Reflections on an elderly man with breathlessness

When a 68 year old man, a smoker, presents with breathlessness and rhonchi in the lungs, with an x-ray chest showing emphysema (increased air trapping), the most obvious clinical diagnosis is COPD. 

Since bronchial asthma is also a disease with rhonchi in the lungs, one may be asked whether this patient has bronchial asthma. As a rule of thumb, one can say that COPD is more likely in older individuals with wheezing while bronchial asthma is more likely in younger people. Having said this, we must not forget that late onset bronchial asthma is possible and COPD can occur in younger individuals with, say, alpha one antitrypsin deficiency. So age is not an absolute differentiating criteria. 

What are the more reliable differentiating points between COPD and bronchial asthma? In the history, an episodic nature of breathlessness or a diurnal variation in breathlessness, with completely asymptomatic periods in between, are strong points in favour of bronchial asthma. Based on spirometry, one can say that if the FEV1: FVC ratio remains below 0.7 after adequate bronchodilator therapy, the diagnosis is COPD. It is important to know that the reversibility of the bronchial tree should be used diagnostically only in the stable phase, not during a time when the patient is having an acute exacerbation.

Rhonchi in the lungs indicate bronchial narrowing. The typical physical sign of obstructive lung disease is rhonchi on auscultation but the absence of rhonchi does not rule out an obstructive lung disease. 

The clinical context in which one detects rhonchi is very important. In elderly people and in those with cardiovascular risk factors, the possibility of heart failure must always be considered as a differential diagnosis when they have rhonchi and crepitations in the lungs. When in doubt, treat with diuretics and bronchodilators until the diagnosis is clear. Based on the proverb "All that glitters is not gold" we have the clinical saying: All that wheezes is not asthma. This implies that wheezing need not always be due to bronchospasm but can also be due to extrinsic compression by edema or a mass.

The PEFR is a useful tool for managing patients with obstructive lung diseases because it gives us an objective parameter to measure the degree of bronchospasm. In this context, I wish to emphasise that even in COPD there is always an element of bronchospasm. The PEFR has both diagnostic and therapeutic implications. With the PEFR we can diagnose asthma and differentiate between asthma and COPD based on the degree of reversibility in readings. With the PEFR, we can also titrate medication in bronchial asthma. We know, for example, that we must prescribe oral steroids to a patient with bronchial asthma whose PEFR remains persistently below 50 percent of expected.

Crepitations in the lungs can indicate a number of possibilities according to the clinical situation. Consolidation of the lung, bronchiectasis, interstitial lung disease and left heart failure are some of the conditions that must come to mind when crepitations are detected in the lungs.

A low PaO2 alone or in combination with a high PaCO2 signify respiratory failure in a patient with COPD. What does a normal PaCO2 in a patient with acute exacerbation of asthma or COPD indicate? It indicates that there is insufficient alveolar ventilation and is a red flag. This is the rule of thumb: In all people who are hyperventilating, the PaCO2 must be low. If it is not low, it means there is insufficient alveolar ventilation. A danger sign.

Hyperinflation of the lungs is generally said to be present when we see that the domes of the diaphragm are flat and the right dome of the diagphram is below the anterior end of the 6th rib. In lungs with hyperinflation, the cardiac show will appear smaller than usual. If it appears normal or enlarged, cor pulmonale or some other form of heart disease must be suspected. 

In patients with COPD, pay particular attention to the pulmonary arteries. The main pulmonary artery is the convexity below the aortic knuckle on the left heart border. It is normally smaller than the aortic knuckle. When the main pulmonary artery is as big as or bigger than the aortic knuckle, one can suspect that it is enlarged because of pulmonary hypertension. Remember: Perihilar shadows in COPD can be due to enlarged pulmonary vessels.

An opacity in the lungs on chest x-ray only means that the air in the alveoli has been replaced by something else. Opacities in the lungs occur in consolidation (inflammatory fluid), pulmonary edema (non-inflammatory fluid), fibrosis and collapse as well as mass lesions. You will need to evaluate the nature of an opacity by looking for associated signs in the x-ray and by knowing the clinical features of the patient. Some opacities have characteristic associations - like consolidation in the upper lobes of the lungs strongly suggest tuberculosis infection. But these are not absolute and therefore not diagnostic. Upper lobe opacities for example can be due to silicosis, malignancies, granulomatous diseases, and Klebsiella pneumonia.

