[level-membership-for-internal-medicine-category]ESSENTIALS OF ELECTROCARDIOGRAM READING
The major components to observe in the interpretation of an ECG are the rhythm, rate, axis and morphology, as shown by the P wave, P-R interval, QRS complex, ST segment, T wave and Q-T interval (see box).
Interpretation of ECG
1. Confirm the name and the date of birth/age of the patient and the date on which the ECG was recorded.
2. Ascertain the number of leads on display (usually 12 leads).
3. Check the calibration: standard paper speed is 25 mm/s (where each small 1 mm square denotes 0.04 s or 40 ms horizontally); vertically each 1 cm square denotes 1 mV.
4. Check the rate.
5. Check the rhythm (regular, irregular): this is best seen in lead II—the rhythm strip.
6. Check the axis (normal axis is between –30° and +120°; if between –90° and –30° it is left-axis deviation and if between +120° and +180° it is right-axis deviation).
7. Analyse the P wave (morphology, regularity and relationship to the QRS complex).
8. Assess the P-R interval (normal is 200 ms).
10. Analyse the ST segment: depression and elevation in relation to the isoelectric line and its significance according to the context.
11. Check the Q-T interval (this is a rate-dependent phenomenon; < 430 ms is normal for the adult male, < 450 ms for the adult female).
12. Study the T wave: height and morphology.
13. Look for special features (e.g. bundle branch block) and possible diagnosis according to the clinical context.
It is not necessary to describe the ECG in the traditional and pedantic way, opening with the rate, rhythm and axis and then going on to describe the rest if they are normal. At the examination this may sound superfluous, and there is no time to waste! Candidates should identify the name of the patient and the date the ECG was done, and immediately start describing the abnormalities with references to the clinical findings. The following is a discussion of the various ECG findings commonly encountered in the long case examination.
Acute (transmural) myocardial infarction
ST elevation of more than 1 mm in two contiguous leads. In anterior infarcts this would be in the chest leads V2–V6. Left heart infarcts show this in leads I, II and aVL. In inferior infarcts it is seen in leads II, III and aVF. Posterior infarctions show up as reciprocal changes in the anterior leads, and the classic findings include R waves, ST segment depression or tall T waves in leads V1 and V2. Acute myocardial infarction can sometimes present as a new bundle branch block.
Q waves are pathological if they are broader than 1 mm or deeper than 2 mm (or > 25% of the height of the following R wave).
Subendocardial ischaemia
ECG changes consistent with subendocardial ischaemia (acute coronary syndrome) are ST segment depression of 1 mm or more, 0.08 seconds after the J point and corresponding T wave changes. The slope of the ST segment may provide some clues to the severity of the ischaemic phenomenon. Upward sloping indicates less severe disease, horizontal sloping indicates more severe disease, while downward sloping is usually considered the most significant and severe. The T wave changes include T wave flattening and T wave inversion.
Left ventricular hypertrophy
Left ventricular hypertrophy is described according to voltage criteria and strain/repolar-isation criteria.
Voltage criteria
1. Length of the deepest S wave in leads V1 or V2, or height of the tallest R wave of lead V5 or V6 > 25 mm
2. Sum of the lengths of the S wave of V1 and the R wave of either V5 or V6 > 35 mm
3. Height of the R wave in aVL > 12 mm and height of the R wave in aVF > 20 mm
4. Sum of the lengths of the S wave in lead III and R wave of lead I > 25 mm
Right ventricular hypertrophy
This may be associated with pulmonary stenosis or pulmonary hypertension.
Right atrial hypertrophy/strain
This is associated with right atrial overload, as in pulmonary hypertension and right heart failure.
Right bundle branch block
This is seen in right heart strain associated with pulmonary hypertension, chronic lung disease, pulmonary emboli and mitral valve pathology. Some people may have non-pathological right bundle branch block, which is of no significance.
Left bundle branch block
This is seen in ischaemic heart disease, hypertension, aortic stenosis and cardio-myopathy. Features to notice:
Left anterior hemiblock
This is the most common cause of left-axis deviation. There is marginal prolongation of the QRS complex with left-axis deviation. Also notice terminal R waves in leads aVR and aVL, deep S wave in lead II, and RSR pattern in leads II, III and aVF. This feature is commonly seen in anterolateral or inferior myocardial infarcts.
Left posterior hemiblock
This abnormality is associated with right-axis deviation of about 120°, Q waves in leads II, III and aVF, R waves in leads I and aVL. When left posterior hemiblock is present it is almost always associated with right bundle branch block. This combination has a poor prognosis, and progression to complete heart block needing a pacemaker is the likely eventuality.
Bifascicular block
Right bundle branch block in combination with a left-sided hemiblock or left bundle branch block. There is a high likelihood of progression to complete heart block requiring a permanent pacemaker.
First-degree heart block
The rate is usually normal and the main abnormality is a prolonged P-R interval (> 200 msec or 5 mm).
Second-degree heart block
Type I (Wenckebach phenomenon)
The sinus rate is normal but the ventricular rate is slower than normal. The main abnormality is the gradual prolongation of the P-R interval until one P wave is not conducted to the ventricles. A new cardiac cycle begins following the non-conducted P wave. Rhythm is usually irregular. This pattern has an association with inferior myocardial infarctions.
Type II
The sinus rate is normal but the ventricular rate is a definite fraction of the sinus rate. There are more P waves than QRS complexes, as only one P wave is conducted for several subsequent P waves. Note the block, which is 2:1, 3:1 or more. This condition is usually associated with anterior myocardial infarctions.
Complete heart block
The sinus rate is normal but the ventricular rate is much slower. The ventricular rate is dependent on the site of the escape pacemaker (if it is in the AV junction, the rate would be around 40–60 bpm; if ventricular, the rate would be < 30 bpm). The P-R interval changes constantly and the P wave has no relationship to the QRS complex (AV dissociation).
Tachyarrhythmias
Ventricular tachycardia
A broad complex tachycardia with a rate exceeding 100 bpm. In practice, however, it is common to see the rate at 140–200. The rhythm is regular. It is called sustained ventricular tachycardia if it persists beyond 30 seconds. The QRS complex is longer than 140 milliseconds. There is evidence of AV dissociation, fusion beats and variable retrograde conduction. QRS pattern of all precordial leads should be in concordance. There may be features of left-axis deviation in the presence of right bundle branch block. A broad complex ventricular rhythm at a rate of less than 100 bpm is called accelerated idioventricular rhythm.
Atrial tachycardia
The rhythm is regular and the rate is 140–280 bpm. QRS complex follows each P wave, but the P wave may also be buried in the QRS complex or the T wave and not be visible.
Atrial flutter
The rhythm is most often regular but may vary if the degree of AV nodal block changes. Ventricular rate may vary between 60 and 150, again depending on the block. There are characteristic atrial oscillations described as ‘sawtooth’-shaped flutter waves. These flutter waves occur regularly at a rate of 250–300 per minute. Depending on the block, the rhythm should be described as atrial flutter with 2:1, 3:2 or 4:1 block.
Junctional tachycardia (AV nodal re-entry tachycardia)
The rhythm is regular and the rate is 100–200 bpm. The P wave appears inverted and is located immediately before or after the QRS complex due to retrograde conduction.
Wolff-Parkinson-White syndrome
This conduction defect occurs due to ventricular pre-excitation due to the presence of an accessory AV conduction pathway. The P-R interval is shorter than 110 milli-seconds and the QRS complex has a slurred upstroke (delta wave). The patient may be in atrial fibrillation. A negative delta wave in lead V1 suggests a right-sided bypass tract.
