A patient with lung cancer and breathlessness

An elderly man with bronchogenic carcinoma was admitted for shortness of breath. Clinical examination showed the trachea to be deviated to the right side. His right chest was dull on percussion with markedly diminished breath sounds. The air entry in the left lung was normal. There were no signs of cardiac failure. Abdominal examination was normal. A chest x-ray showed a large homogenous opacity on the right side of the chest which the attending doctors interpreted as a right pleural effusion. Pleural tapping was attempted three times but was unsuccessful. An ultrasound guided pleural aspiration yielded 50ml of serosanguinous fluid. The patient was treated with nasal oxygen and intravenous fluids.  He gradually improved over a period of four days and was discharged with advice to return for pleural aspiration again if he developed breathlessness.

(Contributed by Azra Kurtovic)

Was this patient’s breathlessness due to his pleural effusion? 



Comment
It is easily evident from the available information that his breathlessness was not due to a pleural effusion. It is not reasonable to assume that aspiration of 50ml of pleural fluid could relieve his breathlessness. We can also infer that the opacity seen in the chest x-ray was not due to a pleural effusion as interpreted by the attending doctors. The trachea, which was shifted to the same side as the opacity, tells us that there is volume loss in the right lung – possibly due to some degree of collapse of the lung caused by the cancer compressing a bronchus.  The radiological opacity seen on the chest x-ray must therefore be due to a combination of the tumour and the lung collapse. A small amount of pleural effusion cannot be excluded. His improvement in the hospital must have been due to the supplemental oxygen which helped relieve his hypoxia.

A patient who did an exercise stress test

A 46 year old man with hypertension and elevated cholesterol levels presented to his doctor with chest discomfort on inspiration. He had no history of chest pain or breathlessness on exertion. He did not have diabetes and he was not a smoker. However there was a strong history of cardiovascular disease in his family.
His physical examination was normal. The resting ECG was also normal. The doctor diagnosed non-cardiac chest pain in him but recommended an exercise stress test.

An exercise stress test using the Bruce Protocol is done. His heart rate and blood pressure are 96/min and 148/86mm Hg respectively at the onset of the test. He progresses steadily from Stage 1 to Stage 4 without any symptoms of chest pain or breathlessness and without any ECG signs of inducible myocardial ischemia. At the beginning of Stage 5, his heart rate is 150/min and his blood pressure is 145/90mm Hg. The exercise stress test is stopped because he feels tired. His peak exercise is recorded as 13 METS.

During recovery, the ECG shows ST segment depression, beginning from 3 minutes of recovery and persisting till the recording was stopped at 6 minutes.

Question: If this patient undergoes a coronary angiogram, which of the following is likely?

1. No coronary artery disease
2. Mild coronary artery disease
3. Severe coronary artery disease

Discussion

An exercise stress test is done for the purpose of detecting inducible myocardial ischemia. Parameters suggestive of inducible myocardial ischemia are: Angina during the performance of the test, ST segment changes, occurrence of ventricular ectopic beats, inability to complete the test, and failure of blood pressure to increase appropriately during the exercise.

This patient showed ST segment depression in the ECG during recovery from the test. Changes in the ST segment during recovery are as significant as ST segment changes during exercise. Hence we can infer that he has coronary artery disease.

When ST segment depression persists more than 8 minutes after the test is stopped or if the blood pressure does not increase as expected during the test, there is a high probability of severe coronary artery disease. Here, the ECG continued to show ST depression at 6 minutes after the test was stopped. Since the ECG was not recorded after that, we do not know for sure how long the ST segment would have remained depressed. Also, his systolic blood pressure did not show an appropriate increase. These tell us that he is likely to have severe coronary artery disease.

