Chest Pain-- Oh What A Pain !

Dear Bloggers

Sorry for almost a week of absence from this blog.  I hope this entry makes up for the short hiatus.

Today I would like to discuss about chest pain.

Chest pain is one of those things that is either something innocuous or on the other hand may be extremely serious. It is up to us as doctors to decipher the 'chaff from the wheat', or in other words, determine whether we need to do lots of tests and treatments or not.

Chest pain is a big topic in itself and too much to go into in detail in this blog. However, when we ask about chest pain we should not just rely on the patient saying that they just have chest pain and we as physicians should not just leave it at that. Chest pain needs thorough investigation through history, examination, radiological, laboratory and electrocardiographic modalities.

If we simply accept the phrase 'chest pain' and do nothing more, then we are short changing the patient and maybe missing a life threatening diagnosis.

So, when we ask about chest pain, we need to know what type of pain.

Cardiac pain is classically heavy / pressing / squeezing -- like someone standing on your chest. It is usually the worst pain ever and patients may say it is 10/10 on the pain scale. The location is usually central chest and may radiate through to the back or into the abdomen especially if it is an inferior MI.  Patients may mention or may have to be asked if the pain radiates to the jaw, neck or either arm or whether there is numbness in the fingers. Associated symptoms of nausea, vomiting, breathlessness and sweating are other classic features of ischaemic chest pain.

Other cardiac causes of chest pain can be aortic dissection which can present with very similar symptoms as patients with acute coronary syndrome. However, patients can develop tearing interscapular pain (between the shoulder blades), cardiovascular collapse from tamponade, limb weakness from arterial occlusion as the dissection occludes the vessels derived from the arch of the aorta. If the dissection moves distally, abdominal organ ischaemia can occur resulting in pain, renal failure and ischaemic bowel. Hence, a patient who starts off with chest pain that then migrates to neck / shoulder blades, lower back and abdomen should be suspected of a dissected aorta until proven otherwise.

Sometimes, fast dysrhythmias can result in chest pain because of rate-related ischaemia and can be due to non-sustained VT, Atrial fibrillation-flutter, Wolff-Parkinson-White syndrome etc. Hence, asking the patient whether they have a fast, regular or irregular pulse may give you a clue to the cause before putting a hand upon the patient.

Another cause of chest pain is pericarditis which is usually infective although non-infective causes are also well known e.g. connective tissue disease, post-AMI, Dressler Syndrome. Such acute pericarditic symptoms include sharp localised pain over the area of the heart, worse on lying flat and better when sitting forwards. Patients may also develop tamponade if severe and especially if taking anti-coagulants or if they are mistakenly given thrombolysis for suspected AMI. However, pericarditis can masquerade as an AMI and hence, it is not always possible to decipher the two conditions without further investigations and intervention.

Pulmonary Embolism is something that should never be forgotten but is not usually high up on physicians differential diagnosis lists in Japan. It should be. Although I have indeed seen far fewer DVTs and pulmonary emboli in patients in Japan, I have nevertheless seen such cases. Symptoms include sudden or gradual onset of dyspnoea, chest pain- typically pleuritic, cough, haemoptysis, palpitations, collapse etc. Sometimes patients will have a classically swollen lower limb containing a DVT although I have found this to be the exception rather than the rule. Remember that patients with pneumonia, cancer, UTI, bed ridden etc can get DVT-PE and just thinking of a single pathology can catch you out. For example, a patient with a pneumonia who remains hypoxic and who may also, for example, have persistent AF despite resolving pneumonic changes should be considered to have a PE until proven otherwise.

Chest pain can also be from lung conditions such as pneumonia, pleurisy and malignancy where the pathology involves the parietal pleural which is innervated by peripheral intercostal nerves and the phrenic nerve of the diaphragm. Hence, such pleuritic pain is a lancinating pain (stabbing) when the patient breathes or moves/coughs etc. This may limit the patient taking a deep breath. Patients may also experience shoulder tip pain on one side and may signify inflammation  of the diaphragm with radiated pain via the phrenic nerve especially around the area of the central tendon of the diaphragm. Inflammation on the other side of the diaphragm e.g. peri-hepatitis, abscess etc can also result in shoulder tip pain.

Pneumothorax and pneumomediastium can result in sudden onset of chest pain. These may produce pain during respiration. The latter may only be considered if there is trauma or gastro-oesophageal symptoms (?? rupture of the oesophagus) and may only then be considered if there is crepitus in the supra-clavicular fossae or air is seen tracking up the mediastinum on chest X-ray.

The ribs of the thorax may also give rise to pain especially if there have been fractures or if there are metastases and asking about bone pain or symptoms of hypercalcaemia are also worthwhile. 

Of course, a common and innocuous cause of chest pain is muscle damage from heavy lifting and this can cause the patient anxiety. 

Back pathology may also cause central chest pain !! Vertebral collapse, fractures, osteoarthritis etc, can irritate the intercostal nerves and produce a lacinating pain over the distribution of these nerves and is worse when the patient moves. This kind of pathology should always be investigated. Many years ago I saw a patient with typical unstable angina who also had pain lacinating round his chest wall who on more detailed examination, had a tender spine. He had two pathologies causing his chest pain!

There are several serious causes of "chest pain" that originate in the abdomen too. 

As mentioned oesophageal rupture is one. Others include pancreatitis, gastric ulceration, cholecystitis, cholangitis etc. 

Because the nerve supply to the abdominal viscuses is from the slower unmyelinated nerves, there is poor localisation of pain unless there is inflammation of the overlying parietal peritoneum. Hence, patients with, for example, pancreatitis can experience lower chest pain / upper epigastric pain and may have some ease of discomfort when sitting forwards. 

Patients with gastric / duodenal ulceration may experience epigastric pain and may also have GERD symptoms such as reflux, retrosternal burning especially when lying flat, flatulence, bitter taste in the back of the mouth and lots of saliva (waterbrash). Patients may not offer up such symptoms unless asked !

Cholecystitis / cholangitis typically gives right hypochondrial or epigastric pain and this can radiate the infrascapular area on the right side. Patients can have fever and jaundice too. However, the patient may define the pain as chest or even back pain and hence, such a diagnosis should always be borne in mind.

Of course, there are several other causes of chest pain that are of no long term consequence. These include the Tietze's "costochondritis" and Bornholme's disease-- coxsackie infection. Elderly patients should also be asked if they have ever had Shingles (VZV dermatomal rash) over the area of the chest pain as post-herpetic neuralgia is occasionally the cause. The give away sign for the diagnosis is the unilateral post-infective scarring of the skin.

