcal pneumonia, H. influenza, Atypical pneumonia e.g. mycoplasma. chlamydia; mycobacterial e.g. TB

--Viral: Influenzal pneumonia, other respiratory viral infections

--Fungal: Cryptococcus

• Endocrine: N/A
• Trauma: N/A

• Inflammatory: Wegener's Granulomatosis, SLE
• Neoplasia: Lung Cancer, Secondary Lung tumours

• Haematological: Leukaemia, Lymphoma, Pulmonary embolism
• Immunological: Goodpasture's syndrome
• Metabolic: N/A

(This is not a complete list-- this was generated during a teaching session)

The patient was examined it was generally normal apart from the superficial chest pain and it was also pointed out that the patient was quite thin.

Chest Roentogen examination was Abnormal. There was a definite discrete circular lesion in the Right Midzone and a possible second circular area in the Left Upper Zone.
The right lesion at its inferior aspect was more radio-dense (white) than the more radiolucent upper area. There was no fluid level present.

The doctors were asked to also examine the bones and one Resident pointed out a 'Moth-Eaten' Left posterior medial rib which was consistent with a pathological aetiology-- perhaps malignancy.

Differential Diagnosis at this Point

Probable Lung Abscess (despite no air fluid level) secondary to Staph aureus after recent influenza; possible anaerobic causation. TB as previously noted, was also considered.
With the presence of a rib lesion, there was a high suspicion of malignancy.
Lastly, Wegener's Granulomatosis also needed to be considered.

CT scan evaluation confirmed abscesses with thick walls and surrounding pneumonia.

No organisms had been grown on culture. The Echocardiogram performed to look for right sided infective endocarditis was Normal although IE could not be ruled out as a cause as the Modified Duke's Criteria show(see previous case of IE). The patient had not been asked if intravenous drugs were used illicitly.

Sputum examination revealed a polymicrobial flora but no specific infecting organism.

TB Ziel-Nielsen stains were negative on two samples.

Samples had also been sent for cytology.

The patient had been started on a second generation cephalosporin without anaerobic cover.

Suggestions

• PCR of sputum for TB, Skin PPD test, Lowenstein-Jehnsen Culture for TB (4-10 weeks wait for growth!)
  
• Add either Clindamycin iv or Metronidazole orally [good bioavailability] (see Sanford Guide 2006 under Lung Abscess)
• Consider bronchoscopy for obtaining brushings, BAL for microbiological analysis (bacteria, mycobacteria and fungi) and cytology and even abscess drainage if necessary
• ANCA test for Wegener's
• Immunoprecipitins for Cryptococcus
• Beta-D-Glucan for identifying presence of invasive fungal infection
• Isotope bone scan to rule in/out metastases in the event that the rib lesion is cancerous
  

The usual cause of lung abscess is from aspiration of anaerobic oral flora. The symptoms consist of fever, cough and dirty sputum. Rigors invariably do not occur in these patients.

Other causes include Staph and occasionally strep species. TB is another cause of lung abscess and should never be forgotten.

Fungal infections include cryptococcus, blastomyces, candida etc...

Atypical type organisms can occur from infections derived from infective endocarditis from the Right Heart in IV drug users.

Non-infective causes include lung malignancy.

Wegener's Granulomatosis results in a necrosis of lung tissue which may simulate lung abscess formation. However, this patient did not have joint symptoms, upper respiratory symtpoms or signs of renal impairment making it an unlikely cause of this disorder.

Dr Aoki

Yesterday, Dr Aoki visited our Institution to be put through his paces on a great case.

The conference went on for 2 and a half hours and I was able to follow most of what was said in Japanese, and even Dr Aoki's jokes !!

It was great to see Dr Aoki's energy for Infectious Diseases and how he broke the case down into its small pieces to come up with a differential diagnosis containing the right answer !!

It reminded me of Dr Tierney's visit last year, although Makoto-san tells better jokes !