References:
1. The significance of ST segment depression that occurs only during the recovery phase of an exercise stress test. (http://www.ncbi.nlm.nih.gov/pubmed?term=2293816)
2. Exercise testing in the evaluation of coronary artery disease. (http://www.ncbi.nlm.nih.gov/pubmed/6979501)
3. The prognostic value of the exercise stress test. (http://www.ncbi.nlm.nih.gov/pubmed/3056676)

Atrial fibrillation

Atrial fibrillation can be either persistent or paroxysmal. When dealing with new onset atrial fibrillation (AF), generally we tend to wait for at least a week before labelling it as persistent AF. The treatment of persistent AF is either rate-control or rhythm-control. When we choose the rate-control strategy, we allow the arrhythmia to persist (atrial rate in AF is more than 350 per minute) but we use drugs to prevent the ventricular rate from exceeding a particular limit (below 90/min at rest and below 110/min during usual activity).

When we choose the rhythm-control strategy, we take measures to change the AF to sinus rhythm. We do this either with drugs (usually Class 1C or Class 3 antiarrhythmic drugs) or by electrical means. Research on atrial fibrillation has told us that both the rate-control and rhythm-control strategies are fine provided patients on rate-control are on adequate long term anticoagulation. It does seem a bit illogical that allowing a fast atrial arrhythmia to remain intact has the same outcomes as changing it back to its normal rhythm. The answer lies in knowing that long term use of antiarrhythmic drugs is not completely safe because they have a pro-arrhythmic effect and can provoke ventricular arrhythmias which lead to complications.

We also know that if we can control the ventricular rate adequately, we can prevent tachycardia-induced cardiomyopathy from developing.

For those who have paroxysmal AF, the treatment options are not so clearly defined even though we know that long term anticoagulation is necessary for them too. Patients with paroxysmal AF tend to be treated with antiarrhythmic drugs. Another option for such patients is catheter-ablation therapy, a procedure where the pulmonary veins in the left atrium are electrically isolated by using radio-frequency energy. All invasive procedures have risks and catheter ablation for AF can lead to strokes (by dislodging microemboli from the left atrium) and cardiac tamponade (by piercing the atrial wall).

A recent study in the New England Journal of Medicine tells us that both drug therapy and catheter ablation are effective for patients with paroxysmal AF and that there is no strong evidence yet that one is better than the other even though we know that those who undergo catheter ablation have less recurrence of AF after two years.

Question: Is it possible to say what the cardiac axis might be just by looking at Lead aVL as shown above?

Answer: It is not possible to say exactly what the cardiac axis is but one can infer in this manner:


1. The current is moving away from aVL. Left axis is the state where the current is moving towards the left side in the segment beyond minus 30 degrees. Therefore lead aVL tells me that this is not left axis.

2. If the current is exactly minus 30 degrees (normal axis) or zero degrees (normal axis), or plus 30 degrees (normal axis), lead aVL should be having a net positive deflection because the electrical scatter is still towards aVL. Therefore the axis is not zero degrees or minus 30 degrees or plus 30 degrees.

3. If the axis is plus 60 degrees, lead aVL should have biphasic deflection (positive and negative deflections are equal) because plus 60 degrees is exactly perpendicular to Lead aVL. Therefore the axis is not plus 60 degrees either.

4. If the axis is plus 90 degrees (normal axis) or beyond 90 degrees (right axis), lead aVL will show a negative deflection because now the electrical scatter is truly away from aVL. Therefore the axis here may be normal (between plus 60 and 90 degrees) or right axis (beyond plus 90 degrees).

Question: Is the ventricular ectopic seen in the given Lead aVL, arising from the right ventricle (RV) or from the left ventricle (LV)?

Answer: If an ectopic beat starts in the RV, it will depolarise the RV first and the LV later. Hence a ventricular ectopic that originates from the RV will have a LBBB pattern. Similarly, a left ventricular ectopic depolarises the LV first and the RV later. Hence it will show a RBBB pattern. So, if a ventricular ectopic shows the LBBB pattern, it is a ventricular ectopic from the RV and if the ectopic beat shows a RBBB pattern, it is a left ventricular ectopic.

The ectopic beat in aVL here (a lead that looks at the left side of the heart) has an LBBB pattern. Therefore it is an ectopic beat that originates from the RV.