Hypertrophic obstructive cardiomyopathy
Patients with hypertrophic obstructive cardiomyopathy may show non-specific ECG features. Evidence of left ventricular hypertrophy and diffuse, widespread, deep and broad Q waves are some commonly seen abnormalities.
HAEMATOLOGICAL STUDIES
Blood test results encountered in the examination include the full blood count, electrolyte profile, renal function indices, liver function studies, endocrine studies and serology. Serological tests can be either infective or autoimmune serology.
Full blood count
Here the focus should be on haemoglobin level, haematocrit, mean cell volume, mean cell haemoglobin concentration, and white cell count with differential and platelet count.
Candidates should know the normal values of all the above so that an abnormal value can be spotted immediately and interpreted accurately. When an abnormality in the blood count is present, ask for the report of the blood film for further clarification and, if appropriate, ask for other tests such as the results of the bone marrow biopsy, haemolytic screen, iron studies and vitamin B12 and folate levels in anaemia, results of the blood culture in the setting of significant leucocytosis and febrile illness, and antiplatelet antibodies in idiopathic thrombocytopenia.
Figure 14.1 ECG showing atrial and ventricular paced rhythm with pacing spikes clearly visible before each atrial and ventricular complex. Also note the left bundle branch block (LBBB) pattern due to the early stimulation of the right ventricle by the pacing lead located there.
Figure 14.3 ECG showing Wolff-Parkinson-White (WPW) syndrome. Notice the short P-R interval and the delta wave visible in most QRS complexes.
Figure 14.5 ECG showing supraventricular bigeminy and left axis deviation
Figure 14.7 ECG showing left bundle branch block (LBBB)
Figure 14.9 ECG showing atrial fibrillation
Figure 14.10 ECG showing supraventricular tachycardia with aberrancy
Neutrophilia
Neutrophilia is diagnosed when the neutrophil count is elevated above 7.5 × 109/L. The possible causes are:
Lymphocytosis
Lymphocytosis is diagnosed when the lymphocyte count is elevated above 4 × 109/L. The possible causes are:
Eosinophilia
Eosinophilia is diagnosed when the eosinophil count is elevated above 0.5 × 109/L. The possible causes are:
Basophilia
Basophilia is diagnosed when the basophil count is elevated above 0.1 × 109/L. The possible causes are:
Leucopenia
Leucopenia is diagnosed when the white cell count is less than 4 × 109/L. The possible causes are:
Microangiopathic haemolytic anaemia (MAHA) should be suspected in an anaemic and coagulopathic patient if the blood film report shows fragment cells, helmet cells, polychromasia and reticulocytosis. The possible causes include:
Thrombophilic screen
This should be performed in cases of thromboembolic disease with a strong family history or recurrent spontaneous venous thrombosis in any patient, arterial throm-bosis in a patient aged under 30 years, and venous thrombosis in a patient aged under 40 years without a predisposing condition.
Thrombophilic screen involves testing for the following:
Electrolyte profile
Look at the sodium level, potassium level, chloride level, bicarbonate level and the renal function indices. If any abnormality is noticed, try interpreting it in the context of the clinical setting or a causative medication.
Sodium
The normal serum sodium level is 136–144 mmol/L.
Hypernatraemia
This can be caused by hypovolaemia and dehydration as well as primary hyperaldosteronism, Cushing’s syndrome and excess salt intake. Patients present with lethargy, irritability, fever, nausea, vomiting and confusion. Management is with controlled hydration using 4% dextrose with 1/5 normal saline or 5% dextrose solution together with judicious diuretic therapy.
Hyponatraemia
This can be caused by inappropriate secretion of antidiuretic hormone (SIADH), congestive cardiac failure, severe hepatic failure, Addison’s disease, aldosterone insufficiency, hypothyroidism, diuretic therapy, salt-losing nephropathy, renal tubular disorders and water retention.
SIADH can be due to small cell lung cancer, central nervous system disorders such as meningitis and subarachnoid haemorrhage, lung disease such as asthma, pneu-monia and tuberculosis, and drug therapy with tricyclic antidepressants, carbamazepine and monoamine oxidase inhibitors. The phenomenon of pseudohyponatraemia occurs in hyperglycaemia, alcohol excess and hyperuricaemia. Significant hyponatraemia (serum sodium of < 125 mmol/L) presents with lethargy, confusion, convulsions and coma. Management of severe symptomatic hyponatraemia uses controlled infusion (1–3 mL/kg/h) of hypertonic saline (3% NaCl) with judicious diuretic therapy. Chronic, asymptomatic hyponatraemia can be well managed with fluid restriction to 1 L/day. Resistant hyponatraemia due to SIADH can also be treated with regular oral demeclocycline.
Potassium
The normal serum potassium level is 3.5–5.0 mmol/L.
Hyperkalaemia
This can be caused by ACE inhibitor therapy, potassium-sparing diuretics, inadvertent potassium supplementation, acidosis, blood transfusion, haemolysis, severe renal failure, rhabdomyolysis and hypoaldosteronism.
Patients present with severe muscular weakness, paralytic ileus, symptomatic brady-cardia and heart block. Management of hyperkalaemia includes administration of 10 mL 10% calcium gluconate if there are electrocardiographic changes of hyperkalaemia (peaked T waves, small P waves and wide QRS complexes). Rapid reversal of potassium levels can be achieved by giving 50% glucose with insulin infusion, but the levels may rise again in a few hours. Concurrently administer oral or per rectum resonium 15–30 g and repeat administration as guided by subsequently measured serum potassium levels. Hyperkalaemia of severe renal failure needs haemodialysis.
Hypokalaemia
Causes of hypokalaemia include loop diuretic therapy, primary hyperaldosteronism, Cushing’s syndrome, renal tubular disease, alkalosis and hyperthyroidism. Therapy with drugs such as verapamil, beta-agonists and amiodarone should be excluded.
Hypokalaemia presents with muscle weakness or tetany. Significant hypokalaemia can lead to rhabdomyolysis. To manage hypokalaemia, usually oral supplementation alone will suffice. If the level is < 2.9 mmol/L, parenteral supplementation with KCl 10 mmol/L over an hour through a central venous line is indicated. The patient’s cardiac function should be monitored during this infusion. It should be repeated as guided by the subsequently performed serum potassium levels.
Calcium
The normal serum calcium level is 2.2–2.5 mmol/L. The serum calcium level varies with the serum albumin level, and the correction can be made using the following formula:
Hypercalcaemia
This can be caused by primary hyperparathyroidism, squamous cell carcinoma of the lung, cancer with bony metastases, multiple myeloma, sarcoidosis, vitamin D intoxi-cation, milk-alkali syndrome and thiazide diuretics.
Significant hypercalcaemia presents with anorexia, nausea, vomiting, constipation, polyuria, severe weakness, stupor and eventually coma.
Steps in the management of hypercalcaemia include, first, hydration with adequate amounts of normal saline, together with loop diuretic therapy. More severe hypercalcaemia needs treatment with a bisphosphonate such as etidronate or pamidronate. Calcitonin injected subcutaneously or intravenously (200 units, 6-hourly) has a short-lived effect. Hypercalcaemia due to multiple myeloma, sarcoidosis or vitamin D toxicity can be treated also with glucocorticoids. Oral phosphate is useful when there is hypercalcaemia together with hypophosphataemia.