The first year doctors have definitely improved in their way of thinking through cases and were easily able to provide answers on how to work up a complex infectious case.

Dr Aoki went through organ systems then specific abnormalities of those systems by using 'VINDICATE' as a medical sieve.

Following the great conference, we went for a meal and ate some great 'Tsubame' locally.

Multiple Pathology-- Pleural Effusions

Today's discussion is about pleural effusions-- it is not a full history today.

A retired male presented with dyspnoea. He was dehydrated and confused and so history was poor.

It was identified that he had a pleural effusion both clinical examination and on chest Xray.

It was noticed that he also had unilateral foot oedema which raised a suspicion of a deep vein thrombosis.

However, his calves were normal temperature, not tender, no distended veins, not red....

The effusion was tapped from the right hemithorax but it became slightly bloody as the liver may have been inadvertedly hit during the procedure.

CT scan was performed which revealed a mass sitting in amongst the pleural fluid.

It was immediately assumed to be a neoplastic lesion, but there were additional ideas !

The analysis of the fluid suggested it was an exudate rather than a transudate making diseases such as heart failure / nephrosis / liver failure unlikely.

On the other hand, with the fluid being bloody and with a possible DVT, it was considered the possibility of PE as a cause for the effusion. Moreover, chronic infections such as Tuberculosis (TB) can cause effusions.

Other causes considered included:

Infection -- as above TB, para-pneumonic effusion, sub-phrenic abscess, unusual parasitic infections
Endocrine -- Hypothyroidism


Inflammatory-- Rheumatoid lung, SLE
Neoplasia: Primary Ca Lung, Secondary tumours, Lymphoma, Lymphangiitis Carcinomatosa

Haematological: Pulmonary Embolism (PE)
Metabolic: Uraemia

The patient underwent ultrasonography revealing a proximal DVT and the spiral CT revealed PE !! However, the pleural fluid was subjected to Ziel Nielsen Stain which was negative BUT the PCR was POSITIVE for TB !!

Hence, in this rather unusual case, it would appear that the cause of respiratory problem was due to multiple pathology.

Infection, for example pneumonia, can increase the risk of PE especially in the first two weeks after an infection although the risk can last for up to a year (Smeeth et al, 2006). This was demonstrated for community acquired pneumonias and not specifically for TB infection.

Moreover, this patient had been lying in bed for several days which again, increased the risk of DVT / PE.

Hence, this patient was treated for TB and PE, both relatively uncommon diagnoses in modern Japan.

Nevertheless, malignancy still needed to be ruled out in this patient, but there were no results confirming this diagnosis.

Things to bear in mind, that despite one cause being found for an underlying disease, if there is a possibility of another cause(s), then they should also be investigated and ruled out alike.

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 !!

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.

NEURO: NAD

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.

ECG: NAD

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.

Seizures

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.

The Tanned Lady

This Case from another hospital has been anonymised.

This 50 year old female was admitted to a hospital with the following Chief Complaints:

1. Fever
2. Back pain
3. Fatigue
4. Muscle Weakness
   

The history was relatively short being only 8 days which started with fever up to 38 deg C and associated back pain. She attended a nearby Clinic and the doctor prescribed antibiotic therapy although it is not known what diagnosis was established at that time. She took the antibiotics for 3 days but there was no symptomatic improvement.

After 6 days she developed Fatigue and Loss of Appetite. After a further 2 days, she was becoming increasingly weak and could not get out of bed. Her husband needed to help her get to the toilet, and on one occasion she experienced diarrhoea.

At this point, several important questions were asked to elaborate on the history such as what type of fever was it? Continuous or Oscillating / Spiking Fever. The latter is very suggestive of a bacterial / viral infection / abscess whereas continuous low grade fevers can represent non-infective aetiologies once infection has been ruled out. It was a continuous fever, although the patient said it was 'up and down' suggesting it was a spiking fever.