A man who could not feel the left side of his body

A 50 year old man was admitted with a sudden inability to feel the left side of his face, left arm and left lower limb. He could speak and he could move all his limbs. He had been diagnosed to have hypertension a few years earlier but he had discontinued his medicines because he felt well. At the time of admission, his blood pressure was 180/106mm Hg and he was conscious and alert. Neurological examination confirmed that he did not have any deficit other than the hemisensory loss. He began improving about 8 hours after admission and within a day, he had recovered his sensations fully. He was diagnosed as having suffered a transient ischemic attack and treated appropriately.

Discussion

Does the diagnosis of a TIA depend only on how soon a patient recovers form a stroke?
It used to be that a diagnosis of TIA was made when a patient recovers from a cerebrovascular event within 24 hours. Now that we know that some of those with a clinical diagnosis of TIA have a visible infarct on brain imaging, the definition of TIA has changed. A TIA, by the new definition, is a transient cerebrovascular event without any visible lesion on brain imaging. 

What about those who recover from a stroke within 24 hours but have a visible infarct on brain imaging?
They should be considered as having suffered a minor stroke. 

Can this patient be considered to have suffered a lacunar infarct if his brain imaging shows a visible infarct?
Yes. A pure hemisensory deficit is a manifestation of a lacunar infarct. The various clinical manifestations of a lacunar infarct, and their corresponding lesions, are given below (MedTutor acknowledges, with gratitude, the contribution for this answer by medical student Wong Wai Kit): 


Pure motor hemiplegia - the affected artery is the lenticulostriate branch of the middle cerebral artery and the lesion is in the internal capsule.
Pure sensory stroke - the affected artery is thalamogeniculate artery which results in a lesion in the ventral posterio-lateral nucleus of  the thalamus.
Clumsy hand syndrome/Dysarthria - the affected artery is the penetrating branch of the basilar artery producing a lesion in dorsal Pons.
Ataxic hemiparesis - the affected artery is the penetrating branch of the basilar artery producing a lesion in the ventral Pons.

A man with breathlessness whose lungs were clear on auscultation

A 57 year old man with diabetes was admitted for breathlessness. His ECG initially showed sinus rhythm with first degree heart block. All the complexes in the limb leads, and most of the chest leads, were of low voltage. A repeat ECG a few hours later showed the same low voltage complexes and a slow regular rhythm of 38 beats per minute. The rhythm was suggestive of an escape ventricular rhythm. P waves could not be identified consistently in the ECG tracing.

Investigations showed that he had advanced renal failure with a serum creatinine of more than 600umol/L. The serum sodium and potassium were normal.

His lungs were clear on auscultation in spite of his breathlessness and the presence of distended neck veins in the neck and a palpable tender liver. His x-ray chest showed significant cardiomegaly. The lungs were clear with reduced vascular markings.

He was treated as congestive cardiac failure due to dilated cardiomyopathy and complete heart block, diabetes, and end stage renal failure.

Discussion
Is the diagnosis of dilated cardiomyopathy correct?
A large heart shadow on the x-ray chest, the presence of congestive cardiac failure and the absence of obvious causes for the heart failure can be the reasons for a diagnosis of cardiomyopathy. However, in this patient with signs of heart failure, the cardiomegaly, the low voltage complexes in the ECG, and the absence of adventitious sounds on auscultation of the lungs should make one consider the diagnosis of a pericardial effusion.

What could be the cause of the pericardial effusion?
The best guess in this situation will be uremic pericarditis with effusion.

Is the slow heart rate due to complete heart block?
I am not in favour of interpreting the ECG as complete heart block because the P waves are not seen regularly. The absence of P waves and a slow regular ventricular rhythm suggests the diagnosis of sick sinus syndrome. Hyperkalemia can be a reason for absence of P waves in the ECG, but that is not the reason in this patient because the serum potassium was normal.

What is the finding in the ECG that differentiates a slow ventricular rate due to complete heart block from sick sinus syndrome?
In complete heart block, the atrial rate is always faster than the ventricular rate and this can be seen from the P wave rate and the QRS rate. In sick sinus syndrome, there will often be no P waves and the slow ventricular rate is either because of a junctional escape rhythm or an escape ventricular rhythm.