Hypocalcaemia
Causes of hypocalcaemia include hypoparathyroidism, vitamin D deficiency, osteomalacia, acute pancreatitis, chronic renal failure, malignancy with osteoblastic metastases, and pseudohypoparathyroidism.
Patients present with circumoral and distal limb paraesthesias, painful muscle cramps, tetany and seizures. Patients may also have Chvostek’s sign and Trousseau’s sign.
Symptomatic hypocalcaemia and corrected serum levels of < 1.88 mmol/L should be treated with parenteral calcium in the form of 10% calcium gluconate.
Acid–base status
Metabolic acidosis
This diagnosis should be suspected when plasma bicarbonate (HCO3) is less than 10 mmol/L and PaCO2 is low with a low pH (a low HCO3 value can be seen in respiratory alkalosis as well as in metabolic acidosis). The anion gap helps the interpretation of metabolic acidosis in more detail, and is calculated as follows:
The normal value is 10–14 mmol/L. Metabolic acidosis could be with a normal or increased anion gap.
Metabolic acidosis with a normal anion gap is due to an associated loss of HCO3 molecules from the body. The possible causes are:
1. HCO3 loss from the gut due to diarrhoea, ureterosigmoidostomy, ileal conduit, pancreatic drainage or biliary drainage
2. HCO3 loss from the kidney due to the use of carbonic anhydrase inhibitor, urinary diversion, renal tubular acidosis (proximal or distal), early renal failure or interstitial nephritis.
This condition is managed with volume repletion and correction of associated hypokalaemia with potassium supplementation.
Acidosis with an increased anion gap is due to the presence of non-volatile acids in the body. The possible causes are:
Metabolic alkalosis
This is caused by excess HCO3 or alkali or the loss of H+ due to metabolic causes. A high HCO3 level and an elevated PaCO2 level together with a high pH characterises metabolic alkalosis. The serum chloride level would give further clues to its aetiology.
Hyperchloraemic metabolic alkalosis is seen in primary hyperaldosteronism, glucocorticoid excess, hypercalcaemia, Liddle’s syndrome and Bartter’s syndrome. Hypochloraemic metabolic alkalosis is seen in gastrointestinal fluid loss (vomiting), diuretic therapy and after hypercapnoea.
Respiratory acidosis
This is caused by alveolar hypoventilation and associated hypercapnoea. A high HCO3 and a high PaCO2 with a low pH is suggestive of respiratory acidosis.
Respiratory alkalosis
This is caused by alveolar hyperventilation. A low HCO3 level and a low PaCO2 with an elevated pH is suggestive of respiratory alkalosis.
Be alert to mixed disorders, where the pH value does not correlate very well with the HCO3 or the PaCO2 level.
RENAL FUNCTION INDICES
Any elevation of the blood urea or serum creatinine level is suggestive of renal failure. Ask for the previous levels, to ascertain whether the renal impairment is acute or chronic and to ascertain whether it is progressive or stable. If the renal impairment is new, further tests should be carried out to find out the cause (as described in ch 6).
LIVER FUNCTION TESTS
Aminotransferases (ALT/AST)
This enzyme has two isoforms: alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Massive elevation of the serum levels of this enzyme is seen in severe viral hepatitis, hepatotoxic-induced liver injury and ischaemic liver injury. Moderate elevations are characteristic of mild acute viral hepatitis, chronic active hepatitis, alcoholic hepatitis, cirrhosis and hepatic metastases.
Usually the ALT elevation parallels AST elevation, but in alcoholic liver disease AST elevation far exceeds that of ALT. The ratio of AST/ALT in this setting is > 2.
Alkaline phosphatase (ALP)
A striking elevation of this enzyme is seen in cholestatic disorders. Moderate and transient elevations are seen in all types of liver pathology, including hepatitis, metastatic disease and hepatic infiltrative conditions such as lymphomas, leukaemia and sarcoidosis.
Gammaglutamyl transpeptidase (GGT)
The level of this enzyme correlates with that of ALP. Its level also goes up in alcoholism, diabetes mellitus, cardiac failure, pancreatic disease, fatty liver and renal failure. Elevation of the level of this enzyme is often non-specific.
Serum albumin level
This marker also reflects the hepatic synthetic capacity, and hence it is low in significant liver disease.
Bilirubin
The conjugated (direct) bilirubin level is elevated in cholestasis. Unconjugated (indirect) hyperbilirubinaemia is seen in haemolysis, ineffective erythropoiesis, Gilbert’s syndrome and the rare Crigler-Najjar syndrome.
Autoimmune markers of liver disease
• Antimitochondrial antibody (AMA)—seen in primary biliary cirrhosis and autoimmune chronic active hepatitis
• Antinuclear antibody (ANA)—seen in autoimmune hepatitis
• Antismooth muscle antibody—seen in autoimmune hepatitis
• Anti-liver kidney microsomal antibody (anti-LKM)—seen in autoimmune hepatitis type II.
ENDOCRINOLOGICAL STUDIES
Thyroid function tests
Commonly performed thyroid function tests include serum free T3, free T4 and thyroid-stimulating hormone (TSH) levels. The most sensitive assay of thyroid function is the serum TSH level (normal range for TSH is 0.3–3 mU/L).
Direct test of thyroid function
Hyperthyroidism is defined as hyperactivity of the thyroid gland. Thyrotoxicosis by definition is excess thyroid hormone due to any cause.
A technetium-99 (Tc99) scan helps to identify the cause of thyrotoxicosis. Causes of thyrotoxicosis include Graves’ disease, toxic nodular goitre, initial phase of Hashimoto’s thyroiditis, excess iodine intake, thyrotoxicosis factitia and subacute thyroiditis. Radioactive iodine uptake is another test that can be performed to assess the activity of the thyroid gland. In the latter three conditions, the uptake of radioactive iodine is reduced. Thyroid scintigraphy using radioactive iodine or Tc99 pertechnetate is also useful for the assessment of hot and cold spots in a goitre.
Autoimmune markers relevant to thyroid disease should be requested in appropriate situations. Antithyroid peroxidase antibody, antimicrosomal antibody and antithyroglobulin antibody are seen in Hashimoto’s thyroiditis and Graves’ disease. In addition, in Graves’ disease, thyroid-stimulating antibodies are encountered.
Ultrasonography of the thyroid gland is done to distinguish between cystic nodules and solid nodules.
In the sick euthyroid syndrome, free T4 levels would be high, low or normal, T3 levels would be low and TSH levels would be low or normal.
Amiodarone causes an elevation in free T4 levels, decrease in T3 levels and an elevation in TSH levels.
Adrenal function tests
Cushing’s syndrome (excess secretion of corticosteroids)
Screening tests for Cushing’s syndrome are the measurement of 24-hour urinary free cortisol or the overnight dexamethasone suppression test.
Confirmatory for the diagnosis of Cushing’s syndrome is a low-dose dexamethasone suppression test (0.5 mg dexamethasone every 6 hours for 48 hours).
To determine the aetiology of the Cushing’s syndrome, a high-dose dexamethasone suppression test can be performed (2 mg dexamethasone every 6 hours for 48 hours). If there is suppression of cortisol secretion, the likely diagnosis is that of an adrenocorticotrophic hormone (ACTH)-secreting pituitary tumour. If there is failure of suppression, the aetiology is likely to be adrenal neoplasia or ectopic secretion of ACTH.