Hence, when taking a history about chest pain, it is simply not accepting what the patient says to you. You must ask more detail!!

Thus, a typical set of questions would include:

• What type of chest pain is it? Can you describe it?
• Is it squeezing, sharp, dull, shooting, stabbing or burning?

AMI QUESTIONS

• Is the pain sqeezing or heavy ? Does it feel like an elephant standing on your chest?
• Is it the worst pain you ever experienced? If 10 is the worst pain ever and 1 is almost no pain, where would you place your pain on this scale?
• Is the pain moving anywhere else, for example, into your neck, jaw or arms?
• Are you getting any tingling in your fingers?
• How long does the pain last? Is it continuous or coming on from time to time (intermittent)?
• Does the pain build up to a crescendo or does it stay the same?
• Is there anything that makes it better or worse?
• What happens if you walk? Does the pain get worse too?
• Is there any associated nausea, vomiting, sweating or breathlessness?
• If you use a nitro-spray / tablet, does the pain get better? (This can relieve cardiac pain AND oesophageal spasm so please don't get caught out!) How long does it take for there to be easing of the pain? Minutes? 

PALPITATION QUESTIONS

• Is you heart ever racing? Do you get chest pain at the same time? Is the racing regular or irregular? If you change your body position, such as squatting or bending over, does the racing stop and chest pain stop? 
• Do you drink lots of coffee or alcohol?
• Any history of problem with your thyroid gland in your neck? Any sweatiness? Any tremor of your hands? Increased appetite and weight loss? How are your eyes? Anyone said they look larger recently?

DISSECTION QUESTIONS

• Does the pain go through to your back? Is it severe or tearing?
• Have you noticed any arm or leg weakness or new back or stomach (abdominal) pain?
• Are you feeling breathless?

PERICARDITIS QUESTIONS

• When you breathe, cough or sneeze, does the pain get worse?
• Does the pain get better on sitting forwards or worse on lying flat?
• If you use pain killers, does the pain become less?
• Any recent fever, cough, cold or sniffles? (URTI symptoms--usually viral origin)

PULMONARY EMBOLISM / PLEURISY / PNEUMONIA QUESTIONS

• Do you have sharp chest pain, fever, cough, phlegm, bloody phlegm, palpitations or sudden or gradual onset of breathlessness?
• Any shoulder tip pain?
• Any history of long haul flights, long car journeys or immobility from illness?
• Do you take any medications such as oestrogens? Have you ever had cancer? Do you smoke? Any exposure to asbestos?

GASTRIC / OESOPHAGEAL QUESTIONS

• When you eat or drink, does the pain get better or worse?
• Do you get symptoms of chest burning, flatulence, a bitter taste in your mouth or lots of saliva, especially when lying flat at night? Does milk or antacids make it better?
• Have you noticed a change in the colour of your stool? Is it black like tar? Is it foul smelling? Do you feel dizzy on standing? Do you get breathless or have palpitations?
• Are you under lots of stress? Do you take aspirin or pain killers or steroids? Have you ever had an ulcer?

PANCREATIC / LIVER / GALLBLADDER QUESTIONS

• Have you noticed any change in the colour of your eyes, skin or urine? Have they turned yellow / dark brown? Does the chest pain get better when sitting forwards? Have you been vomiting?
• Does the chest pain come on several hours after eating? Is it mainly when you eat fatty foods? Do you ever get pain under the right shoulder blade or shoulder tip pain ? (sub-phrenic abscess)
• Do you get shivering or shaking with a fever? (may signify gram negative septicaemia e.g. ascending cholangitis, sub-phrenic abscess) 

MUSCULOSKELETAL SYMPTOMS

• Do your bones hurt? If you press on your own chest, do the bones ever hurt? Do you get pain worse at night? Does it ever keep you awake? Have you had any recent injury to your chest? Do you take steroids? Any recent weight loss, night sweats or fever?
• Do you have any back pain? Worse when coughing or sneezing? Is this ever associated with the chest pain?
• Do you get pain in your muscles or chest when you lift something heavy? Have you done any recent heavy lifting at all?

SKIN AND SOFT TISSUE RELATED QUESTIONS FOR CHEST PAIN

• Have you noticed any recent skin complaints such as a rash? Have you ever had shingles in the area of the chest pain? 
• Have you noticed any breast pain or recent lumps that are of concern to you (especially female patients).

NON-SPECIFIC INFECTION RELATED QUESTIONS

• Any recent foreign travel?
• Any recent contact with another sick person?
• Any recent common cold symptoms?

CONNECTIVE TISSUE RELATED QUESTIONS

• Any pain or swelling of any joints in your body?
• Do they get stiffness? How long for? More or less than one hour in the mornings?
• Anyone in the family with rheumatoid arthritis or other types of immune related diseases?

QUESTIONS FOR INVESTIGATING HYPERCALCAEMIA

• Are you thirsty or passing lots of urine ? (nephrogenic diabetes insipidus)
• Do you get confused or have problems with concentration?
• Do you get constipation or abdominal pains?
• Have you had any recent kidney stones? Have you ever passed a stone in your water?
• Do you get pains in your bones?
• Have you had a recent bone fracture?

The above can be remembered as the 'Bones, Stones, Abdominal Groans and Psychic Moans'.

As you can see from the above, asking about chest pain is not just a five minute chat!! It takes time but must be done if you are to find the true pathology.

Of course, the physical examination may help you a lot. Pressing on the chest may elicit bone pain, percussion may reveal hyper-resonance of a pneumothorax or reduced percussion sound of a pneumonia. Crepitus in the neck may alert you to the pneumomediastinum, or the supraclavicular lymph nodes and unilateral dorsal muscles wasting of the hand may alert you to the Pancoast tumour in the apex of the lung. Of course, the aortic diastolic murmur may be attributed to acute aortic regurgitation and reduced valvular sounds from the ensuing tamponade of a dissection etc....

Therefore, putting together the detailed history with the physical examination is necessary to provide a clearer idea of what the likely underlying process is. Without these two essential and complementary elements, the doctor will have no way to understand the problem and follow on tests will be unfocused and may miss the problem.

Only with the detailed history and physical will one have an idea of what to investigate, and remember from the above non-exhaustive list, there are many potential causes to investigate.

