CT scanning, Magnesium Hydroxide and Collapse!

Dear Bloggers

An 80 year old patient was admitted with collapse. He was found to have severe bradycardia and hypotension requiring emergency transvenous pacing which was successful.

On later assessment, the patient was found to have new onset renal failure whereas two weeks prior his renal function had been normal.

The patient was found to have hypercalcaemia and hypermagnesaemia. The hypercalcaemia had been appropriately worked up with tests for PTH, myeloma screen, vitamin D, thyroid function and so on. However, there had been no assessment of the hypermagnesaemia.

The cardiac enzymes had been completely normal.

The patient had been previously admitted into the hospital two weeks prior with a urinary tract infection which was successfully treated and the patient was discharged back home.

So essentially, what were the causes of the complete heart block, the new onset renal failure, the hypercalcaemia and hypermagnesaemia?

This is why the history is so, so, so important. The chronological set of events can provide the answer and doing additional reading can help the physician understand what may have gone wrong.

Following the chronology here, the patient received a contrast CT scan prior to discharge and no further renal function tests were performed. Then on the re-admission, the FeNa test revealed an intra-renal defect rather than pre-renal defect. The renal ultrasound scan was within normal limits ruling out obstruction.

Hence, a contrast induced nephropathy was highly suspected in this case.

However, in most cases of contrast induced nephropathy, there is usually only a modest rise in creatinine and it is usually self-limiting after about 5 days. About 5% of patients who develop this problem actually have permanent renal damage requiring dialysis. Hence, the renal failure in this case could be due to another unseen problem.

Why the hypercalaemia? Well, renal failure can result in parathyroid hormone abnormalities and cause hypercalcaemia. On the other hand, it would seem to have occurred too soon for such an acute renal insult. Hypercalcaemia itself can result in renal failure. Conditions such as multiple myeloma can result in amyloid kidney, light chain deposition and hypercalcaemia all causing renal failure. The patient could simply have a parathyroid adenoma causing the problem! However, at the bedside the patient had digital clubbing suggesting that malignancy could be yet another cause!

Why the hypermagnesaemia??

Well, this is the most interesting part. When the drug list was examined in detail, the patient was using magnesium hydroxide for constipation. Levels of >5mmol/L (this patient's was >6mmol/L) can cause prolongation of the P-R interval, widening of the QRS interval, increased T-wave amplitude leading to cardiac arrest. Hypotension is yet another feature. 

Hypermagnesaemia occurs especially when there is a combination of taking magnesium containing products e.g. purgatives (as in this case), with the presence of, yes you guessed it, renal failure !

Hence, tracing the set of events backwards it was possible to work out the likely causes to therefore work out why the patient developed heart block and collapse.

The lessons learned here include:

• Only do a CT scan when it is absolutely necessary; even then, in the elderly, be mindful about using contrast even in patients with seemingly normal renal function. Ensure that the patient remains well hydrated and follow-up blood tests are done to see if renal function deteriorates. 
• Try and think if you can get the same information in a different way e.g. waiting to do a colonoscopy rather than CT abdomen in cases of lower GI haemorrhage.
• Hypermagnesaemia can occur with magnesium hydroxide for treating constipation especially with concomitant renal failure ! 
• Once the acute problem e.g. complete heart block, has been effectively treated (in this case transvenous pacemaker insertion), the underlying cause must be investigated.
• Every problem whether it be a history problem, a physical examination problem, a radiological problem or a lab data abnormality MUST have an assessment and plan in order to avoid missing obvious and treatable causes of disease. Without an assessment there can be no treatment or further investigations.

It is entirely possible in this patient that the constipation was caused by the hypercalcaemia and use of purgatives resulted in the patient's heart block and collapse exacerbated by iatrogenic renal dysfunction.

My advice as always is to thoroughly analyse the history and its chronology, and moreover, check the drugs !!!!!!!!! In this case, a very commonly used drug caused a serious problem.

The current evidence suggests that either oral n-acetylcysteine or intravenous bicarbonate which are given before and after the contrast-requiring procedure, may reduce the incidence of contrast induced renal failure with similar numbers needed to treat of about 8. Please consider in at risk patients.

Treatment for hypermagnaesemia is circulatory support with intravenous fluid, cardioprotective calcium gluconate, furosemide (which causes magnesium loss via the kidneys) or failing that, dialysis.