The plasma ACTH level may also give clues to localising the focus of hypersecretion. An elevated plasma ACTH level may suggest a pituitary or an ectopic origin. To localise the pituitary tumour, imaging studies with cranial CT or MRI should be done. But for the localisation of pituitary microadenomas that do not manifest in the imaging studies, selective venous sampling of the inferior petrosal sinus is necessary.
A suppressed plasma ACTH level is highly suggestive of an adrenal neoplasia and should be followed up with pelvic imaging studies such as CT.
Tests for adrenal insufficiency
In patients presenting with symptoms of weakness, anorexia, weight loss, hypotension, postural drop in blood pressure, syncope and vitiligo as well as investigational findings of hyperkalaemia, hyponatraemia, hypercalcaemia and low bicarbonate levels, adrenal insufficiency should be considered as a top differential diagnosis. Screening for adrenal insufficiency involves performing a short Synacthen® test. This test involves checking the plasma cortisol level 30–60 minutes after an injection of 250 mg cosyntropin.
To localise the level where the secretory function is defective, plasma ACTH should be checked 30 minutes after the injection of 250 mg cosyntropin. If the ACTH shows an elevatory response, the likely site is the adrenal gland, and if there is no elevation the likely site is the pituitary.
Test for hyperaldosteronism
When a patient presents with diastolic hypertension, headache, muscle weakness with fatigue and if there is associated hypokalaemia in the electrolyte profile, consideration should be given to the possible diagnosis of hyperaldosteronism. The first test to be performed is the plasma renin/aldosterone ratio. If it is normal or elevated, go on to measure the plasma aldosterone level before and after saline loading. If there is no suppression of aldosterone secretion with a salt load, consider aldosterone-secreting adrenal tumour and perform relevant imaging studies of the abdomen and pelvis in the form of CT and MRI.
Test for phaeochromocytoma
Phaeochromocytoma should be considered in hypertensive patients presenting with a history of headache, profuse sweating, palpitations, anxiety and weight loss. The screening test for phaeochromocytoma is the assessment of the levels of metanephrines and free catecholamines in a 24-hour urine collection. If there are excess levels of the above markers, abdominopelvic imaging studies and an MIBG scan should be done to localise the tumour.
Parathyroid hormone tests
Test for hyperparathyroidism
This condition is commonly diagnosed incidentally in middle-aged women who are discovered to have hypercalcaemia. However, in any patient with hypercalcaemia it is important to exclude metastatic malignant disease, squamous cell carcinoma, multiple myeloma, chronic renal failure, hypocalciuric hypercalcaemia, thyrotoxicosis, multiple endocrine neoplasia (MEN) type 1 and MEN type 2A.
The initial test for suspected hyperparathyroidism is the serum parathyroid hormone assay. If this is elevated, surgical exploration by a skilled surgeon is the best way of localising the involved parathyroid adenoma or the hyperplastic gland. Remember to exclude chronic renal failure, as there is hyperparathyroidism associated with autonomously hypersecreting parathyroid glands in tertiary hyperparathyroidism of chronic renal failure.
Pituitary function tests
In suspected growth hormone excess, the best initial tests are:
When inadequate secretion of growth hormones is suspected, the best initial test is to assess the growth hormone response to insulin, levodopa or L-arginine challenge.
In both the above situations, an abnormal test should be followed up with pituitary imaging studies in the form of MRI.
In suspected prolactin excess, the best test is the assessment of serum prolactin level.
LUNG FUNCTION TESTS
Formal lung function studies include a flow–volume curve demonstrating the inspiratory flow rate in litres per second as depicted by the curve below the meridian, and the expiratory phase as depicted by the curve above the meridian. The candidate should be able to interpret the curve to diagnose obstructive lung pathology, restrictive lung pathology, the severity of each condition, large airway obstruction and its exact location, as well as mixed airway disease.
The other component of the lung function study is the carbon monoxide diffusion capacity. This would indicate whether the lung pathology is confined to the airways alone where the diffusion capacity is normal, or whether the pulmonary parenchyma is affected where the diffusion capacity is reduced.
By combining the two sets of information, the candidate should be able to make a diagnosis of the lung condition as guided by the clinical findings. The FEV1/FVC ratio is an age-related phenomenon. However, a ratio less than 75% in a young individual or less than 60% in an older individual is considered consistent with obstructive airway disease. An FEV1/FVC ratio of 80% or more with both FEV1 and FVC values being very low is suggestive of restrictive lung pathology.
Following are some possible patterns of lung function study findings that can be expected at the examination:
1. Severe obstructive lung disease (FEV1/FVC ratio < 50%) without impairment of the carbon monoxide diffusion capacity—likely diagnosis is asthma
2. Severe obstructive lung disease with significant impairment of the carbon monoxide diffusion capacity—likely diagnosis is emphysema
3. Severe restrictive lung disease (FEV1/FVC ratio > 90%) with impaired carbon monoxide diffusion capacity—likely diagnosis is pulmonary fibrosis.
NUCLEAR IMAGING
Lung scan
Lung scans are performed to confirm or exclude a clinical diagnosis of pulmonary embolism or to ascertain lung function (gas exchange).
Ventilation-perfusion (V/Q) scan
This is performed to confirm or exclude a clinical diagnosis of pulmonary embolism. It is of further help in the follow-up of treatment for pulmonary embolism. Radioactive Xe133 or Xe127 gas is used for the ventilation scan. Perfusion is assessed with injection of Tc99m macroaggregated albumin (MAA). A plain chest X-ray should be obtained before or soon after the scan, for reference purposes. Mismatched areas show normal ventilation with impaired perfusion. A patient whose V/Q scan has a reported high probability of pulmonary embolism should be treated with therapeutic anticoagulation, first with IV heparin and then with oral warfarin for a total of 6 months.
The finding of a high probability scan has high correlation with the findings of pulmonary angiography, which is the gold standard test. Scans reported as being of intermediate probability should be followed up with a pulmonary angiogram to confirm the diagnosis. If a scan is reported as low probability, the likelihood of pulmonary embolism is remote and other possible diagnoses should be looked for.
Follow-up scans should be performed several weeks or months after the initial study. Follow-up scans may show resolution of the initial defects as well as recurrent pulmonary embolism. A normal perfusion scan with impaired ventilation is usually due to atelectasis. Chronic airflow limitation and emphysema manifest as matched defects.
Thyroid scan
A thyroid scan is used to assess global as well as differential activity (e.g. hot or cold nodules). Scans are performed using radioactive iodine (I123) or Tc99.
Increased uptake of the nuclear marker is seen in:
Decreased uptake is seen in:
Adrenal scan
Metaiodobenzylguanidine (MIBG) is a neurotransmitter precursor that is taken up by the diseased adrenals and the thyroid gland. This agent is used to image the adrenals on blocking its uptake by the thyroid by administering Lugol’s iodide solution. A normal gland shows minimal or no uptake. Uniform increased uptake bilaterally is seen in adrenal hyperplasia. Unilateral increased uptake is suggestive of neuroectodermal tumours such as carcinoid, phaeochromocytoma and neuroblastoma. Distant meta-stases of these tumours can also be identified by their increased activity.
Renal scans
Tc99m DMSA is used to assess the renal cortical anatomy. Tc99m DTPA or Tc99m MAG3 is used to assess renal dynamics—perfusion and function. These are technetium-labelled radiopharmaceutical agents with low toxicity and low radiation.
These tests are useful in the assessment of renal artery stenosis in the hypertensive or vasculopathic patient. Other uses include assessment of the effects of renal revascularisation therapy, assessment of differential renal function prior to nephrectomy, assessment of glomerular filtration, and ascertaining the aetiology of transplant failure (rejection, tubular necrosis, cyclosporin toxicity).