Moreover, where was the back pain? It was in her central back. Then, what type of pain? Was in continuous? Intermittent? Dull? Sharp? Associated with movement? Tearing? Worse on breathing deeply?

The importance of back pain can represent many different aetiologies here especially with fever such as a discitis, vertebral osteomyelitis, paravertebral abscess, myeloma, inflammatory arthropathies, metastatic disease, dissection, chest infection, pulmonary embolism, UTI, renal pain from rhabdomyloysis??....the list is extensive and by no means complete here, and by asking the right questions can lead the doctor to a more accurate idea of what is going on.

The patient had diarrhoea but it was not asked whether the diarrhoea was painful, the colour, the amount, whether there was any associated blood or mucus. This could possibly fit with inflammatory bowel disease which can cause diarrhoea (bloody), fever, fatigue, and arthropathy or a reactive arthritis / Reiter's Syndrome. The diarrhoea of course could be just due to antibiotic therpay!

Was the back pain due to pancreatic cancer invading the retroperitoneum and causing malabsortion and steatorrhoea?? The importance of asking the most minute details about diarrhoea cannot be taken lightly.

Were there night sweats? Weight loss? These questions needed to be asked and in addition, any history of TB exposure, chronic cough, haemoptysis-- TB can cause fever, and if it spread to the spine it may cause back pain too (Pott's disease).

The patient's past history included some congenital hip problems only and the patient had never smoked, did not drink alcohol and had never had a blood transfusion.

She was taking no medications apart from the antibiotic therapy.

No Family History or Detailed Social History was asked which is unfortunate as these may have given some clues.

Physical Examination: She was sleepy and hardly answered questions which may account for the paucity of history.

Temp: 39.1 Deg C, BP 82/40, SpO2 96% ? with Oxygen or Room Air. No Resp Rate or heart rate were recorded which in this situation was very important as the patient was clearly ill.

There were no meningeal signs-- no neck stiffness, No Kernig's Sign. Babinski was not performed.

The rest of the examination was described as normal.

Clearly, from the above examination, it was not entirely clear what the problem was with this patient.

However, the patient was clearly shocked and with a high fever and low blood pressure one has to consider Septic Shock as the primary problem.

Chest Xray revealed a left sided pneumonia. CT Chest again confirmed the pneumonia seen on chest xray.

Blood tests:

WBC 11,200, Platlets 9.4 , CRP 29.3, INR 1.46, D-Dimer 2.7, [FDP not tested]
CK 615
BUN 76, Creat 4.57, K 4.0, Na 128
Hb 10.3, MCV 84.2

AST 97, ALP 1434, gamma-GT 266, Bil 3.4 (Direct 2.4, Indirect 1.0), LDH 295, Alb 2.5

Urine: WBC 10-19. No bacteria. Myoglobin 1632.

ABG: pH 7.5, Low pCO2, HCO3 19.6, PO2 54.4 and BE -0.9

The above results signify severe problems for this patient including:

• Acute [probably Bacterial] Pneumonia with Hypoxaemia and Respiratory Alkalosis
  
• Disseminated Intravascular Coagulation
• Rhabdomylosis
• Acute Renal Failure [probably from combination of Shock, Sepsis and Rhabdomyolysis]
• Severely abnormal liver function [? Shock Liver -- unlikely here as usually ALT and AST are very high in shock liver; this picture looks more obstructive]

The patient was treated with a 3rd generation cephalosporin and this was changed to meropenem by the 13th day.

No organism was identified by blood culture which may be due to previous antibiotic therapy.

She also received gamma-globulin, Anti-Thrombin III for the DIC and under went plasmaphoresis for endotoxin related shock and renal failure on several occasions.

The HDF was stopped when the plasma creatinine reached 0.94 although the bilirubin was now 5.7

Antibiotics were stopped 14 days after admission.

However, she was complaining of itching. She was otherwise saying that she felt well.

The most striking thing that was noticed was her tanned skin which was not the yellow one sees with Jaundice, but a tan from being in the Sun.