However, a patient with chest pain should have the following basic and cheap examinations despite the underlying cause to exclude serious pathology:

1. Chest roentogen (Chest X-ray) --ERECT TYPE IS BETTER to look for perforation, pneumonia, pneumothorax, widened mediastinum, etc
2. Electrocardiogram (ECG) e.g. AMI, pericarditis, AF
3. Cardiac enzymes, most particularly a Troponin T at a minimum of 6-12 hours after the onset of chest pain (positive in AMI, PE, Myopericarditis, CPR-Trauma, PCI)
4. D-Dimer (positive in DVT-PE; good negative predictive value)
5. Amylase and liver function test (Amylase raised in Pancreatitis, cholecystitis, perforation, dissection, DKA, Macroamylasaemia, etc )
6. Complete blood count to look for signs of a raised white cell count and neutrophil left shift
7. Temperature, pulse oximetry, respiratory rate and blood pressure measurement
8. Corrected Calcium and ALP check in case of bone pathology.

There are many other basic tests that one could do but they would depend on the results of the above investigations e.g. cardiac echo if suspicious of aortic regurgitation, treadmill test. Modalities like CT, MRI should not be launched into without first assessing the underlying cause and determining whether it will give you the appropriate answer.

Of course, patients with non-specific chest pain can end up being over-examined on occasion. However, ruling out serious pathology is necessary. 

Today's discussion is just the tip of the iceberg when it comes to discussing symptoms and how to ask the right questions. My advice to you is to think of the potential serious causes of pathology when thinking in terms of the presenting symptoms. Then once considered, ask yourself how these illnesses present as symptoms and ask those same questions to the patient. Without a deep background knowledge of how diseases present themselves, then one becomes reliant on machines making the diagnosis rather than the doctor. 

Machines are not always right.

Please consider.....

Answer To Recent Case

Here are the answers to the recent case-- I am sorry if it is overly long to read but I hope it will cast some light on this difficult scenario.

Question 1: Please make a problem list soley from the history and physical examination findings.

Problem list

• Unsteadiness
  
• Slurred speech
  
• Periperal numbness (on history and physical)
  
• Diplopia
  
• Meningoencephalitis
  
• Seizures
  
• Medications- Phenobarbital / Phenytoin / Sodium Valproate / Flunitrazepam / Metoclopramide
  
• Fine tremor
  
• Coarse Facies
  
• Alopecia
  
• Cerebellar signs
  
• Absent reflexes

Question 2: What other specific question(s) would you like to learn from the history that might help you with this diagnosis?

The drug history is very important here and the drug doses and frequency should be investigated in addition to searching for hidden alcoholism.

The fact that the patient is happily married does not exclude her from being infected with a sexually transmitted infection by her partner and hence, a discussion with the partner might be in order especially if an unusual infectious aetiology were to be found e.g. neurosyphilis.

Moreover, the fact that the patient works in the 'fashion industry' is very non-specific. For example, she might make jewellery!! She might be using Lead!! Lead can cause cerebellar disease too ! Hence, a more in-depth questioning about her occupation would be in order here.

Question 3: What particular feature of the oral examination might give you a further clue regarding the cause of this problem.

Given the fact that the patient takes Phenytoin, one chronic side effect is gum (gingival) hypertrophy. This might give the clinician a clue regarding the cause of some of the symptoms and signs.

Question 4: What is the diagnosis?

The fact that the patient has severe cerebellar signs, peripheral neuropathy, a resting tremor, coarse facies, alopecia and gum hypertrophy, a diagnosis of acute on chronic phenytoin toxicity would be top of the list.

However, when one thinks of cerebellar dysfunction, one needs to consider various other causes such as:

Acquired

Drugs- Phenytoin, flunitrazepam (can cause drowsiness, slurred speech, tremor), Phenobarbital (known to cause ataxia), Na valproate (known to cause tremor, ataxia, speech disorder.

Salicylates, aminoglycosides, sedatives ( e.g. benzodiazepines), chemotherapy agents e.g. fluorouracil, cytarabine

Infection- Viral encephalitis, HIV, CJD, abscess

Trauma

Connective Tissue- SLE, Sjogren’s disease, Hashimoto’s thyroiditis, Auto-Ab associated Cerebellar Ataxia

Neoplastic- primary ( e.g. meningioma, haemangioblastoma) or secondary brain tumour (melanoma, lung, breast, thyroid etc), and Primary CNS Lymphoma. Cerebellar pontine angle tumour e.g. acoustic neuroma associated with neurofibromatosis type 2.

Paraneoplastic cerebellar dysfunction can occur with Breast Ca, Lung Ca (mainly SCC), Ovarian Ca, Uterine Ca and Cervical Ca.

Haematovascular- posterior circulation stroke (infarction or bleed), dissection.

Immune- Multiple sclerosis, Guillain-Barre Syndrome (Miller-Fisher variant)

Metabolic- Alcoholic cerebellar degeneration, Lead poisoning.

Granulomatous- sarcoidosis

Degenerative- olivopontocerebllar disease (may be part of a multi-system atrophy)

Congenital- Friederich’s ataxia- cerebellar degeneration, peripheral neuropathy, spinal degeneration, pes cavus, autosomal recessive, onset age 20; 1:50,000 prevalence (one of the several causes of absent reflexes but extensor plantar response). There are several other more rare congenital ataxias.

Question 5: Which one laboratory test would give you the diagnosis?

The primary lab test to be done is the serum phenytoin level. This correlates well with symptoms when there is toxicity.

Phenytoin is a well established drug used for various conditions including seizures and dysrhythmias (although the latter used less commonly these days). It can be given intravenously or orally.

Normal range for phenytoin in Japan is 10-20mg/L.

Above 20mg/L, nystagmus is common. Above 30mg/L, tremor, ataxia and slurred speech occur. When levels exceed 40mg/L, lethargy, confusion and unconsciousness occur. There have only been a handful of patient cases who have survived with levels >100mg/L.

Phenytoin is protein bound and hence, in patients with low albumin levels or renal failure, patients may experience toxicity at lower serum concentrations.

Phenytoin exhibits dose-dependent elimination kinetics, and toxicity can occur easily in patients on chronic therapy especially when there are drug interactions or slight alterations of daily dose. As the phenytoin level reaches therapeutic range, the liver elimination of the drug becomes saturated and therefore becomes Zero-Order in Kinetics. Hence, the half-life increases as serum levels rise e.g. T1/2 = 26 hours at 10mg/L, 40 hours at 20mg/L and 60 hours at 40mg/L respectively.

There is no specific antidote available for treatment of phenytoin toxicity whether iatrogenic or intentional and treatment is supportive e.g. charcoal for elimination (if orally administered) and maintaining airway, breathing and circulation.