Please consider...

p.s. the results to the latest mind boggling case will be available soon.... keep reading!

Now Its Time to Teach The Nurses

Dear Bloggers

Yesterday was my very first session for teaching nurses in Japan.

The lecture concentrated on physical examination of the chest with emphasis on basic treatment of the patient such as using a semi-recumbent position rather than prostrate position to reduce aspiration pneumonia and to improve ventilatory function in patients with COPD and cardiac failure.

The reason for such physical examination training? Well, doctors are not always around when you need them and it is useful for nursing staff to make an initial basic assessment so that when they inform the doctors,  the urgency of a particular problem can be better understood.

For example, knowing whether the JVP is raised in a breathless patient, counting the respiratory rate using a 'old fashioned watch' rather than relying on machines (which can sometimes be inaccurate), feeling the pulse rate and volume, knowing the signs for CO2 retention, knowing the difference between fluid or consolidation on basic examination of the patient's chest.

You may say that these are the job of the doctor. To some extent yes. However, doctors do not have a monopoly on physical examination and the fact is, there are simply not enough doctors in Japan per head of population. Hence, for nursing staff to be able to aid the doctors and spot the deteriorating patient early is essential, especially in a busy hospital.

Traditionally, there has been a separation between the job of the doctor and the job of the nurse. That separation is not practical or logical in today's society. In the UK, it is now becoming commonplace for emergency nursing staff to be able to take a history and perform a physical examination which helps the doctors see the patients more quickly after such an initial assessment. There are emergency specialist clinics for cellulitis and DVT which are run by nursing staff following a strict protocol. 

There is no reason why such specialist nurses with higher level skills and motivation should not be able to help with initial patient assessments.

The nursing staff were amazed to hear that examination of the chest starts by just observing the patient and of course, looking at the hands for clubbing!

The photo below shows the nurses checking for the normal diamond shape created when the two index fingers are put together back-to-back which is lost in advanced clubbing of the fingers. It would have been a good time to play the famous music from YMCA :-)

Teaching will continue monthly covering various aspects of physical examination, radiology, dermatology, diabetes medicine and so forth.

Luckily, I have an excellent translator to help me! :-)

Another Mind Boggling Case

Dear Bloggers

The following case has, as always, been anonymised to safe guard patient confidentiality and anonymity.  International physicians are also welcome to answer this case history. Please feel free to send in your answers which I will then publish.

This 61 year old male presented with a six-week history of

• Cough
• Fever
• Fatigue and Malaise
• Numbness and pain in the right hand
• Pain in the proximal lower limbs, buttock pain and dragging of the left leg

The cough commenced six weeks before admission and the patient considered this to be due to a common cold. The cough was non-productive. There was no associated sinus pain, rhinorrhoea, throat or ear pain. 

The fever had started gradually and had reached up to 38 degrees. There was no associated chills or shaking with the fever. No associated sweats.

The fatigue and malaise had been of relatively rapid onset and the patient had lost his appetite only being able to eat half of his food.

The numbness in the right hand had developed just prior to admission into the hospital. The numbness initially affected the thumb, index and middle finger but then became confluent over the entire palmar aspect of his hand. He did not complain of numbness on the back of his hand. He also described joint pain and was unable to make a fist. 

The pain in the proximal lower limbs was described as a dull ache in the back of his thighs. It was not worsened by movement or coughing. There was no history of any previous spinal pathology and no history of trauma. There was no 'shooting' quality to the pain. The patient had also developed a heaviness of the left leg and he was dragging it when walking. Although he was able to walk  he preferred to be prostrate because of the fatigue and malaise. 

The buttock pain was described as an ache and was localised without radiation. The patient preferred not to lie on his buttocks in bed and instead, laid on his side.

Prior to admission, the patient had sought medical advice from a local clinic on several occasions and several courses of antibiotics had been prescribed which had not resolved the problem.

On further questioning (Body Systems Review):

CVS: No chest pain, no palpitations, no breathlessness.

RESP: No sputum, no haemoptysis, no history of lung disease or TB exposure.

ABDO: No abdominal pain, no nausea or vomiting. No diarrhoea or constipation. No jaundice, normal coloured stool and urine.