However, she said she never went out in the sun and she did not come from a Southern area of Japan. She said her skin had become increasingly tanned since last year BEFORE she was unwell with this acute problem. She otherwise was feeling well.

She had never had Hepatitis B or C infection and as mentioned, she did not drink alcohol.

This suggested, before examination, that the liver problem pre-dated the infection and was chronic in nature.

On examination, she looked well. There was no asterixis [liver flap], slight palmar erythema [red palms], and mild excoriations [scratch marks] on her arms.

She had deep tanning in exposed and non-exposed area of her skin.

JVP was not raised. No lymphadenopathy. Eyes were jaundiced. No liver breath [fetor hepaticus].

Pulse 80/minute, No heaves / Thrills. Heart sounds were normal. Mild peripheral pitting oedema.

Respiratory rate was 18/minute. Chest revealed some mild left basal crepitations [crackles] which did not clear on coughing consistent with resolving pneumonia.

Abdominaal Examination was abnormal: The patient had one spider naevus [vascular spider] on the left supraclavicular area. The liver was enlarged about 3 fingers below the costal margin and was mildly tender but smooth to the touch. Splenomegally could not be identified from palpation, but Traub's Space was Dull on percussion consistent with mild splenomegally.

Bowel sounds were normal.

Clinical Impression

The acute problem had clearly resolved.

However, she had obvious Hepatosplenomegally, Deeply Tanned Skin, Signs of Chronic Liver Disease and Liver Biochemistry consistent with an Obstructive Picture and particularly a High Alkaline Phosphatase.

The CT abdomen confirmed the physical findings and ultrasounds showed no dilatation of the Common Bile Duct.

Obviously, the above findings are consistent with Primary Biliary Cirrhosis. A differential diagnosis, if this were a Caucasian patient, would be Haemochromatosis especially because of the Deep Tanning of the skin.

Autoantibodies were performed and ANA was positive 160 (+), Anti-Mitochondrial M2 Antibody 49.4 (+)

Hence, the diagnosis here was likely to be PBC. It would fit the clinical features of this patient in that it is common in females aged between 30-60 years and approx 50% have no symptoms prior to diagnosis. Particular features include pruritis [itchy skin], tanning of the skin[due to increased Melanin deposition NOT BILIRUBIN], and smooth Hepatomegally in advanced stages. Most other causes of chronic liver disease produce a small liver. However, acute hepatitis can produce an enlarged liver.

PBC is associated with other autoimmune phenomena such as Sjogrens syndrome, autoimmune thyroiditis, CREST syndrome and autoimmune arthritides.

Most patients thesedays are identified by picking up blood abnormalities when asymptomatic with a raised ALP being one of the first signs.

Obviously, this patient had advanced disease and it is a surprise that it was not identified sooner than this when it could have been more amenable to therapeutic intervention.

Most patients are commenced on ursodeoxycholic acid as this is the only drug known to alter the natural history of PBC although it does not prevent chronic liver failure or the need for transplantation. Other drugs that have been used in the past include: colchicine and methotrexate although in randomisd trials they have shown no statistical benefit. [please see UpToDate 15.1 for further details]

It suggested that other causes of liver disease should also be ruled out including Haemochromatosis [ferritin level], Wilson's Disease [caeruloplasmin], and alpha-1-antitrypsin deficiency. Note that copper metabolism is abnormal in PBC and Keyser-Fleischer Rings can occur in these subjects.

An ERCP was recommended to rule out Primary Sclerosing Cholangitis.

Moreover, the patient would have needed a liver biopsy to confirm the diagnosis and stage of liver involvement.

Ultimately, the patient would require a liver transplant.

Other things to consider include checking levels of fat-soluble vitamins including A, D, K [ and E, but not clinically relevant]. Vitamin A deficiency can lead to night blindness in severe disease especially in those with raised bilirubin levels. A prolonged clotting time can be indicative of vitamin K deficiency and vitamin D deficiency can lead to osteomalacia. If levels are low, they need to be replaced.