The perspective gap

In the book 'Give and Take' by Adam Grant, psychologist and professor at Wharton Business School, there is a term called the perspective gap. This refers to our inability to fully appreciate another person's distress when we ourselves are not experiencing a similar kind of distress. The perspective gap explains why physicians often underestimate the severity of the pain that their patients report. In this context, the author of the book gives an account of an incident that occurred in a San Francisco hospital where a respected oncologist wanted a spinal tap done for a patient with advanced metastatic cancer because he wanted to determine if the reason for that patient's deteriorating level of consciousness was meningitis.

The neurologist, who was requested to do the spinal tap, however had his doubts about the need for such a procedure because, not only would the procedure be painful for the patient, he believed it would not result in any significant clinical improvement. The patient and his relatives too did not want the procedure. However, after repeated explanations and much persuasion by the oncologist, the patient and family members agreed to the procedure believing that the oncologist could not be wrong. The neurologist finally did the spinal tap. Soon after that, the patient developed a pounding headache, slipped into a coma and died three days later from the cancer.

The neurologist goes on to say that this incident showed him how the oncologist uncritically accepted the notion that he was doing good. This is the perspective gap that we, as doctors, must always be aware of. The only way to avoid it is to always look at the advice we give to our patients from the point of view of the patients themselves. We should remember the perspective gap when we advice our patients about diabetic diets and also when our prescriptions contain too many medications.

Treating acute ischemic strokes with antidepressants

Depression is common after strokes. This is something that we can all relate to intuitively because a catastrophic event like a stroke is bound to affect one's emotions. A study published in the Medical Journal of Malaysia (April 2, 2013) reinforces this point and made me look up an article that had caught my attention a few months ago. In February 2011, the Lancet Neurology had published a study involving 113 patients with ischemic strokes and hemiplegia / hemiparesis, 57 of whom were treated with 20mg of Fluoxetine daily within five to eleven days of the stroke. At the end of three months, the researchers noted that those who had been treated with Fluoxetine (and physiotherapy) showed better motor recovery than those who received only physiotherapy.

When patients are depressed, they are unlikely to be motivated to do the post-stroke exercises that will help them recover motor function. While this may be a good reason to diagnose and treat depression after a stroke, the authors of this study also postulate that fluoxetine may have direct beneficial effects on neurons. It may turn out that antidepressants like fluoxetine are good for stroke recovery irrespective of whether the affected person is clinically depressed or not.


References:
1. Prevalence of depression in stroke patients with vascular dementia in University Kebangsaan Malaysia Medical Centre.

2. Fluoxetine for motor recovery after acute ischemic stroke (FLAME): a randomised placebo-controlled trial. 

Atypical pneumonia

Atypical pneumonia is often due to Mycoplasma or Chlamydia infections when the pneumonia is community-acquired. This type of atypical pneumonia responds well to macrolide antibiotics. In this week's issue of the New England Journal of Medicine (article), there is a report about a healthy young woman who developed a form of atypical pneumonia that rapidly progressed to respiratory failure. Hence this is a good opportunity to discuss some clinical aspects of severe atypical pneumonia acquired from the community.

Atypical pneumonia - other than Mycoplasma and Chlamydia - should be suspected when the respiratory illness does not respond to treatment with the usual antibiotics for community acquired pneumonia.

1. Think of Legionella pneumophilia when there are associated symptoms and signs of involvement of the CNS and / or gastrointestinal tract.

2. Think of Leptospiral infection when there is associated severe myalgia, headache or neck pain. Involvement of the liver and kidney and the presence of a skin rash are further points in favour of suspecting this condition.

3. Think of fungal pneumonia if the patient is immunocompromised and if there is exposure to an enviroment where fungi are likely - mouldy and damp places like caves, for example.  

4. Think of Toxoplasma and Pasteurella infections if there is close exposure to cats.

5. Think of Lyme disease, Rickettsial infections and Tularemia if there is a history or physical evidence of tick bites.

A woman with diarrhoea

A patient without a pituitary gland?