Administration of captopril 50 mg (captopril-perfusion scan) increases the diagnostic accuracy of renal artery stenosis. The stenotic kidney shows decreased or delayed perfusion and delayed clearance of nuclear contrast. Substitution of captopril with high-dose aspirin has been shown to be equally efficacious with less toxicity.
Delayed images visualise the distal drainage system. Obstructive uropathy should be suspected if there is:
Cardiac scans
Nuclear scans are useful in the assessment of cardiac perfusion abnormalities and dynamic function. The nuclear test is more sensitive than the standard exercise stress (ECG) test for ischaemia, but has similar specificity. Agents commonly used in the assessment of the heart are thallium (TI201) chloride and technetium (Tc99m) sestamibi. Tc99m sestamibi gives images with better resolution and has better tissue pene-tration, and is therefore useful in obese subjects.
Perfusion imaging
Differential perfusion of myocardium at rest and with increased activity (after exercise) or vasodilator administration (pharmacological stress test) is indicative of significant coronary artery stenosis. When the coronary artery is stenosed less than 90% but more than 50% (considered significant), perfusion during rest is preserved. But with activity or administration of vasodilator, there is relative impairment of the perfusion to the areas supplied by the relevant artery. For impairment of perfusion at rest, the artery should be narrowed by more than 90%. This differential perfusion is suggestive of significant coronary artery disease.
For the exercise stress study, the patient is exercised on a treadmill or a bicycle ergometer. The patient should be exercised to the maximum stress according to the protocol used, or to a heart rate of ≥ 85% of the maximal predicted. Fatigue, dyspnoea, angina, hypotension, arrhythmia and significant ECG changes suggestive of ischaemia are indications to terminate exercising. Nuclear agent is injected at peak exercise to obtain the initial ‘stress’ image. Imaging is repeated after 4 hours of rest to look for redistribution of the coronary flow. Beta-blocker or calcium channel blocker therapy should be withheld for at least 12 hours prior to the study.
Pharmacological stress testing with the use of a vasodilator agent is used for those who cannot perform physical exercise. This test has similar sensitivity and specificity to the exercise test. Commonly used vasodilator agents are dipyridamole, adenosine and dobutamine. Coronary flow usually increases with the administration of the vasodilator agent in the normal arteries. But in stenotic vessels this change is not significant, so there is differential distribution of the nuclear agent, highlighting coronary ischaemia. Patients should not consume any caffeine or xanthine-containing food material for 24 hours before the study. A resting study is performed later to assess redistribution.
Reversible areas of hypoperfusion indicate significant coronary artery disease. Fixed defects highlight areas of previous myocardial infarction. False-positive results are seen in cardiomyopathy.
Acute myocardial infarction
Tc99m pyrophosphate is used to diagnose subacute myocardial infarction. But this test is not commonly used because ECG and cardiac enzyme or troponin assessment is readily available.
Gated heart pool scan
This study is used to assess ventricular systolic function. Tc99m-labelled red blood cells are used to image the blood pool. Imaging is gated according to the sequence of cardiac cycle. This test also allows the assessment of segmental wall motion in the ventricle. A gated heart pool scan is of value in the assessment of myocardial damage due to ischaemia, cardiomyopathy, and cardiotoxins such as anthracyclines.
RADIOLOGICAL IMAGING STUDIES
Chest X-ray
Interpretation of the patient’s chest X-ray is almost an integral part of the long case. Candidates should be able to identify and interpret the most obvious and most striking abnormality in the radiograph immediately. The most commonly encountered conditions are consolidation, pulmonary oedema (alveolar or interstitial), bronchiectasis, hyperinflation associated with emphysema, pneumothorax and mass lesions. An ideal approach is as follows:
1. Start by giving the name of the patient and the date of the investigation as mentioned on the film.
2. Name the projection (frontal or lateral).
3. Identify the abnormality and describe its appearance in detail.
4. Give a comprehensive list of differential diagnoses relevant to the clinical picture of the patient.
5. If relevant, ask for other imaging to further clarify the lesion.
Following are some examples of commonly encountered X-ray abnormalities.
• Opacification of a section of the lung field—Describe the nature of the opacification (confluent, patchy, homogeneous, heterogeneous) and the exact distribution (mention the possible lobes involved). Identify additional features (air bronchograms, miliary seeding etc). Ask for a lateral projection to define the exact distribution of the lesion.
• Cystic lesions—These may be due to cystic bronchiectasis, lung abscess (notice air-fluid level) or emphysematous bullae. Request a high-resolution CT scan to further clarify the lesion.
• Mass lesions—Consider primary or secondary malignancies, progressive massive fibrosis or benign tumours. Request a chest X-ray done at least 3 months previously to look for the presence of the same lesion, again asking for the CT scan with lung windows to further clarify the lesion and mediastinal windows to look for any lymphadenopathy.
• Bronchogenic carcinoma—This appears as a solitary mass lesion in the central or peripheral lung field. Look for cavitation. If present, it is more suggestive of squamous cell carcinoma. Look for hilar enlargement and mediastinal widening due to lymphadenopathy. There may be segmental or lobar atelectasis due to airway obstruction by the mass. Check for the presence of any post-obstructive pneumonia. The presence of asymmetry of the diaphragmatic shadows may suggest involvement of the phrenic nerve.
• Cardiac failure—A cardiothoracic ratio of more than 50% is suggestive of cardiomegaly. The hilar shadows may appear prominent due to congestion of the large arteries. Vascular shadows directing to the upper lobes may appear prominent (upper lobe diversion). These vessels seem as thick as or thicker than those vessels supplying the lower zones.
• Pulmonary oedema—In addition to upper lobe diversion, look for cuffing of the walls of the bronchi. This is due to the accumulation of interstitial fluid around the bronchi, and is a sign of interstitial oedema. Further progression of cardiac failure can lead to alveolar oedema, which manifests as patchy and diffuse opacifications. Septal oedema gives rise to Kerley B lines, which appear as horizontal linear opacifications in the lung peripheries that extend perpendicularly to the pleura, and Kerley A lines, which appear as long, fine linear shadows that radiate up from the hilar regions in the upper lung zones.
• Bronchiectasis—There may be increased lung markings due to retained secretions. Look for cystic spaces due to dilatation of bronchi and loss of definition of lung markings due to peribronchial fibrosis. Severe cases may also have the appearance of ‘honeycombing’. There may be compensatory hyperinflation of the uninvolved lung in cases with unilateral disease.
• Interstitial lung disease—Manifests as linear and/or nodular opacifications. In the acute setting there may be peribronchial cuffing, blurring of hilar shadows and blurring of vascular shadows. In the chronic setting look for fine reticulations, an appearance that suggests potentially reversible active pneumonitis. Coarse reticulations and honeycombing (nodular radiolucencies with background opacity) suggest progression to potentially irreversible fibrosis.
• Emphysema—Look for hyperinflation of the lung with flattening of the diaphragmatic shadows. There may be pulmonary vascular pruning and peripheral bullae. Cardiac shadow is likely to demonstrate right heart enlargement. If the height of the anterior border of the cardiac shadow in the lateral view chest X-ray is more than one-third the height of the sternum, it may suggest right heart enlargement.
• Cystic fibrosis—Look for longitudinal shadows of mucous plugging, tramline appearance with surrounding cystic bronchiectasis, areas of atelectasis and large pulmonary arteries suggesting pulmonary hypertension.