Malabsorption can lead to steatorrhoea and reduced nutritional absorption. In such cases, either fatty acid intake is reduced and / or pancreatic enzyme substitutes are given.

The patient should have also been considered for a diagnostic-therapeutic upper GI endoscopy as the patient has a high risk for oesophageal varices even in the absence of obvious cirrhosis. Treatment consists of banding varices and reducing portal pressure with non-selective beta-blockers and calcium antagonists.

This case, once again, underlines the importance of obtaining a thorough history and physical examination.

Finally, causes of Hepatosplenomegally should be reviewed here and include:

• Liver disease and Elevated Portal Pressure including PBC

• Infections: Malaria, Schistosomiasis, Toxoplasmosis [cats: social history!], CMV, EBV, Acute Hep B, C infection, Weil's Disease [Rat's urine -- Social History!], Brucellosis [food history part of social history!]
  
• Haematological-Neoplasia: CML, CLL, Lymphoma, Extramedullary haematopoiesis of myeloporliferatice disease e.g. polycythema rubra vera
  
• Granulomatous: TB, Sarcoidosis
• Inflammatory: Amyloidosis
• Vascular: Budd-Chiari Syndrome

Causes of Hyperpigmentation should also be reviewed and include:

• Racial
• Sun Related
• Dermatological: severe chronic eczema, freckles, acanthosis nigricans, chloasma [pregnancy related]
• SunTan Supplements e.g. Tanning Creams (がんがろ！！)
• Tattooing, arsenic exposure, gold, argyria.
• Drugs: chloroquine, chlorpromazine, minocycline, amiodarone.
• Topical Agents: benzoyl peroxide, tretinoin, flurouracil
• Berloque hyperpigmentation: phototoxicity from citrus or celery
• Drug Eruptions: Septrin, NSAIDs, Tetracyclines
• Oral Supplements: Beta-carotenaemia
• ACTH related: Primary Hypoadrenalism, ACTH secreting Pituitary adenoma, ACTH secreting tumours e.g. Ca Lung
• GI related: Haemochromatosis, Primary Biliary Cirrhosis, Wilson's Disease, Whipple's Disease, Hyperbilirubinaemia from any cause.
• Infection: Visceral Leishmaniasis

Collapsing Patients and Drugs

This case has been anonymised for patient safety but provides good examples of investigating collapses in elderly patients.

This elderly female patient was recently admitted to another institution due to 1) symptoms of a chest infection and 2) Collapse.

The patient was demented and was unable to provide any history of what happened. The brief history was provided by the care home.

The patient had recently developed a cough, sputum and fever and had been seen by a local community physician who had diagnosed a chest infection for which levofloxacin had been prescribed.

The patient had been getting better and the sputum had stopped although the patient had developed rhinorrhoea and general upper respiratory symptoms for which a further course of levofloxacin had been prescribed.

The patient had been eating her dinner when she suddenly collapsed at the table with her head falling forwards on to the table. Within a few minutes, the patient had regained consciousness. The patient could not remember anything of the event. There was no description of seizure activity. It was not clear whether the patient had bitten her tongue or developed urinary incontinence during the episode.

Further questions I would have liked to ask include: pre-syncopal dizziness, palpitations, chest pain, sudden onset of headache and visual aura before the collapse. Also, was the patient coughing prior to the syncope (cough syncope), any history of collapse / dizziness on turning of her head (hypersensitivity of baroreceptor response). Any cardiac history such as dysrhythmias, valvular disease, ischaemic heart disease?

Previous history included hypertension and dementia plus borderline diabetes.

Drugs included amlodipine, topical GTN patch, oral cough medication (opiate based I think), and levofloxacin.

The care home did not mention about angina but the patient was clearly taking medication that would be used for her heart!

No known drug allergies.