MUSC-SKEL: No bone pains, no back pain, no joint swelling or stiffness. 

UROGEN: No urinary symptoms e.g. dysuria, haematuria, frequency, nocturia, urgency, hesitancy, incontinence, feeling of incomplete voidance etc...

CNS: No headaches, no pulsating head pains, no visual disturbance, no jaw claudication or tongue pain on eating. No description of facial numbness or pain. No dizziness or vertigo. No visual disturbance. No auditory disturbance.

ENDO: No thirst, no polyuria, no changes in ability of concentration, no tremor, no sweating, no previous fractures, no recent weight gain  or weight loss. 

SKIN: No complaint of skin rashes or ulceration.

Previous Medical History

Appendicectomy when aged 15 years

Left sided weakness at age of 30 years. No formal diagnosis made. Recovered within 6 months.

Medications- nil

No know drug allergies (NKDA)

Family History

No IHD, no AMI, no HTN, no hyperlipidemia, no diabetes mellitus, no connective tissue diseases.

Social history

The patient was normally well and independent and he worked part-time in a grocery store. He had not been able to work for 1 week prior to admission because of the worsening symptoms.

He was a non-smoker and drank occasional alcohol. He lived with his wife and had two adult sons.

On Examination-- please pay careful attention to the detail here!

General Impression: The patient looked unwell but not seriously ill.

Vital Signs: Temp 38.4 C, BP 140/80, Pulse 110/min (regular), respiratory rate 14/min, SpO2 98% breathing ambient room air. BMI 38.2

General: No clubbing, no splinter hemorrhages, no Janeway lesions or Osler nodes. No conjunctival hemorrhages.  No lymphadenopathy.

CVS: Apex not displaced. No heaves or thrills. Heart sounds 1 + 2. No systolic or diastolic murmurs. No lower limb swelling or evidence of deep vein thrombosis (DVT)

RESP: trachea central and no tracheal tug. Expansion, percussion and auscaultation were normal. Palpation of the chest revealed tenderness along the anterolateral aspect of the ribs bilaterally.

ABDO: Subcutaneous fascia ++. Soft, non-tender, no obvious masses or hepatosplenomegaly. No abdominal bruits and normal bowel sounds. No renal angle tenderness. 

CNS: normal cranial nerve examination.

PNS: tone, reflexes and coordination were all within normal limits. Gross sensation of the upper and lower limbs was normal except the right hand. Sensation of the hand was reduced over the entire palmar aspect including the fingers and the distal dorsal aspects (nail area). The dorsal aspect of the hands had normal sensation. Babinski sign negative bilaterally.

MUSC-SKEL: The right hand was held open in extension. The patient was unable to make a fist because of pain. Examination of each small hand joint revealed pain in the metocarpophalangeal joints of the index and middle finger. There was no increased warmth or swelling. Several of the proximal interphalangeal joints were also painful but not obviously swollen. The wrist joint was not painful or swollen. 

Movements were reduced in extension but particularly flexion of the fingers. The patient was unable to grip paper between his thumb and index finger (pincer grip) or between the index and middle and the middle and ring finger. Testing these movements was not painful.

Power (MMT) of the other remaining limbs was 5/5 (normal)

Examination of the left hand was normal.

Examination of hip movements revealed a normal range of movements which was non-painful. Straight leg raising test was non-painful bilaterally.

Springing of the pelvis with the patient lying on his front elicited pain over the sacro-iliac regions.

Other joints e.g. elbow, shoulders, spine, knees and ankles were within normal examination limits.

ENDO: no tremor, no exopthalmos, no goitre, no pretibial myxoedema, no necrobiosis lipoidica diabeticorum, no acromegallic features, no Cushingoid features (moon face, shoulder hump, striae etc), normal genital size and testicular volume.

SKIN: no focal abnormality identified. No evidence of alopecia.

Questions:

1. From the history and physical examination, please make a problem list.
2. What are the possible differential diagnoses in this case?
3. What tests would you undertake to investigate this patient's problem including both simple and advanced tests?
4. Give your top three differential diagnoses.

GOOD LUCK !!!

Muscle fasciculation

Dear Bloggers

Muscle fasciculation is something that we have all read about but which we rarely see---unless you actively look for it.