• Bronchiolitis obliterans with organising pneumonia (BOOP)—Manifests as unilateral or bilateral patchy consolidation of air spaces. There may be widespread nodularity and irregular linear opacifications. Also look for pleural thickening and effusion.
CT scan of the chest
Computed tomography (CT) of the chest is necessary to further clarify information gathered from the chest X-ray. There are different types of chest CT scan—the high-resolution scan, the helical scan, the scan with lung windows and the scan with media-stinal windows. The candidate should be familiar with the different types so that the scan most appropriate to the clinical setting can be requested.
High-resolution CT scan
Slices of the images are 1 mm thick and are made 1 cm apart. These scans can demon-strate fine changes in the parenchymal architecture. This helps examine the lung parenchyma in more detail to better define interstitial lung pathology. It is indicated in parenchymal lung disease, alveolar disease, emphysema, pneumonitis, drug effects, BOOP and small airway disease.
It is most useful in the diagnosis of interstitial pneumonitis and lung fibrosis. If the pneumonitis shows a ‘ground glass’ appearance, this is consistent with an active inflammatory process progressing to fibrosis. Some reversibility may be achieved in this situation, and a trial of systemic corticosteroid therapy is indicated. If the picture is that of ‘honeycombing’, the fibrosis has progressed beyond reversibility.
Normal-resolution CT scans
These images are of 1 cm slices taken in a contiguous run. They give a good overall impression of the lung architecture.
• Lung windows—This setting is indicated for the diagnosis of lung masses, abscesses, bullae, consolidation, and pleural diseases such as plaques and mesothelioma. In the lung window the air spaces appear black and the tissue appears white.
• Mediastinal windows—These pictures better define mediastinal anatomy and differentiate between fat, blood vessels and solid structures such as lymph nodes. They are indicated in the study of mediastinal mass lesions, lymphadenopathy and for visualisation of the mediastinal vessels.
Helical CT scan
This scan looks at the pulmonary vasculature, and the indication is for the diagnosis of pulmonary thromboembolism, particularly involving larger arteries. Contemporary radiography involves helical or spiral scanning on all occasions.
The following are some commonly encountered conditions where CT scan of the lung may be indicated.
• Interstitial lung disease—Look for sharp interstitial nodules, ‘ground glass’ opacifications or ‘honeycombing’ that appear in the subpleural region as a reticular pattern with small cystic changes. Ground glass appearance is a manifestation of acute or subacute pneumonitis and is consistent with potential reversibility. Honeycombing is associated with (irreversible) fibrosis.
• Bronchiectasis—In the high-resolution CT scan, look for tramline opacities and signet-ring sign of thickened bronchi in end-on profile.
• Emphysema—Look for discrete, well-demarcated areas of radiolucency and pulmonary vascular pruning.
• Lung tumours—To better define the anatomy and characteristics of the mass lesion and look for metastases.
• Post-primary tuberculosis—To better define the lesion and look for necrosis, and to distinguish from an apical tumour with secondary pneumonia.
Abdominal imaging
Abdominal imaging should be requested when there is suspicion of abdominal malignancy, intestinal obstruction, organomegaly, liver disease, pancreatitis, septic collections or biliary obstruction.
Abdominal ultrasound
Look at the hepatic parenchyma, gallbladder, cystic duct, hepatic duct and common bile duct. Dilatation of the common bile duct (> 6 mm diameter) suggests possible obstruction. Ultrasound can show hepatic mass lesions, stones in the gallbladder, stones in the duct system, chronic cholecystitis and tumour of the gallbladder or the bile duct. To further clarify the above lesions, ask for the abdominal CT scan or the result of endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP), depending on the clinical setting.
Abdominal X-ray
This is indicated in the setting of intestinal obstruction (look for air-fluid levels in the erect film), suspected intestinal perforation (look for gas under the diaphragm), chronic pancreatitis (pancreas appears calcified), gastric dilatation and megacolon.
Barium swallow
This is performed to assess mechanical or functional obstruction of the oesophagus.
Abdominal CT scan
This is usually performed with oral as well as IV contrast. Look at the hepatic parenchyma, porta hepatis, stomach, duodenum, gallbladder, bile duct, portal vein, small and large intestines, abdominal aorta, inferior vena cava, pancreas, kidneys, pelvic organs and retroperitoneum as clinically indicated.
Abdominal MRI scan
This is used to define the anatomy of abdominal and pelvic organs and vasculature with better resolution and definition. It is a preferred imaging modality to better identify pathology.
Cranial imaging
Cranial imaging is done to look for intracranial mass lesions, intracranial haemorrhage, cerebral oedema, cerebral atrophy and hydrocephalus. Investigations for suspected intracranial or intracerebral haemorrhage should be done without the injection of radiocontrast media, as fresh blood is highlighted in white.
Cranial CT scans
Following are some common conditions encountered in cerebral CT scans.
• Subarachnoid haemorrhage—In the cranial CT scan, look for white opacifications (hyperdensity) in the subarachnoid space around the brain (around sulci and gyri), sylvian fissure, the basal cisterns, superior cerebellar cistern and the ventricles. Look for evidence of obstructive hydrocephalus.
• Epidural haemorrhage—This lesion appears as a biconvex (lenticular) extraaxial fluid collection. Also look for the mass effect that manifests as an anatomical shift in the intracranial content and effacement of gyri and sulci.
• Subdural haemorrhage—This lesion manifests as an extraaxial peripheral crescentic fluid collection with concavity in the inner margin. A convex outer margin follows the contour of the cranial vault. The lesion appears as a hyperdensity in the first week, with transformation to isodensity around the second week. It becomes hypodense from the third week onwards (chronic subdural).
• Metastatic lesions—These appear as haemorrhagic, cystic or calcified space-occupying lesions. Most often the cerebral metastases are located in the corticomedullary junction, but remember to look in the subarachnoid space, subependymal space and the skull. They manifest as hyperdense lesions when imaged without injection of radiocontrast material and as hypervascular lesions when imaged with contrast.
• Primary brain tumours—Glioblastoma multiforme accounts for almost 50% of intracranial tumours. In the contract-enhanced CT scan it appears as a homogeneous or non-homogeneous mass lesion with ring enhancement. Request MRI scan for further clarification.
• Ischaemic stroke—Acute stroke (within the first 24 hours) appears as a localised hypodensity in the basal ganglia region or the grey–white matter junction. In the subacute stage (at 1–7 days), its appearance takes a wedge-shaped hypodensity with the base facing the cerebral cortex. Note the localisation to a vascular distribution and the manifestation of mass effect with sulcal effacement and/or transtentorial herniation due to the surrounding oedema.
– Basal ganglia infarct—Manifests as a dense homogeneous enhancement outlining caudate nucleus, putamen, globus pallidus or thalamus.
– Lacunar infarct—Manifests as a discrete area of hypodensity between 3 and 15 mm. The usual area of location in the order of frequency is the upper two-thirds of putamen, caudate nucleus, thalamus, pons and internal capsule.
• Binswanger’s disease—This condition is due to arteriosclerosis of the poorly collateralised distal penetrating arteries, and it correlates with hypertension and ageing. The CT scan shows multifocal hypodense lesions in the periventricular white matter. There may be evidence of lacunar infarctions in the basal ganglia. There is sulcal enlargement and dilated lateral ventricles, signifying brain atrophy.
• Multiple sclerosis—In the CT scan there is non-specific atrophy of the brain. Foci of active demyelination may appear as areas of hyperdensity in the contrast-enhanced CT scan during acute attacks.