From the history alone it was convincing that this was a Cardiac Syncope possibly induced by drugs (combination of calcium blocker, nitrate, opiate derivative) plus there is the possibility of Torsade de Pointes from a Long QT interval induced by Levofloxacin especially on a back ground of probable ischaemic heart disease.

Vitals revealed a BP of 151/57 (large pulse pressure), pulse 70 regular, Resp Rate 20/min, Sats 97% on RA. Patient was afebrile.

Pulse examination revealed a Bounding and Collapsing pulse suggesting possible Aortic Regurgitation. JVP was not raised. There was an obvious Carotid Murmur originating from the heart and a Soft systolic mumur at the Aortic area.

Chest examination was normal with no crackles.

Leg examination revealed mild oedema probably as a result of the Amlodipine, which is a known side effect.

Chest Xray revealed calcification of the rib ends which is a normal sign of aging. There was some mild shadowing behind the heart which was consistent with consolidation with current or recently treated infection.

ECG revealed sinus rhythm but with first degree heart block and a corrected QT of 416ms. There were no acute changes.

Urine revealed 4+ bacteria and 2+ white cells.

Bloods showed a raised CRP and white cell count was normal. CK and CK-MB were normal. There was some mild chronic renal failure consistent with the patient's advanced age.

Clinical Impression:

1) Syncope due to drop in cardiac output possibly from combination of hypotensive drugs and opiate-derivative (which causes venodilatation).

2) Possible Torsade de Pointes from Levofloxacin ( a rare but well described phenomenon)

3) Post-pneumonic changes on chest Xray

4) Current Urinary Tract Infection

Suggestions

It was suggested that the Levofloxacin be stopped and continue with the already started Ceftriaxone. The patient coming from a Care Home might have a multi-drug resistant bacterium and hence, urine culturing and sensitivity would be of prime importance here plus blood cultures. Levofloxacin is an excellent drug for treating UTI, but with the urine being positive suggests to me that the infection was not being effectively treated.

It was also suggested obtaining a cardiac echo to ascertain if there was underlying aortic regurgitation because if moderate-severe, it can be dangerous using nitrate drugs as these can cause sudden drops in cardiac output and collapse.

It would also be of advantage to obtain continuous cardiac monitoring or at the very least a 24 hour Holter monitoring to see if a dysrhythmia can be identified.

It was also suggested that if the above tests proved negative the Carotid Sinus Massage (CSM) could be performed to see if there was any underlying hypersensitivity of the carotids to cause sudden heart block and collapse.

This is done with the patient in a recumbent position wired up to a monitor. The patient must not have any carotid stenosis (otherwise stroke might occur!) and hence, it should be done on the side with no murmur. If a patient has bilateral murmurs, then a Carotid Doppler would need to establish if the carotids have any disease and hence, whether it would be safe to perform CSM. If safe to do so, the carotid on ONE SIDE of the neck is massaged with light pressure for 30 seconds to one minute to see if there is any cardiac slowing. If the patient feels unwell during the procedure such as dizziness, then the procedure should be terminated.

If the patient's heart rate slows, then it should be recorded and printed out if possible.

If this test is normal, then a Dix-Hall-Pike test can be performed which involves cardiac monitoring and manouvers angulating the patient. This can reveal underlying problems causing collapse.

Every Breath You Take- Every Move You Make

Professor Lonny Ashworth, MEd, RRT.

Today we had the pleasure of having Professor Lonny Ashworth from Boise State University in the USA attend the hospital to lecture on how to use ventilators.

His visit was brief, just for 4 hours only, with him previously having been visiting a hospital in Chiba.

Today, he hosted two identical practical sessions whereby junior doctors could try Ventilators for themselves to see how CPAP feels, in additon to Square Wave Forms, Assisted ventilation and SIMV to mention but a few topics discussed and tried.

Each doctor got to be a 'patient' on a ventilator with the other doctors changing the controls.