A man with COPD and frequent ventricular ectopics

A 94 year old man with chonic obstructive pulmonary disease was admitted in hospital because of increasing breathlessness and cough. This was his 3rd admission in 2012 (a period of 8 months) for similar problems. At the time of his admission, his ECG showed sinus rhythm, low voltage complexes in the limb leads and most of the chest leads, frequent ventricular ectopics and ST segment depression and T wave inversion in the chest leads V2 to V6. The ventricular ectopics were no longer present two days after he was treated for his COPD with bronchodilators, glucocorticoids, antibiotics and nasal oxygen. The ST segment depression and the T wave inversion also resolved.

Discussion

What was the reason for his ventricular ectopics and ST segment and T wave changes at presentation?
Myocardial hypoxia secondary to arterial hypoxia must have been the precipitating cause for these ECG changes. It is very likely that he has underlying stable coronary artery disease.

What is the reason for the low voltage complexes in the ECG?
He has hyperinflated lungs. This must be reason for the low voltage ECG complexes.

Should this patient be treated with inhaled glucocorticoids when he is discharged?
Yes. This patient has, by definition, frequent exacerbations of COPD (more than 2 episodes in a year). He should receive long term inhaled glucocorticoids in addition to inhaled long acting beta-agonists and/or long acting anticholinergics.

Is it necessary to prescribe long term oxygen therapy for him?
Long term oxygen therapy (LTOT) is indicated only in those who have direct or indirect evidence of persistent hypoxia - for example, an arterial oxygen partial pressure of less than 56mm Hg (7.3kPa), pulmonary hypertension, cor pulmonale or secondary polycythemia. If these are not present, this patient need not be given LTOT.

A teenager with fever and a low blood pressure

A 17 year old boy was admitted in a state of peripheral circulatory failure with cold clammy hands and feet and a blood pressure of 78/60mm Hg. He had been unwell with fever, headache and aches in various parts of his body for 5 days but had not sought medical treatment. He had noticed slight bleeding from his gums when he brushed his teeth. He did not complain of abdominal pain, nausea and vomiting or cough and breathlessness. Initial investigations in the A&E showed that he had a hemoglobin value of 11.2gm/dL, a total white cell count of 4200/uL and a platelet count of 68000/uL. He was diagnosed with dengue shock syndrome and treated intensively with intravenous fluids while the results of further tests were awaited.

Discussion

Can dengue shock syndrome be diagnosed in a patient like this without any obvious excessive bleeding?
Yes, we can. Dengue shock syndrome occurs in Dengue hemorrhagic fever (DHF), not in classical dengue fever. The distinction between these two types of dengue fever does not lie in the degree of bleeding but in the presence or absence of plasma leakage from the vessels. Having said this, I must also state that generally, one expects a greater degree of bleeding in DHF than in classical dengue. 

How do you recognise capillary leakage of plasma in a patient with dengue fever?
The clues to this are: 
1.An increase of 20 percent in hematocrit from the previous value, or the reverse - that is, a fall in hematocrit by 20 percent after hydration is initiated.
2. A pulse pressure less than 20mm Hg 
3. A low serum protein level 

We know that fluids are the mainstay of treatment for dengue shock syndrome. How do you initiate fluids and when will you consider colloid infusions?
Crystalloids - normal saline or dextrose saline or Ringer Lactate - can be initiated at 6ml/kg per hour for 2 hours. If the blood pressure does not increase, we can infuse at 10ml/kg per hour for another two hours. If the BP is still low at this point, colloids (like Dextran 40) can be considered. 

IgM antibodies to the dengue virus are generally detected after 5 days of the illness. Is there any test that can detect the dengue virus in the first one or two days of illness?
Yes, there is a commercial test kit for the NS 1 viral antigen (Non Structural viral protein). This test can help to confirm dengue infection within 24 to 48 hours of the onset of fever. 