This patient developed a peripheral neuropathy with wasting of the thigh, anterior lower leg and calf muscles causing a foot drop as a result of a vasculitis.

As can be readily seen in the video below, with this patient sitting at rest (hence not using the lower limb muscles), there is spontaneous, involuntary, gross muscle contraction and fasciculation. Please pay close attention to the trough formed between the quadraceps and medial thigh muscles.

   

B's Clinical Images in Medicine- A Quick Case-- The Answers

Dear Bloggers

Here are the answers to the recent blog case.

Professor Alan Lefor, Professor of Surgery at Jichi Medical School, Japan has provided an excellent set of answers to the case below:

It appears that with a history of dyspnea, cough, fever, poor dental hygiene and the attached x-rays, as well as hx of smoking, that this is a lung abcess. It looks like the superior segment of the left lower lobe. It could be a tumor with overlying infection, but there is an air-fluid level in the lung mass which to me suggests at least infection. It could be from Tuberculosis, or oral flora. Aspiration of oral flora is most common, and they typically occur in the posterior segments of the upper lobe or the superior segments of the upper lobe.

I would suggest a bronchsocopy for further evaluation, with cytology etc. Also AFB studies to r/o TBc. The pt needs a transtracheal aspiration to get definitive dx.

The treatment of this, at the least, would be antibiotics, but it may require surgical drainage if the pt does not respond to antibiotics, which should be done using a minimally invasive approach (VATS).

Thank you Professor Lefor.

Professor Tierney, Professor of Medicine, USCF, commented on a similar case some time ago on lung abscesses and I would like to share his words of wisdom with you today.

A lung abscess without teeth is cancer of the lung until proven otherwise.

The notion here is that edentulous patients have a much smaller oral burden of anaerobic organisms, which ordinarily originate in the teeth, and thus a cavitary, abscess-like lesion virtually always implies bronchial obstruction. In a series of several hundred similar infections reported from the West Los Angeles Veterans Hospital this rule was never broken. In general, drainage is as important as antibiotics in such patients, performed by sequential rigid bronchoscopies.

Thank you Professor Tierney.

Gurpreet Dhaliwal, M.D., Associate Professor of Medicine, UCSF, has also kindly commented on this case.

1) What is the diagnosis from the history, physical examination and X-ray findings?

There is an irregular air-fluid level and cavity in the mid-left lung, perhaps in direct communication with the bronchus. Differential diagnosis is listed below. If forced to choose among them, the reported fever provides modest weight for an infection (lung abscess), as does the poor dentition and the diabetes mellitus. Putrid sputum and weight loss, which also characterize abscess, are not mentioned. There is no reason it can not be TB or malignancy, both of which bacterial lung abscess is known to mimic, and vice-versa. The ischemic ulcer on the right lower limb is quite common in a smoker with diabetes, but could be a portal of entry for a blood-borne infection.

2) List the likely cause(s)

Common offenders are lung abscess (aspiration or hematogenous), tuberculosis, lung cancer or metastases, and autoimmune syndromes like RA or Wegeners. Uncontrolled DM (and its associated nonspecific immunodeficiency) might expand the possible list of infections.

3) What other tests would you do?

A sputum study for cytologic, mycobateriologic, and bacterial examination. CT imaging, bronchoscopy, or both may be required if sputum is unrevealing.

4) What is the current evidence based treatment of such a condition?

I don’t know the latest with regards to lung abscess (if that’s the correct dx). Usually prolonged treatment with antibiotics will suffice, with some very old data favoring clindamycin over PCN. Lung abscesses are “drained” by their communication with the bronchial tree.

Thank you Dr Dhaliwal

What happened with the patient?

The patient deteriorated with an increasing size of the abscess despite standard antibiotic treatment for this condition. At presentation, the abscess diameter by chest xray measurement was 6.5 cm (a poor prognostic feature). The patient did not receive a bronchoscopy.

Several days into the hospital admission, the patient developed sudden chest and abdominal pain. Radiological investigations revealed breakdown of the abscess with a resulting pyopneumothorax which required intervention by chest drainage.

Usual cultures of the fluid remained negative.

However, the pleural examination revealed the following: LDH 5021, total protein 4.2 and Adenosine Deaminase (ADA) was 70 U/L.