The ventilators used were very hi-tech, the ones that I am used to seeing in the UK.

The junior doctors appeared to enjoy themselves very much and with the help of a translator, were able to understand well.

Here some junior doctors pretending to look studious but really being comedians!

Looks like SCUBA diving but a great lesson in ventilator control !!

No sleeping or time to be intubated and ventilated ! !

During his lecture, Lonny made a joke and said 'Every breath you take....' and I said 'Every move you make....' and he said --- ah no that's a song!!! Yes, from Sting and the Police ! A great respiratory song.

Some panoramic views of the study session....

Lonny, we really enjoyed your session and you are welcome back anytime!

History and Physical Revisited: a neurological quandry

This case has been anonymised for patient confidentiality.

A male patient of advanced age who presented with a sudden history of collapse. The patient apparently did not lose consciousness and returned to his home. Following this, the patient's conscious level began to decrease, and his breathing became laboured and his family admitted him to hospital.

It was not clear exactly what was described when the patient's breathing became abnormal. For example, did respiratory rate increased or decrease? Did the patient develop asthma-like symptoms, was there any pulmonary oedema, cough, sputum, haemoptysis?

Also, there is no history about what happened before the collapse. Where was the patient? What was he doing? Was there a sudden onset of headache? Were there any other features? Was there seizure activity and if so, was it sustained?

With the paramedics attending his home, his GCS was described as 3/15 but on admission to hospital, the GCS had apparently increased to 14/15 and the patient was able to speak and follow commands during examination.

However, following this, his breathing became further laboured with there being identification of hypoxaemia on blood gas analysis and the patient was intubated and ventilated.

The patient had not apparently sustained any head injury but other details of history such as sudden onset headache / chest pain / neck stiff were not elicited.

The previous medical history was that of hypertension only for which he took medication, although on admission, it was not known what medication he was taking.

Vitals signs were slightly abnormal, with the patient being normotensive, afebrile but with a of pulse 100/min and regular.

From what was relayed to me, the CNS examination was relatively unremarkable and the only positive finding on the rest of the physical examination were bilateral crackles at both bases on chest exam.

The patient had had the usual tests including chest Xray and Chest CT which showed old changes which looked like fibrosis, but there was no obvious pneumonia.

CT head showed a very small area of fibrosis near the thalamus on the right side, but this looked old. There was no blood or space occupying lesion (SOL). The MRI scan showed no abnormality apart from some artifact over the left frontal area. The diffusion MRI was otherwise normal.
The vascular scan showed no obvious abnormality.

Bloods revealed a slightly raised BUN of 27 but a normal creatinine. White cell count was slightly raised and CRP was increased to 2.1. CK, CK-MB, Troponin T were all normal. All other usual bloods were normal.

ABG- revealed a normal pH but CO2 and HCO3 were decreased and the SpO2 was approx. 50mmHg consistent with a compensated respiratory alkalosis and hypoxaemia.

The team were concerned that a pneumonia may be causing the chest symptoms but were unable to ascertain the cause for the collapse and coma, especially as the examination and tests had been normal.

My Opinion.......

On hearing this rather brief history, the differentials that come to mind include:

• Subarachnoid haemorrhage -- initial collapse from bleed and then as vascular constriction ensues, and intracranial pressure increases, the patient can become comatosed from ischaemia. Some SAH cannot be picked up on CT and only a Lumbar puncture performed, usually after 18 hours will pick up Xanthochromia.

• Stroke: a sudden onset phenomenon with sudden loss of neurological function either from infarction or bleeding. When considering thrombotic stroke, one should remember that thrombo-emboli can originate from the heart chambers, the valves, myxoma, platelet rich emboli from the carotids and primary thrombosis from atherosclerotic plaques. Paradoxical embolus and stroke can occur from a patent foramen ovale giving a right to left shunt through the atria. Emboli can pass from right to left cardiac circulations and cause stroke! This however is very rare. Patients may regain some level of consciousness but this may deteriorate with cerebral oedema.