A man who did not know he had renal disease

A 45 year old man with diabetes and hypertension was admitted in the ward because of cardiac failure. After his admission, investigations showed that he had advanced renal failure. Subsequently he underwent two sessions of hemodialysis through a double-lumen femoral catheter. He never knew he had renal disease until this admission. He had been regularly reviewed by doctors for diabetes and hypertension in a government clinic near his house for about ten years. Four years ago, he had been referred to an ophthalmologist in a specialist government hospital and had undergone laser treatment for retinopathy.

The doctors attending to him during this admission feel that he may have end-stage renal disease and have recommended that he should undergo the creation of an AV fistula for the purpose of regular maintenance hemodialysis in the future.

Discussion

Is his kidney disease a recent development?

No. He must have had chronic kidney disease 4 years ago at the time when he was treated for diabetic retinopathy because there is a close association between these two microvascular complications.

If his chronic kidney disease had been detected 4 years ago, would it have benefited this patient?

Yes, it might have benefited him because, with early detection, we could have attempted to slow down the progression of renal failure and give him a longer period of life without renal replacement therapy.

What are the treatment options to slow down the rate of renal deterioration in diabetes?

Treating diabetes to achieve target blood sugar values, treating hypertension to target values and the use of medication that inhibit the renin-angiotensin system have been shown to delay the progression of renal failure in diabetes.

Why should one be cautious about using the serum creatinine value during this admission to label him as end stage renal failure?

During this admission he has cardiac failure and, consequently, reduced renal blood flow. His serum creatinine on admission will therefore be the result of both his chronic kidney disease and the acute renal injury secondary to cardiac failure. Only after the acute event (cardiac failure) has been treated will the serum creatinine truly reflect the impact of his chronic kidney disease. Hence, one should not use his initial serum creatinine to label him as end stage renal failure. A repeat serum creatinine, after one or two weeks of treatment, will be a better measure of his chronic kidney disease and the need for maintenance hemodialysis.

A woman with deteriorating renal function

A 46 year old woman with diabetes, hypertension and bronchial asthma was admitted with signs of a respiratory infection and bilateral pedal edema. She was treated appropriately with antibiotics, diuretics and her usual medicines for diabetes, hypertension and asthma. Her ECG was normal.  Her renal function was impaired and she had a serum creatinine of 135umol/L. Her 24 hour urine protein estimation showed a value of 5.52grams protein. A diagnosis of diabetic nephropathy with renal impairment was made and treatment with Enalapril 10mg BD was initiated. One month later, she was asymptomatic even though she still had pedal edema. At this time her serum creatinine was 140umol/L.

Two months later her serum creatinine was 129umol/L. At this time the dose of Enalapril was increased to 20mg BD because her blood pressure was higher than the target value of 130/80mm Hg. A month later her serum creatinine was 150umol/L and Tab Telmisartan 80mg OD was added to her existing medication because the blood pressure was still above target value. When reviewed three months later, her blood pressure was normal but her serum creatinine was 178umol/L. At this point the Telmisartan was discontinued but, even after that, her serum creatinine continued to increase and touched a value of 222umol/L two months later. Seeing this, her doctors decided to stop Enalapril also and to treat her hypertension without any ACE inhibitors or angiotensin receptor blockers.

Slowly, within the next six months, her serum creatinine decreased and it returned to her earlier baseline value 135umol/L.


Discussion

In view of her deteriorating renal function after angiotensin inhibition, can this woman be considered to have renovascular hypertension?
No, I do not think she has renal artery narrowing because her renal function did not deteriorate even with high doses of Enalapril. 

Then what was the cause of her serum creatinine touching a value of 222umol/L?
I believe that this rapid deterioration in renal function was due to the combination of  Enalapril and Telmisartan. A high dose of Telmisartan was added soon after the dose of Enalapril had been doubled. Rapid angiotensin inhibition can lead to deterioration in renal function. 

Can this patient be started again on Enalapril now?
Yes, she can. It is in her best interests to introduce an ACE inhibitor again because of the renal protection it offers. But the medication must be started in a low dose and dose increases must only be done gradually.