The above results are mainly consistent with the presence of either an abscess, empyema, carcinoma, rheumatoid lung or tuberculosis. However, the ADA level was >60 U/L making tuberculosis a more likely candidate.

As can be seen by the above observation chart, following drainage with a chest tube, the fever and pulse began to settle (red- pulse, blue- temperature).

As a physician, in a case such as this, I would rely more heavily on the observation chart such as the pulse and fever rather than watching the C-reactive protein. Remember, CRP is not a vital sign and is expensive whereas, pulse and temperature ARE vital signs and can be measured for free and actually show how the patient is improving!

The Current Evidence

In a recent review of the literature from UpToDate version 16.1 the vast majority of abscesses are caused by anaerobic organism inhaled into the lungs when in a recumbent position i.e. when sleeping.

Various organisms are involved in the infective process including peptostreptococcus, Prevotella, Bacteroides species and Fusobacterium species. There are other bacteria that can also cause lung abscess e.g. streptococcus, Tb, but the anaerobic organisms are by far the most common.

Indeed, as Prof Lefor mentions, the infection tends to affect posterior lung segments or upper segments of lung lobes where there can be infection in the recumbent position.

The history is usually one of cough, sputum, chest pain, fever and sometimes a foul putrid smell to the breath or a bad taste in the mouth.

It is important to try and obtain sputum for gram stain and culture. Tracheal aspirates are performed in Japan via the nasal cavity but can be uncomfortable and cause localised trauma to the nasopharyngeal mucosa. Bronchoscopy to obtain a specimen is considered controversal and should be performed by an experienced operator because spillage of fluid from the abscess cavity can result in further lung infection.

However, in cases where the abscess is unresolved by antibiotic therapy, bronchoscopic placement of a pigtail catheter to drain the abscess may be of use or percutaneous drainage can also be performed. In unresolving cases, surgery is sometimes required.

Antibiotic therapy is aimed at the underlying cause. The common antibiotic therapy for anaerobes is Clindamyin 600 mg IV Q8h, followed by 150 to 300 mg PO four times daily. The duration of therapy is at least 3 weeks and/or until there is symptomatic and radiological resolution.

Of course, malignancy should always be ruled out especially in a smoker. Hence, sputum should also be sent for cytology. In uncertain cases, a bronchoscopy and obtaining brushings, aspirates and bronchoalveolar lavage may provide helpful clues to the underlying cause.

Moreover, ruling out tuberculosis must be considered in 'at risk' patient e.g. from high risk areas, immune suppression e.g. HIV, and should prompt the physician to check a ZN stain on 3 daily sputa, TB PCR, a Tuberculin Skin test and Adenosine Deaminase in the pleural fluid. Fluid should be sent for long term TB culture and if still undecided, a Quantiferon test may help.

For a more indepth discussion on this subject I would suggest reading the current evidence in UpToDate 16.1

Please Consider....

Rheumatology, oh joy, rheumatology

Dear Bloggers

Professor Stein joined us for two-days to do his famous teaching through case examples.

Being an expert in rheumatology, he was presented with various difficult cases covering rheumatology and general internal medicine. Cases, that were presented in English by the Japanese 1st, 2nd and 3rd year residents, included:

• Infective endocarditis due to streptococcus bovis
• Rheumatoid arthritis-systemic sclerosis overlap syndrome
• Churg-Strauss syndrome

Professor Stein then instructed the residents how to take a rheumatologic physical examination and how to understand the problems of the history, physical examination, lab data and radiology in order to construct a problem list and assessment to decide on what would be the best way to proceed with further tests and / or treatment.

Here are some photos of his current visit.

B's Clinical Images in Medicine- A Quick Case

Dear Bloggers

Below is a set of radiographs of a patient who presented with increasing cough, dyspnoea and fever.

The patient had long-term untreated diabetes mellitus and there was a history of chronic, heavy smoking.

On examination, dental hygiene was poor and the physical examination of the chest revealed no abnormalities to percussion or auscaultation. Abdominal examination was normal.

The patient had an ischaemic ulcer present on the right lower later limb.

Questions:

1) What is the diagnosis from the history, physical examination and Xray findings?

2) List the likely cause(s)

3) What other tests would you do?

4) What is the current evidence based treatment of such a condition?

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.....