In this case, the patient was also taking several other drugs and hence, drug-drug interactions must be considered here and include:

Phenytoin-Valproic Acid interaction- valproate displaces phenytoin from protein binding causing toxicity

Phenobarbital - Valproate Interaction- valproate reduced metabolism of Phenobarbital and can result in toxicity. One case report of decreased valproate effect through increased metabolism.

Phenobarbital – Flunitrazepam interaction- decreased effect of benzodiazepine through increased metabolism induced by phenobarbital. Increased risk of respiratory failure with combination of benzodiazepine plus phenobarbital (one case report 1986).

Benzodiazepine – Phenytoin interaction - decreased effect of benzodiazepine through increased degradation via liver enzyme induction. Possible toxicity when phenytoin and benzodiazepine combined although mechanism not established.

Benzodizepine – Valproate interaction – possible benzodiazepine toxicity by displaced protein binding by valproate and also possible decreased detoxification by the liver (glucuronidation).

Hence, there are several potential drug interactions at work in this patient. Other drugs being used to control the seizures may result in phenytoin toxicity, and toxicity or reduced activity of other drugs.

I have no doubt that drug-drug interactions contributed to the acute on chronic toxicity. However, another part of the history found out later was that the patient had poor daily compliance and she took sometimes more medication than prescribed in order to make up for lost doses.

The usual daily dose is up to 300mg of phenytoin and only several cases has there been doses up to 500mg/day. This patient was apparently taking doses far in excess of the recommended daily dose.

Other clues to the diagnosis of phenytoin chronic administration were the mild leucopenia and thrombocytopaenia which are also well described. The CT and MRI scan of the cerebellum were both entirely normal.

Case Response From Dr Masami Matumura from Kanazawa Medical University. As usual, Dr Matsumura provided an excellent breakdown of the case, and is as follows;

Question 1:Please make a problem list soley from the history and physical examination findings.

#1 Ataxia

She showed unsteadiness when walking, gait- wide based, staggering in nature, heel to toe test positive, heel to shin test positive R>L, finger to nose test positive bilaterally, dysdiadochokinesis positive bilaterally, nystagmus, slurred speech, and fine resting tremor.

#2 Polyneuropathy

She had numbness of her arms and legs, mildly reduced light touch, and no reflexes.

#3 Diplopia

#4 Pinky-red cheeks

#5 Coarse skin

#6 Alopecia.

#7 Viral meningoencephalitis

#8 Post-meningitis seizures treated with medication

Interestingly, she has two neuro-anatomical disorders, ataxia and polyneuropathy.

I have to pick up all possibilities in this case.

Differential diagnosis:

• Vascular: Cerebellar infarction, Subdural hematoma
  
• Infection: Cerebellar abscess, HIV, Acute viral cerebellitis, Lyme disease, Syphilis, Lepromatous leprosy,
  
• Neoplastic: Paraneoplastic syndrome, Cerebellar glioma, Cerebellar metastasis
  
• Collagen (autoimmune): Systemic lupus erythematosus, Sarcoidosis, Sjogren’s syndrome, Dermatomyositis, Primary biliary cirrhosis, Guillain-Barre syndrome, Post infection syndrome
  
• Toxic/Metabolic: Phenobarbital, Sodium valproate, Metoclopramide, Lead, Aluminum, Hypothyroidism, Vitamin B12 neuropathy, Diabetes
  
• Trauma/Degenerative: Spinocerebellar atrophy
  
• Iatrogenic: Phenobarbital, Sodium valproate, Metoclopramide
  
• Idiopathic: Amyloidosis, Multiple sclerosis
  
• Congenital: Fabry’s disease, Friedreich’s ataxia, Porphyria

She could not describe onset of symptoms. I assume these conditions were acute course or subacute course. If it was true, infection, neoplastic, collagen, toxic, and metabolic causes must be considered.

Question 2: What other specific question(s) would you like to learn from the history that might help you with this diagnosis?

I would ask her whether she has episodes of skin rash after sun exposure or not. And I would ask her change of voice and feeling cold or not.

Question 3: What particular feature of the oral examination might give you a further clue regarding the cause of this problem?

I seek oral ulcers!

Question 4: What is the diagnosis?

Systemic lupus erythematosus (SLE) is highly suspected in this case. She had two neuro-anatomical disorders, pinky-red cheeks, coarse skin, and alopecia.

Second candidate is autoimmune thyroiditis. She is Japanese woman.

Interestingly, both SLE and Hashimoto’s thyroiditis can be associated in several cases.

I can’t explain the cause of diplopia. Opthalmopathy is not described.

Metoclopramide is often prescribed in many patients. This drug can cause extrapyramidal sign. Tremor might be caused by metoclopramide in this case.

Question 5: Which one laboratory test would give you the diagnosis?

Serum antinuclear antibodies.

If it is possible, I would order CBC, FT4, and TSH.

Comments from B:

Dr Matusmura raises some very interesting points with his case interpretation. SLE is still a possibility. However, the pink cheeks on this patient did not involve the bridge of her nose, which the classical ‘Butterfly Rash’ of SLE does. Moreover, skin rashes are known to be a manifestation of phenytoin administration as well.

Alopecia is indeed a feature of SLE although it is not a pathognomic feature and can be found in phenytoin toxicity too—as can hirsuitism!

However, interestingly, phenytoin has been associated with inducing SLE in several patients although this tends to be a discoid-type rather than systemic.

Lastly, when the phenytoin dose was decreased, the symptoms began to resolve, and if this were purely SLE, one might not expect such a rapid improvement.

In order to diagnose SLE, the must be several criteria met and they include the following:

1) Malar rash

2) Discoid rash

3) Photosensitivity

4) Oral ulcers

5) Arthritis

6) Serositis- pleurisy or pericarditis

7) Renal disorder- persistent proteinuria >0.5g/24h or cellular casts

8) Neurological Disorder- seizures or psychosis (having excluded other causes first)

9) Haematologic disorders

• Haemolytic anaemia or
  
• Leucopaenia <4.0x109/litre>
  
• Lymphopaenia <1.5x109/l>
  
• Thrombocytopaenia
  

10) Immunological disorders-

• Raised anti-DNA antibodies
  
• Anti-Sm antibody
  
• Positive anti-phospholipid antibodies
  

11) Raised titre of Anti-nuclear antibody

SLE can be diagnosed if 4 or more of the above criteria are met either simultaneously or serially over time.

(1982 revised criteria of the American Rheumatologu Association [now American College of Rheumatology] for the diagnosis of SLE)

From the above criteria, at most, the patient may have only had two criteria for suspecting SLE, those being the haematological disorders and the possible Malar rash. Cerebellar dysfunction although well recongised in SLE is not one of the diagnostic criteria. Unfortunately, antibodies for SLE were not performed in this patient.