How much of an increase in serum creatinine is allowed after introducing an ACE inhibitor or an angiotensin receptor blocker?
An increase of up to 30 percent from the baseline is permissible. This acute increase in serum creatinine does reflect impaired glomerular filtration but it may reverse over time. The long term benefit of angiotensin inhibition outweighs the slight, and often short-term, acute renal dysfunction. 

What is the likely cause of her pedal edema?
From the available information, nephrotic syndrome has to be considered as the most likely cause of her edema. 

A man with fever who fell down

A 46 year old man presented 8 days ago with fever and a fall. He had struck his head on the edge of a table during the fall. He never lost consciousness. When he was first seen by doctors, his blood pressure was low at 88/70mm Hg and he had a subconjunctival haemorrhage in his right eye. He was diagnosed to have septic shock and treated accordingly. When he complained of pain in his upper abdomen, an ultrasound of the abdomen was ordered and this showed features of acute acalculous cholecystitis. A CT scan of the head showed no skull fractures and no brain injury.

He was initially treated with Ceftriaxone, IV fluids and infusion of Dopamine. Blood cultures grew Pseudomonas aeroginosa in one and Burkholderia cepacia in the other.

His ECG showed sinus rhythm with ST segment elevation (concavity upwards) in chest leads V2 and V3.

In spite of treatment with Ceftriaxone, his fever persisted and, on day 5, Ceftriaxone was changed to Cefepime. Fever persisted in spite of this and, after seeing the second blood culture which grew Burkholderia, Ceftazidime replaced Cefepime. Two days after introducing Ceftazidime, he became afebrile. His blood pressure has been normal from the second day after admission. The Dopamine infusion was tapered and stopped after four days.

He is not a diabetic; his renal function is normal and his liver function tests are also normal.

Discussion

1. How was the diagnosis of acute acalculous cholecystitis made by ultrasound imaging?
Thickening of the wall of the gall bladder (wall thickness more than 3mm) is a diagnostic sign of acute cholecystitis. The absence of gall stones on imaging makes it acalculous. Apart from this, tenderness elicited by pressure on the ultrasound probe while imaging the gall bladder (sonographic Murphy’s sign) is also diagnostic.

Although acute acalculous cholecystitis is more common after abdominal trauma, it can occur in healthy, young and middle aged people in the community.

2. What are the common infections caused by Pseudomonas aeroginosa?
Pseudomonas aeroginosa is a gram-negative aerobic bacterium that is seen in water and moist soil. It can colonise human beings without producing disease. It can cause skin infections, cellulitis, otitis externa, and urinary infections in immune-competent hosts. In those who are immune-compromised, it can cause bacteremia and sepsis with resultant pneumonia, meningitis and endocarditis.

3. What is Burkholderia cepacia and what is its clinical significance?
Burkholderia cepacia was previously called Pseudomonas cepacia. It was first discovered as the cause of “onion rot”, a bacterial infection of onions. Now we know that it can be a cause of hospital acquired, catheter-related infections in the blood and urinary tract. It is also an important cause of infection in the lungs in those with cystic fibrosis.

4. Is there any significance to the ST elevation seen in the chest leads of this patient?
The ST elevation in this patient was limited to V2 and V3 and it was concave ST elevation. Hence, it is most likely not related to a myocardial infarction or to acute pericarditis. The absence of RBBB also rules out the Brugada syndrome. Transient ST elevation has been seen in patients with blunt chest trauma and attributed to cardiac contusion. This may be the reason for the ST elevation seen in this patient because he had presented after a fall. Of course, his ST elevation may have been a pre-existing finding, being a benign early repolarisation pattern. Repeat ECGs are necessary for a more accurate interpretation.

ST segment elevation is judged either in relation to the PR segment or the TP segment. If judged in relation to the PR segment, the J point is taken as the reference. If judged in relation to the TP segment, then a point 0.08sec after the J point is taken as the reference. ST segment elevation is considered to be significant only if it is more than 1mm in the limb leads or more than 2mm in the chest leads.