• Sudden Cardiovascular Collapse: Loss of cardiac output for any reason such as a dysrhythmia, can lead to collapse and patients may suffer cerebral hypoxia and brain damage or head injury. With the latter, injuries to the temporal area can cause laceration of the middle meningeal artery and tense extradural bleeds and reduced consciousness.

• Dissection: Dissection can lead to acute collapse from sudden loss of valvular competency and / or tamponade, and if there is a proximal dissection, it can occlude the arteries supplying the head and neck leading to stroke.

• Pulmonary Embolism: Large PEs can cause sudden collapse and unconsciousness due to sudden cardiovascular compromise. PE can be chronic in nature and cause fibrotic change. Hypoxaemia from a massive PE can lead to hypoxaemia and reduced conscious level.
  

From the scans and data, there was neither an obvious large stroke nor an SAH. There was no evidence of a dissection or head injury either. The CT chest, which showed contrast imaging of the pulmonary vessels, did not reveal any PE.

Further results revealed a normal CSF examination with a slightly raised protein level only.

Urine results revealed no sugar but two plus of ketones (probably explained by fasting state)
Blood sugar approx 210. Could have this been an undiagnosed DKA with respiratory compensation??? I think unlikely in view of the absence of glucose in the urine.

Examination

Examination of the patient was difficult due sedation from propofol. However, at the end of the bed, the patient was making some unusual movements of adducting his shoulders and turning his wrists slightly inwards. He also had twitches which I thought might be sub-clinical seizure activity.

On examining him, his pupils were approx 4mm bilaterally and responded rapidly to light and were hence intact. Response to pressure on the nailbeds on both hands revealed Extension to Pain. Babinski responses were bilaterally positive as was Achille's Tendon Pinch which also causes plantar extension. Just to ensure that this was not just a withdrawal response, the patient was tested with a noxious stimulus, which in the case was a blunted pin. A normal response should be to plantar flex away from the pin tip when applied to the dorsal aspect of the toe. A positive response is dorsiflexion towards the pin tip. This patient showed bilateral Positive Signs confirming bilateral Upper Motor Neurone impairment.

Chest examination revealed bilateral crackles with them being of higher intensity of the right side.

Clinical Impression

Following this most revealing examination, it showed that the patient actually had developed severe neurological signs. With the signs being Bilateral this suggested that both cerebral hemispheres had probably become involved.

With the patient Extending to pain, this is a decerebrate condition. However, his pupillary responses were spared and when examined by a very astute neurologist, the Doll's Eyes reflex was also normal suggesting a normal midbrain.

Hence, a definite abnormality was identified which could now account for some of the features of the history.

The basic neurological examination helped reveal the problem that no scan could identify.

This underlines the importance of a good history (where possible from the patient / family /friend /bystander) and detailed physical examination.

Please remember that detailed physical examination should be able to reveal gross physical abnormalities. When performing a neurological examination on a conscious or unconscious patient, the Babinski Response can be of paramount importance. There are many other tests for finding upper motor neurone signs such as Hoffman's Sign in the fingers and many other in the feet which can be found in any good neurology textbook.

Don't forget to check for Clonus as more than three beats is signifcant og UMN signs.

Don't forget the Reflexes. It does not take long to do but can reveal the possible level of the problem and determine absent, decreased, normal or increased reflexes, which are all significant of either normal or abnormal neurological states.

Don't forget to do sensory testing in the conscious patient as this again can determine the level of a lesion.

This patient had a repeat scan but again this was normal.


After discussion with the neurologist, it was suggested that the clinical features and a normal set of scans with 24 hours of admission could be accounted for by:

• Diffuse bilateral hypoxic-ischaemic damage of the cerebral hemispheres

• Multiple embolic phenomena

Hence, the history of sudden collapse and waxing-waining consciousness might be accountable from a cardiovascular cause leading to cerebral ischaemia or multiple infarction.