Hence, it is still possible that phenytoin may have induced some features of SLE, and checking autoantibodies would be certainly worthwhile.

Finally, the haematological disorders in phenytoin toxicity are related to depleted folic acid and hence, checking this blood level and giving replenishment would be one way to correct the problem.

I think this paper from 25 years ago sums up what needs to be said:

1: Acta Neurol Scand Suppl. 1983;97:49-67.


Side effects of phenobarbital and phenytoin during long-term treatment of epilepsy.

Iivanainen M, Savolainen H.

Phenobarbital and phenytoin have good antiepileptic effect, but clinically significant untoward effects occur during their long-term use. Phenobarbital may cause hyperactivity, behavioral problems, sedation, and even dementia; these effects are dose related to some extent. Side effects of phenytoin include sedation, a cerebellar syndrome, phenytoin encephalopathy, psychosis, locomotor dysfunction, hyperkinesia, megaloblastic anemia, decreased serum folate level, decreased bone mineral content, liver disease, IgA deficiency, gingival hyperplasia, and a lupus-like hypersensitivity syndrome. Especially susceptible to the neurotoxic effects of phenytoin are epileptic children with severe brain damage who are on multiple drugs. In those children, balance disturbance may develop and be followed by gradual loss of locomotion. Among 131 mentally retarded epileptic patients, phenytoin intoxication occurred in 73 (56%), of whom 18 experienced persistent loss of locomotion. There is experimental evidence that the toxic action of phenytoin lies at the cellular level, predominantly in the cerebellum. Many experts avoid the long-term use of phenytoin because of its insidious and potentially dangerous side effects.

Thank you very much Dr Matsumura.

Another response was from Professor Lefor of Jichi Medical University who made an excellent attempt to answer this very difficult case. Professor Lefor’s way of working up this case is also very thorough and indeed, the diagnosis for this case does fall into that ‘other’ group. His reponse is below:

1.My problem list includes:

a. Unsteady gait

b. Diplopia x2y

c. Sensory changes

d. Slurred speech

e. Hx seizures in the distant past, on meds

f. PE showed no bruits, nystagmus, slurred speech, tremor, decr sensation and wide gait

2. What other questions?

I would want to know more about the time course of onset of these various symptoms.

3. Oral Exam: I am not sure what to look for

4. What is the diagnosis?

This is a tough case. There is a wide variety of disparate neurologic findings here. It is difficult to put it all together. The major etiologies would include vascular, infectious, tumor, and other. I doubt it is vascular given her age, physical findings and onset. Infectious is possible, but the time course does not support this. Tumor is certainly possible, but the wide variety of symptoms makes it hard to assign to a mass lesion. My number one is in “Other” category, and I believe that this is most consistent with some global neurologic disorder such as Multiple sclerosis which affects a wide area of the CNS as a de-myelinating disease. She is a little bit old for the usual patient (in the USA the onset is rarely over age 40), but this disease, or some other de-myelinating condition seems most probable given the wide range of structures affected as evidenced by her symptoms.

5. What is the one test: For MS, there is no one absolute test, but MRI is quite good and is the one test I would get. MRI would also rule out a brain tumor, which is also a possible dx, and must be fully ruled out quickly to avoid “missing it”.

Thanks for letting me participate

Alan Lefor

Comment from Dr B： Professor Lefor’s consideration of MS is very thought provoking especially as diplopia can be a symptom of MS. Moreover, the onset of cerebellar dysfunction can also occur in MS and neurological deficits occuring in various places over time is one feature of this disorder. Indeed, exacerbations of MS with acute deterioration can occur although this is usually related to an underlying infection which there is no history of in this case. Moreover, the generalised loss of peripheral tendon reflexes is not a usual presentation of MS. However, with an acute deterioration, one might expect the loss of reflexes e.g. in a single limb, and for them to return in time and become hyper-reflexic signifying a previous upper motor neurone lesion.

However, the pinky cheeks, coarse face, alopecia etc do not fit with MS or with a tumour and hence, a metabolic or autoimmune condition would be considerably higher up on the list. However, things such as tumours and MS should always be ruled out in such conditions as has been described above.

Thank you very much Prof Lefor.

Learning Points From This Case

If a detailed history is taken, if it is a common disorder, the cause will usually become obvious quickly.

Taking a thorough drug history, drug doses and frequency is very important. One must not just re-prescribe the drugs just because that is what the previous physician did or that is what the patient says they are taking. You must check the correct doses if you do not already know.

In this case, the drug doses and frequencies were purposely omitted in order to draw your attention to the fact that they were missing. They should never be over-looked or omitted from the history and young physicians should always be asking about drugs the patient takes. Drug doses and frequencies must be checked to avoid toxicity. This case demonstrates this example very clearly.

Checking drug-drug interactions is also essential. I would suggest obtaining a handbook on drugs that deals with this or perhaps one for PDA e.g. Epocrates (epocrates.com [free]) or the Handbook of Adverse Drug Interactions (skyscape.com).

Generally, as physicians we all have to know an awful lot about drugs but it is something that can cure or curse a patient but we must know when that happens. The only way is learn throughly about drugs and especially about commonly used ones in daily practise. One textbook that I used as a student was Rang & Dale's Pharmacology with an updated edition just last year. You can never know too much about a drug.

Common Things Are Common and 'When You Hear Hoofbeats, Don’t Expect To See A Zebra'~~(Theodore E. Woodward M.D) are very important ideas. Obviously, things such as drugs, alcohol, stroke and infection are high up on any list for cerebellar diseases. These should be excluded initially and if ruled out, investigation for other causes such as MS, SLE and even Friederich’s ataxia which lie somewhere further down the investigative road.

Usually, if you prioritise your differential diagnosis according to the history and physical plus specific lab and radiological tests, the answer will soon become apparent.

But remember this, the answer usually lies somewhere within the history but you have to elicit the right answers to find it.

Please consider and have a good week!

Finally, thank you to Dr T and his team for showing me such a great case.

A new case-- time to put your thinking caps on

Dear Bloggers

Today I have another great case for you supplied by a distant hospital in Japan. The case has been anonymised to safeguard patient confidentiality.

Presenting complaint: unsteadiness when walking

The patient was a 47 year old female working for a busy fashion design company. She developed unsteadiness when walking at work. She was uncertain whether it was of sudden onset but she remembered she did not have this problem when on the bus and then train that she took daily to her job.The unsteadiness was not associated with dizziness, new visual disturbance, nausea, vomiting or hearing loss and she denied motor symptoms. She denied vertigo and dizziness on standing.