"Please see my MRI. Something is very wrong," my patient, Ms L. said to me.

I looked at her carefully. She appeared to be close to tears. Then I opened the large folder containing her MRI scan pictures and looked at the radiologist's report first. It read: Empty sella syndrome. There was no other abnormality in the scan.

"Who sent you for this scan?" I asked.

She looked embarrassed when she told me that she had been referred for the scan by a doctor in a private hospital because of her headaches. Of course I knew that she had been suffering from headaches because she had been my patient for over 2 years and I was treating her for migraine.

"I went to this doctor because some of friends told me that I should get a second opinion for my headaches," she explained.
"So, what did the doctor say after seeing this scan?"
"He said that I did not have a pituitary gland. He said I needed tests for different kinds of hormones." After a pause, she continued, "I cannot afford the costs of all those tests."

It was a familiar story. Patients are often attracted to doctors who "scan them" believing that scanned images of their bodies are better than clinical judgement.

I looked sympathetically at Ms L. How should I start explaining to her that she could not have lived all these years if she did not have a pituitary gland? Then I told her that the empty sella syndrome is a radiological diagnosis only. It simply means that the pituitary gland is not seen on MRI scans. Just because it is not seen on the scan, does not mean it is not there. Many people with the empty sella syndrome have normal pituitary function.

I ordered the tests for the relevant anterior pituitary hormones - TSH, FSH, LH, ACTH and Prolactin - and spent time reassuring her that her headaches were not due to a brain tumour. Two weeks later, I reviewed the results of these tests and found them all to be normal. Ms L was relieved.

"I wonder where my pituitary gland is hiding," she murmured.
With a straight face I told her, "We will not search for it with any more scans."

Even after she left, her question kept haunting me. Where was the gland if it was not in the sella tursica? I must find the answer to that.

When a doctor prescribes a drug with uncomfortable side effects.....

A 35 year old woman came to my clinic in the hospital because she had noticed discharge of milk from both her breasts. Her last pregnancy was more than 4 years ago. Her physical examination was normal. I wondered if she had hyperprolactinemia and I requested a test for the same.  I also asked her about her menstrual cycles and whether she experienced any hot flushes because I was aware that increased prolactin levels diminished secretion of estrogen from the ovaries. She said that her menstrual cycles were erratic. She did not have any hot flushes. I should have discussed about libido but I did not. Anyway, the serum prolactin levels were high in her and that made me suspect that she had a prolactin secreting tumour in the pituitary. I examined her cranial nerves, pupils, optic disc and visual acuity and field of vision. Nothing abnormal was detected.

The patient was worried when she realised that she might have a tumour in the brain. I explained to her that such tumours were never malignant and that, in most cases, it was so small that we did not even call it a tumour. Instead we called it a microadenoma. She wanted to know how small it was. I told her that a microadenoma is, by definition, something that is less than 10mm in diameter and I showed her how small it looked on paper.

An MRI was then done for her. It confirmed a microadenoma of the pituitary. I then tested her thyroid function and her serum cortisol level because, even though it was only a microadenoma, I wanted to make sure that it was not impinging on the function of the adjacent parts of the pituitary gland. These tests were normal.

In consultation with an endocrinologist she was then offered treatment with a dopamine agonist. We offered her bromocriptine because that was the only drug available with us in the hospital. I knew though that the best dopamine agonist for reducing serum prolactin was cabergoline. Dopamine agonists are also used to treat Parkinsonism and my patient had an uncomfortable moment when the pharmacist who dispensed her medication told her that she had Parkinsonism. It took me awhile to reassure her that she did not have that neurological disease.

When she began to suffer nausea and vomiting because of the bromocriptine, she consulted another doctor in a different hospital. Following the advice there, she underwent transsphenoidal resection of the microadenoma. This is a technique where the tumour is excised through an incision in the nose so that the lesion can be approached through the sphenoid sinus.

She came back to see me after the surgery, happy that she did not have to take the bromocriptine anymore. I learnt something useful from this encounter: when a doctor prescribes a drug that causes uncomfortable side effects, the patient blames the doctor, not the drug!