Cranial MRI
• T2-weighted scans—Cerebrospinal fluid appears white. Oedema and fluid accumulations also appear white. This weighting helps to better identify abnormalities, so it is important to look at the T2-weighted image first.
• Diffusion scans—This scan helps identify acute stroke as early as within 2 hours of onset. The infarcted tissue appears white, and it is important that all images highlight the relevant area to diagnose stroke conclusively.
• Perfusion scans—Segmental images are made with the injection of gadolinium contrast. There is evidence of decreased perfusion in areas of ischaemic stroke.
The following are some conditions in which MRI scan of the brain is indicated.
• Multiple sclerosis—MRI is the imaging modality of choice in this condition, with 95% specificity. Areas of demyelination are usually distributed in the undersurface of the corpus callosum, the periventricular region and the brainstem. They appear as well-demarcated, discrete foci of increased signal intensity on the T2-weighted and proton density scans. These foci are hypodense in the T1-weighted scans. However, there is gadolinium-DTPA enhancement of the lesions in the T1-weighted scans.
• Stroke—Lesions appear as described above.
Skeletal imaging and arthritis
It is appropriate to ask for skeletal and joint imaging in patients with arthritis, joint pain or back pain, if the condition is relevant and important in the current clinical setting. Rheumatoid arthritis, chronic or acute backache, seronegative arthropathy, Paget’s disease and crystal-induced arthropathy are some of the more commonly encountered conditions in the long case examination where the candidate should consider skeletal and joint imaging as appropriate to clarify the diagnosis and assess the disease severity.
The following are some common radiological appearances with which the candidate needs to be thoroughly familiar.
• Rheumatoid hand—Describe the apparent deformities, such as ulnar deviation of the fingers, ‘Z’ deformity of the thumb, and swan-neck and boutonnière deformity of the fingers. Other common radiological abnormalities in the rheumatoid hand are joint space narrowing, subluxation of the metacarpophalangeal joints, periarticular erosions, juxtaarticular demineralisation, evidence of previous joint surgery or replacement, soft tissue masses suggestive of pannus formation or periarticular oedema and absence of the ulnar styloid.
• Osteoarthritis—Look for joint space narrowing, periarticular osteosclerosis, subchondral cysts and marginal osteophyte formation.
• Ankylosing spondylitis—Look for the loss of definition of the sacroiliac joints due to erosion and sclerosis. Later this may progress to joint fusion. The vertebral column may lose its curvature (loss of lumbar lordosis and thoracic kyphosis) and manifest syndesmophytes (vertical bony bridging between vertebrae). Individual vertebrae become square-shaped. Look for calcification of the longitudinal ligaments and fusion of the facet joints. These changes together with syndesmophytes give rise to the characteristic ‘bamboo spine’.
• Diffuse idiopathic skeletal hyperostosis (DISH)—This disorder manifests radiologically as flowing ossification of the anterior and lateral aspects of the vertebral column due to bony overgrowths and ligamentous calcification. Similar changes may be seen in the extraspinal locations, particularly in the lower limbs. Clinical manifestation of this condition is relatively silent.
The following pages contain some radiographic imaging studies commonly encountered in the examination. The text underneath each image gives an example of the way in which it needs to be interpreted.
Figure 14.11 This is a frontal projection, postero-anterior view chest X-ray. It is of normal appearance.
Figure 14.12 Diffuse alveolar opacification of the right lung with evidence of preexisting CAL and normal heart size. The appearance is consistent with atypical pneumonia, especially due to Legionella. Other differential diagnoses include unilateral pulmonary oedema, pulmonary haemorrhage and unilateral bronchiolitis obliterans with organising pneumonia (BOOP).
Figure 14.13 There is a coarse interstitial pattern with central and basal predominance. Cystic spaces are a prominent feature. Apices are relatively spared. Mediastinum is normal. Appearance of this chest X-ray is consistent with Pneumocystis carinii pneumonia in a patient with HIV infection.
Figure 14.14 Extensive irregular opacity in the right lung apex, with cavitation and a fluid level. This has the appearance of a cavitating abscess. There is elevation of right hemidiaphragm. Other differential diagnoses include post-primary tuberculosis of right apex, Klebsiella pneumonia, and right apical malignancy with cavitation.
Figure 14.15 There is obliteration of the upper segment of the left heart border and opacification of the mid-segment of the left lung. There are air bronchograms. This is consolidation of the lingula.
Figure 14.16 There is hyperinflation of both lung fields and increased lung markings. Multiple cystic areas are present in both lungs, suggesting bronchiectasis. Appearance of a large main pulmonary artery segment suggests pulmonary arterial hypertension. This picture shows diffuse bronchiectasis consistent with cystic fibrosis.
Figure 14.17 There is a band of opacification behind and running parallel to the sternum, thicker superiorly. There is slight elevation of the left hemidiaphragm and mediastinal shift to the left. These features suggest left upper lobe collapse.
Figure 14.18 There is absence of the left breast shadow. There is a coarse reticular pattern throughout the right lung with perihilar predominance. The left lung is clear. This picture is highly suggestive of lymphangitis carcinomatosis in a patient who has had left-sided mastectomy for cancer of the breast.
Figure 14.19 This chest X-ray shows a mass in the lateral basal segment of the right lower lobe with widening of the upper mediastinum and irregularity of the outline of the trachea. This appearance is consistent with metastatic carcinoma of the lung.
Figure 14.20 This chest X-ray shows an interstitial pattern throughout the lung fields with septate lines (Kerley A and B) and perihilar haze. There is interstitial oedema, suggesting high left atrial pressures. There are widespread areas of confluence, suggesting alveolar pulmonary oedema, and therefore left atrial pressure should be above 40 mmHg.
Figure 14.21 There are reticulonodular markings in the lower zones bilaterally. This is the honeycomb pattern of pulmonary fibrosis. The differential diagnoses include rheumatoid arthritis, asbestosis, scleroderma, idiopathic pulmonary fibrosis and chronic aspiration with fibrosis.
Figure 14.22 This high-resolution CT scan of the lung shows widespread air space opacification bilaterally. This opacification has the ground glass appearance suggestive of active interstitial inflammation.
Figure 14.23 This high-resolution CT scan of the lung shows asymmetrical transradiancy between the two lungs. There are peribronchial cuffing, tramline markings and cystic spaces. This is bronchiectasis of the left lower lobe.
Figure 14.24 This thoracic CT scan performed in the mediastinal window shows mediastinal lymphadenopathy in both preaortic and aortopulmonary areas. The differential diagnoses include soft tissue malignancy, metastatic lung cancer and lymphoma.
Figure 14.25 This X-ray of left and right hands shows periarticular osteopenia, ankylosis and deformity of the carpus, subluxation and deformity of the radiocarpal and distal radioulnar joints. There are periarticular erosions and erosion of the ulnar styloid. There is loss of joint space at the first metacarpophalangeal joint. This picture is consistent with rheumatoid arthritis of the hands.
Figure 14.26 The MRIs show an area of abnormality in the left parietal lobe. There is a wedge-shaped area that is slightly hypointense on the T1-weighted picture and hyperintense on the T2-weighted picture. This is consistent with an area of infarction. In addition there are areas that are hyperintense on T1-weighted, T2-weighted and intermediate images consistent with extracellular methaemoglobin. This picture is consistent with subacute haemorrhage.