She did however admit to the following symptoms including:

1) Diplopia- a two year history that had not got worse and was corrected by her prescription spectacles; this occurred mainly when she looked upwards.

2) Numbness of her arms and legs- this had occurred several days before the onset of the unsteadiness and was throughout the entire length of her limbs. She did not have any facial numbness according to her account.

3) Slurred speech- this occurred around the same time as the onset of unsteadiness.

Previous medical history included

• Viral meningoencephalitis (20 years before)
• Post-meningitis seizures treated with medication; no seizures for many years.
• Glaucoma

Medications included

• Phenobarbital
• Sodium valproate
• Phenytoin
• Flunitrazepam
• Metoclopramide

No known drug allergies (NKDA)

She was otherwise fit and healthy and was a hard working mother of two children and was happily married. She was fully independent and was a non-drinker and had never smoked. There was no family history of cardiac, respiratory, abdominal or CNS disease.

Pertinent Negatives

She denied the following:

GEN- no fever, no sweats, noshakes/chills, no constitutional symptons

HEAD- no sinus pain, no otalgia and no throat pain.

CVS- no palpitiations, no chest pain, no dyspnoea

RESP- no recent cold, no cough, no sputum, no haemoptysis

ABDO- no nausea, no vomiting, no jaundice, no pain, no constipation or diarrhea. Normal appetite and no weight loss.

MUSC- no weakness, no muscle pain, no joint pains or swelling

UROGEN- normal menstrual periods, no menorrhagic, no abnormal vaginal discharge, no urethral pain, no urgency, no frequency and no haematuria. No new sexual partner—not using barrier contraception.

CNS- no sudden onset headache, no hx of migraines, no blurred vision, no loss of vision, no swallowing problem, no hearing disturbance, no facial numbness.

PNS- no falls, no collapse, no uni- / bi-lateral weakness, no loss of bladder or bowel control. No back pain.

Endocrine- No polyuria, no polydipsia, no disturbance of concentration, no increased or decreased appetitie, no lactation, no recent increase or decrease in weight / size of hands or feet, no Hx of hypertension.

Skin- she denied any new skin problems

On examination

The patient was alert and looked otherwise well. She was afebrile, BP 120/80mmHg, Pulse 80/min regular, Resp rate 14/min regular, O2 sats 98% breathing ambient room air.

General- pinky-red cheeks, coarse skin and evidence of alopecia.

No jaundice, anaemia, clubbing, cyanosis, oedema or lymphadenopathy (JACCOL)

CVS- Hands warm and well perfused. Pulse good volume. JVP not elevated. Heart sounds 1 & 2 normal with no added sounds or murmurs. No carotid bruits. No peripheral oedema.

RESP- Trachea central and no tracheal tug. Expansion normal. Percussion note normal. Normal vesicular breath sounds.

ABDO- Soft, flat, non-tender, no masses. Bowel sounds normal. Genital and rectal examinations not performed.

Breast exam- normal.

CNS

I normal sense of smell

II normal visual fields. Pupils equal and reactive to light and consensual reflex normal.

III / IV / VI – Normal range of movement but Nystagmus bilaterally (mild) and some vertical nystagmus on vertical gaze.

V- motor and sensory normal.

VII / VIII - normal

IX / X / XI / XII - individual nerve testing normal.

Mild slurring of speech noticed.

PNS

Fine resting tremor- not ‘pill rolling’ type.

Tone- normal throughout

Power- normal throughout

Reflexes- absent throughout

Sensation- mildly reduced light touch throughout; other modalities not tested

Coordination- finger to nose test positive bilaterally. Dysdiadochokinesis positive bilaterally. Heel to shin test positive R>L.

Babinski sign negative bilaterally

Gait- wide based, staggering in nature (ataxic) and heel to toe test positive.

Question 1: Please make a problem list soley from the history and physical examination findings.

Question 2: What other specific question(s) would you like to learn from the history that might help you with this diagnosis?

Question 3: What particular feature of the oral examination might give you a further clue regarding the cause of this problem?

Question 4: What is the diagnosis?

Question 5: Which one laboratory test would give you the diagnosis?

Tendon Hammers and Patient's Feet

Dear Bloggers

Today I would like to advise on what I consider to be the correct use of a Tendon Hammer to perform the Babinski sign for determining upper motor neurone lesions.

Essentially, the end tips of most of the modern hammers are far too sharp and can be very uncomfortable to use on a patient's foot especially when there are a team of doctors and students all having a try to practise their skills to elicit the sign.

Unless the end of the tendon hammer is blunted it is therefore not appropriate to use the sharp tip for eliciting the Babinski sign. Please try and use another type of blunted instrument.

In order to understand just how uncomfortable it is to perform Babinski sign on a patient with a sharp tipped tendon hammer I suggest you take off your own shoes and socks and get a colleague to perform it on you. It is not a pleasant experience. Never do to a patient what you would not have done to yourself!

Use of the tip of the tendon hammer by doctors in the UK MRCP examinations can lead to failing that section of the examination. Never put your patient through unnecessary discomfort. Things that can be used are 'orange' sticks, your thumb (although not in an formal examination!), a blunt tipped tongue depressor. The former and latter can be disposed of although I would recommend washing your thumb rather than trying to dispose of it :-p

Just to remind you of the correct technique, ensure that the toes are neutrally positioned e.g. not pointing up or down. Use the blunt instrument to excite the lateral border of the foot starting at the heal and running caudally towards the fifth metatarsal head followed by a medial turn across the foot towards the remaining metatarsal heads in the direction of the great toe.

A negative sign is visualised by the toes plantar flexing [true flexion]. A positive sign is visualised by the toes moving into dorsiflexion [plantar extension]. The most sensitive aspect is visualising the movement of the Great Toe because it may be the only toe that moves.

Sometimes the excitation of the plantar elicits no response at all and it can be due to peripheral neuropathy or myopathy although it may also be seen in early stroke or spinal cord injuries. Drugs also temporarily influence the Babinski response and include sedative drugs such as propofol, general anaesthetics etc.

Please consider....

Antibiotics and Evidence versus Eminence Based Medicine

Dear Bloggers

I hope that you are having an enjoyable Golden Week. The weather is not particularly golden and more like 'lead'- grey with it being overcast :-(

Today I would like to focus on the duration of antibiotic usage for treatment of pneumonia. The 'recommended' duration of intravenous antibiotic use is widely accepted to be a week to 10 days or sometimes longer. From one colleague I had heard that intravenous antibiotics are routinely given for infections resulting in positive blood cultures for a standard of two weeks even if the patient has recovered, despite the underlying cause. In many of the traditional textbooks and handbooks covering the use of antibiotics, there is the standard use of 7-10 days of antibiotic use in pneumonia. However, where is the evidence for this widely accepted dogma??

A team from the Netherlands attempted to investigate whether an abbreviated three-day course of intravenous amoxicillin was inferior to an 8-day course of amoxicillin consisting of 3 days of initial intravenous therapy followed by 5 days of orally administered amoxicillin for use in mild to moderate-severe community acquired pneumonia.

Patients were included in the study if they had symptoms and signs of pneumonia plus radiological evidence of the diagnosis. They all received high-dose intravenous amoxicillin for 3-days after which, if there was seen to be improvement e.g. feeling better, reduced sputum, fever reduction etc, the patients either received placebo or high dose oral antibiotics for a further 5 days.

The results were astonishing in that a 3-day course of intravenous amoxicillin was observed not to be inferior to an 8-day course of amoxicillin for the treatment of mild to moderate-severe community acquired pneumonia.

As 60-80% of admitted patients have mild to moderate-severe pneumonia [pneumonia severity score <110], it is therefore conceivable that most hospitalized patients with CAP could be treated with high dose intravenous amoxicillin for just 3 days.

The majority of bacterial isolates were the usual culprits of Streptococcus pneumoniae followed by Haemophilus influenza.

The study had less than 200 patients and the 3-day-treatment-placebo group had worse symptoms than the 8-day-treatment group on admission but the overall cure outcome in the 3-day group was statistically non-inferior to the 8-day group.

It seems logical that antibiotics when given either orally or intravenously for specific infections e.g. CAP, uncomplicated UTI, should be done so at high-dose and for a short period of time if there are no complicating factors. The idea behind this is that the Minimum Inhibitory Concentration can be achieved as the serum level is high and with a short duration of administration reduces the exposure of bacteria to prolonged periods of antibiotics which is known to promote antibiotic resistance.

Moreover, the longer that antibiotics are continued, the more side-effects that one gets such as drug-associated fevers, drug induced rashes and antibiotic associated colitis e.g. Clostridium difficile infection.

Short course antibiotics lead to reduced expense on antibiotics, reduced hospital stay and reduced exposure to hospital acquired infections.

Patients should not be kept in hospital just because of the widely accepted dogma that 10-days of antibiotics have to be administered. There needs to be a re-evaluation of the current thinking so that evidence is used when treating patients rather than eminence based opinion.

One thing I have noticed commonly is the use of low dose prolonged courses of antibiotics. I cannot see the use for such prolonged courses especially when side effects are increasingly common. In the BMJ study, the three-day course was associated with no observed side-effects as opposed to the 8-day course which was associated with side-effects. Moreover, if low-dose antibiotics are used, then the MIC cannot always be effectively achieved and would also promote resistance and failure to achieve a clinical and/or bacteriological cure.

To rely on rigidly fixed doses for use of antibiotics is not logical because patients have all different weights, volumes of distribution depending on body fat, and they may have underlying renal or liver disease which ultimately affects the final dose that can be used. Just consider for one moment the use of weight per kilogram per day of antibiotic administration akin to childrens dosing.

The following examples may surprise you of just how much antibiotic is recommended. Obviously, doses and duration of antibiotics depends on the underlying infection, the patient’s immunity, renal and hepatic disease plus local bacteriological resistance factors.

For example, the maximum allowed oral dose of amoxicillin in Japan is 250mg three times daily. However, if one uses the paediatric dosing according to world standards e.g. 40mg/kg/day and if for example an adult patient is 40kg, the total daily dose required is 1600mg. Divided into thrice daily dosing, this equates to over 500mg per dose [533mg to be precise]. Hence, the dose allowed to be prescribed is half of what is recommended to be given to adult patients according to world standards.

As a consequence, with this single example, it may to some extent explain why some community acquired pneumonias and urinary tract infections are only partially treated in the community thereby requiring hospital admission for higher dose intravenous antibiotic administration.

A further example is the use of clarithromycin-- maximum daily dose in Japan is 200mg twice daily. However, if one uses the pediatric world dosing standard which is 7.5mg/kg/day every 12 hours, in a 40kg patient, the dose would be 300mg per dose. Obviously, for larger patients the dose would be higher. In fact, the recommended world dose for adults is 500mg twice daily.

One other final example is the aversion to use Benzylpenicillin (Penicillin G) in pneumococcal pneumonia for fear of not covering the Penicillin Resistant Streptococcus Pneumoniae [PRSP]. This aversion is unfounded because pneumococcal pneumonia can be effectively treated with this well established antibiotic even for PRSP so long as it is used at high-dose e.g. 2 mega units, six times daily [total of 12,000,000 units daily].

A recent example from another hospital was a female patient with a typical uncomplicated community acquired pneumococcal pneumonia who was treated with the high-dose Penicillin G regimen and who had antibiotics stopped after just 4 days because of complete resolution of symptoms. She was discharged on day 5 with early outpatient follow-up. Penicillin G does work ! :-)

Finally, in the Netherlands 3-day pneumonia treatment study mentioned above, the intravenous dose is not mentioned but the 5-day oral course was 750mg three times daily-- hence, high dose!

This study demonstrates that for specific case definitions e.g. mild to moderate-severe community acquired pneumonia, the use of a three day course of intravenous amoxicillin is not inferior to three days of intravenous therapy followed by five days of high dose oral amoxicillin [total of eight days treatment].

If you are interested in reading this fascinating research it can be read for free on www.bmj.com.

The reference is:

el Moussaoui et al. The effectiveness of discontinuing antibiotic treatment after three days versus eight days in mild to moderate-severe community acquired pneumonia: randomised, double blind study. BMJ. Vol 333, 30 Sep 2006.

Please Consider....

Ethics in Medicine

Dear Bloggers

I sometimes like to do an article based on ethics. Medicine is not just about trying to make a diagnosis and treating everything that is a problem. Medicine is not just a science project that can be controlled like a laboratory experiment. Medicine is a mix of science, personal interactions, subjective and objective opinions from the doctor, the patient and the family with the abundance of feelings all intermingled.

Ethics is a very important part of medicine and is used perhaps unknowingly all the time when making decisions on how to proceed with patient care.

I have observed that the ethical dilemmas are different in Japan compared to the UK. For example, sometimes patients in Japan do not have the finances to be able to pay for expensive treatments and so on occasion, families will make the decision for the patient which may sometimes lead to an alteration of therapy which may not be what the medical staff would advise or think is appropriate. In the UK, taxation pays completely for the medical system and use of medical services is free at source, and hence, treatments are started if there is a clinical need and the patients and their families do not consider the financial aspects as is done in Japan. However, in the UK, I have said that treatments may be started if there is a clinical need. This is where ethics comes into play because although certain treatments are available, all patients are different, and just because certain investigations and treatments can be done it does not necessarily mean that it is appropriate to do such things either because of the patient's refusal or because of severity of illness, reduced life expectancy, poor quality of life etc...

There is often the saying here of 'All or Nothing' treatment. Either you do everything for the patient or do nothing. I have to say that I really do not agree with such a concept to apply to every patient scenario. Life is not always so black and white-- in fact, life is different shades of grey.

For example, should an elderly patient with a pre-morbid history of severe debilitating chronic disease with profound sepsis and fulminant multiorgan failure with a poor quality of life receive expensive extra-corporeal Polymixin therapy, haemodialysis and receive cardiopulmonary resuscitation when such interventions are very unlikely to cause the patient to survive and moreover, would be unlikely to alter the underlying pathology and importantly, cause more unneccessary discomfort?

There are doctors who might say yes. There would be many who would however say no. This is where ethics comes into the situation. Not everything is so clear cut.

Although haemodialysis removes the toxins from the blood, in the presence of DIC, the use of heparin during dialysis in the treatment of renal failure can worsen bleeding! Haemodialysis is a renal replacement intervention but it does not make the kidneys recover any better! It is purely supportive whilst waiting for the kidney to hopefully recover. However, fulminant renal failure might not recover leaving a patient with an additional chronic diseases and worsening quality of life left on thrice weekly haemodialysis which the patient and their family might not be able to afford. Such therapy might prolong life but might be seen by the patient as inhumane and intolerable. From my observations over the years, doctors frequently forget to consider the end outcome when starting major intervential therapies such as haemodialysis or intubation with ventilation therapy in such patients e.g. terminal lung cancer with respiratory failure.

The great anf famous textbooks show us how to think about symptoms and signs of disease, how to investigate and treat but never about the ethical issues and appropriateness of treatment. For this, the only real textbook is experiencing these situations yourself in the hustle and bustle of daily hospital life. Yes, there are many ethics books available with excellent examples of dealing with difficult issues and I would highly recommend reading such books.

Continuing on, patients with severe sepsis have a very high mortality [over 50% ] in various studies despite optimal treatment. Hence, in such a severe situation, even if there is eventual cardiopulmonary arrest, is it appropriate to perform cardiopulmonary resuscitation? One has to think about the overall outcome. If cardiopulmonary resus is successful, will that stop it from happening again? Will it make the other organs recover? The answer is usually no. One has to consider factors such as cerebral damage of CPR, the potential chronic heart disease resulting from ischaemia of the cardiac arrest, the likelihood of success and I come back to the point once again of Quality of Life.

Many patients with severe chronic disease have a shortened life expectancy and poor quality of life. In the UK, patients are asked directly about whether they would want to be resuscitated rather than asking the family. The family memebers are not the patient and in the UK, they are regarded as separate entities and therefore are not able to make such life and death decisions about the patient unless the patient is a child. On occasion, UK patients will directly state that they do not want to be resuscitated despite the contrary opinion from their relatives. Obviously, if the patient is not confused and not suffering from a psychiatric illness, and is considering such an opinion in a logical, clear way, the doctors have to respect the decision of the patient over that of the relatives. The patient is put first.

However, in Japan, the wishes of the family sometimes over-ride the wishes of the patient and sometimes, the patient is not directly consulted. There is the fear of family members that such discussions might make the patient's mental condition worse and that they will somehow 'die from shock' or that the patient would somehow not want to know their fate. From my experience of direct talking to patients in the UK, I have never experienced such spontaneous death from a discussion about the patient's condition directly with the patient and hence, such thoughts are somewhat unfounded in my opinion. Moreover, doctors siding with family members to avoid informing the patient of the diagnosis is again unfounded. As I have mentioned in a previous blog dealing with ethics, by informing the patient allows family members to be entirely honest with eachother in the final days, weeks or months of terminal illness which has the benefit of bringing family members closer together.

Hence, when we are considering whether to institute a treatment, we need to consider not only the medical problem in front of our eyes, but also the social factors and particularly Quality of Life issues. Doing knee-jerk reactional therapy with the 'Do All Or Nothing' approach is ignoring the Ethical issues which might be in direct conflict of the wishes and the interests of the patient.

Another concern I have about family oriented decisions rather than patient oriented decisions is when family members have a potential vested financial interest to gain from the patient's death. Hence, it is my belief that medical personel should be making the decisions when it comes down to investigating and treating the patient albeit still taking into account the opinion and feelings of the family. However, medical personel can look at the patient and their problems in an independent, unfettered manner to decide just what therapies are appropriate. In doing so, it removes a serious conflict of interest that might potentially exist between the patient and the family members interests.

Palliative care is another area which needs much development in Japan and it is entrenched with ethical issues. I have written on Palliative Care in the past and I see this as a very important arm of medicine. Patients should not be put through pointless operations for cancer that have no hope for prolonging life when the other intervention would be controlling pain and other symptoms to make life as happy and tolerable as possible during the final stages of illness. Using a palliative approach is Not a Failure of the Doctors! Sometimes, diseases can no longer be controlled by 'modern' medicine and pursuing treatments which do not alter the final outcome and cause more pain and suffering is not putting the patients first. Although as medical people it makes us feel better that we have tried our best and shows the family that we are really trying to do everything, the patient can get lost in the mix and it might not be the best for them!

One has to ask what is best? Doing everything to make us and the family feel better at the expense of the patient's feeling both mentally and physically or putting the patient first and using ethics based ideology to decide on whether the patient really wants such treatment and whether it will lead to a favourable outcome. Hence, palliative care is sometimes better than 'full active' treatment as pain, agitation, dyspnoea etc can be controlled through symptomatic measures and medications.

When I started off in medicine I thought that medicine was just about saving people from dying of illnesses. Yes, that principle I still hold true and is the driving force for my love of medicine. However, I learned over the years, that not all patients can be saved from the natural course of their illness and having a humane passage out of this world by using appropriate palliative interventions rather than futile active treatment, is sometimes better than doing everything and still losing the battle with the patient suffering more as a result.

Please remember about ethical issues and think about your patient as a whole being, rather than just a system disease based approach. Please consider....

Have a nice day....