Figure 14.27 There are moderately well-defined low-density areas in the left posterior temporal, parietal and occipital cerebral lobes and similar smaller areas in the right posterior parieto-occipital regions. This picture is consistent with areas of watershed infarction.
Figure 14.28 Cirrhotic liver with a contrast enhancing mass lesion
Figure 14.30 MRI of primary sclerosing cholangitis
CORONARY AND CARDIAC IMAGING
Coronary angiography
Study the left coronary tree first. Notice the calibre of the vessels along their length and estimate the percentage stenosis of the diameter of narrowed segments due to atherosclerosis. Define the left main segment and the left anterior descending artery (LAD) (the artery that spans all the way to the cardiac apex) and the left circumflex (LCX) artery. The LAD has diagonal and septal branches arising from it. The LCX has obtuse marginal branches and posterolateral branches originating from it. Then go on to examine the right coronary artery and the posterior descending branch (PDA) arising from it. In 10% of the population the PDA arises from the LCX and this is described as left coronary dominance. If the patient has had coronary artery bypass grafts, study the graft angiograms for any stenoses or disease. The grafts could be vein (saphenous) grafts, radial arterial grafts, or left or right internal mammary artery (LIMA or RIMA) grafts. Usually the LIMA is grafted to the LAD.
Echocardiogram
Study the echo images or the report first, looking at left ventricular dimensions and the contractility. Check the ejection fraction. Look at the sizes of the four chambers and left ventricular wall and septal thickness. Then study the valves for stenosis and regurgitation. In the febrile patient look for valvular vegetations. Study the septi for any left/right communications or shunts. If there is a septal defect, note the direction of blood flow. Read the pressure gradient across the stenotic valve. Study the chamber pressures and the estimated pulmonary pressure. In the patient with atrial fibrillation look for intracardiac thrombi, particularly in the left atrial appendage. Examine the pericardial space for any effusion and the pericardium for calcification.
Coronary CT
Coronary CT is gaining rapid popularity as a less invasive imaging modality of the coronary arterial anatomy. The study is useful as a screening test for coronary or vein graft stenosis. It is useful in the investigation of patients who are stable and in an intermediate risk category. Calcification of the arteries and metallic stents can cause interference and shadows, compromising its definition. The images are acquired during diastole in the cardiac cycle, and therefore heart rate needs to be slow for satisfactory results. If the heart rate is too rapid, beta-blocker administration is indicated.
Cardiac MRI
Useful in defining cardiac anatomy. Motion artifacts compromise the quality of images.
Intracoronary ultrasound
Useful in studying the cross-section of a coronary artery by introducing a rotating ultrasound transducer into the coronary artery. This is more sensitive at detecting and measuring coronary stenosis. This modality is useful in studying stent apposition to the vessel wall after coronary stent deployment.
Intracardiac ultrasound
This imaging technology facilitates a closer scrutiny of the cardiac chambers by introducing an ultrasound probe into the right atrium via the inferior vena cava. The access is from a femoral vein. This modality is particularly useful in the device closure of intracardiac shunts and in performing septal puncture to access the left atrium from the right-sided circulation.
Electrophysiological study/RF ablation
These studies are done to identify and isolate aberrant conduction pathways in the heart that create rhythm disturbances. Catheters are introduced into the heart and placed in the areas of interest, which may include the cardiac chambers, bundle of His, coronary sinus (allows access to conduction pathways to the left ventricle) and pulmonary veins (to study atrial fibrillation). When the culprit pathways have been identified and isolated, they can be ablated with radiofrequency energy (RF ablation) and thus, on most occasions, cure the patient of the rhythm disorder.
Figure 14.31 Technetium-sestamibi scan showing normal coronary perfusion at rest and impaired perfusion during stress. The top row of each view depicts perfusion during activity and the bottom row depicts perfusion at rest. In this scan the stress images show a defect in the left ventricular wall that normalises during rest.
(reprinted from Niederkohr R D, Daniels C, Raman S V 2008 Concordant findings on myocardial perfusion SPECT and cardiac magnetic resonance imaging in a patient with myocarditis. Journal of Nuclear Cardiology 15(3):466–8)
Figure 14.32 An abnormal sestamibi scan. The stress and rest tomographic images are labelled and the equivalent stress views are above the corresponding resting views. In this scan there is reversible ischaemia in the anterior wall.
(Image courtesy of Dr P Sullivan)
Figure 14.33 A 65-year-old man presented with exertional angina with a background history of hypertension and hypercholesterolaemia. His exercise stress test was positive for reversible coronary ischaemia. (a) Subsequent coronary angiography showed a significant stenosis of the right coronary artery. (b) This lesion was treated with angioplasty and stent placement.
Figure 14.34 A 31-year-old woman presented with exertional dyspnoea. On examination she had fixed splitting of the second heart sound. On echocardiography there was a septum secundum type atrial septal defect (ASD). She was treated with percutaneous closure of the defect.
Figure 14.35 A 44-year-old man presented with progressive dyspnoea and peripheral oedema in the background of chronic alcoholism. On examination there was bilateral pitting oedema of the ankles and an elevated JVP. There was an audible S3 gallop in the precordium. There were bibasilar crepitations in the lung fields. Echocardiogram showed (a) left ventricular dilation and (b) impairment of systolic function. His coronary angiography was normal. (C and D) Left ventriculography showed severe impairment of systolic function.
Figure 14.36 A 71-year-old man was brought in by ambulance after a cardiac arrest and successful resuscitation in the local shopping mall. Upon presentation the ECG showed deep T wave inversion in the septal and left lateral leads. Urgent coronary angiography showed significant narrowing at the osteum of the left main coronary artery (A and B). The patient was referred to the cardiac surgeon for urgent coronary artery bypass surgery, and in the meantime was anticoagulated with heparin.
Figure 14.37 A 75-year-old woman with diabetes presented with 2 hours of retrosternal ache radiating down the right arm. She also complained of nausea. Her ECG showed ST segment depression of 2 mm in the inferior leads. She had cardiac biomarker positivity. Coronary angiography showed diffused, critical stenoses in all three coronary arteries (triple vessel disease). The patient was referred to the cardiac surgeon for coronary artery bypass surgery.
Figure 14.38 A 20-year-old woman was referred by the family practitioner upon the incidental finding of a machinery murmur heard all over the precordium. The murmur was loudest in the left subclavian region. Echocardiography showed a patent ductus arteriosus (PDA). This was confirmed by ascending aortography. Note the 10-cent coin placed over the patient’s chest during aortography to help estimate the size of the PDA. This PDA was closed percutaneously with a ductal occluder.
Figure 14.39 An 86-year-old woman presented with sudden loss of consciousness. On examination she had a slow rising pulse and a harsh ejection systolic murmur that radiated to her carotids bilaterally. Echocardiography demonstrated a calcified aortic valve with a critical gradient on Doppler assessment. Note the maximum and mean pressure gradients of significance. She was referred to the cardiac surgeon for valve replacement.
Figure 14.40 A 60-year-old man who presented with retrosternal chest pain was diagnosed with acute coronary syndrome. There were deep T wave inversions in the lateral lead in the ECG. He had significant troponin level elevation. He subsequently developed an apical systolic murmur that radiated to his left axilla. Echocardiography showed an eccentric jet of mitral regurgitation on colour flow Doppler assessment. Coronary angiography showed a tight stenosis of the large left circumflex coronary artery. This lesion was treated with angioplasty and stent placement. Subsequent echocardiography showed significant improvement of the mitral regurgitation. The valve defect was due to papillary muscle ischaemia associated with the circumflex artery stenosis.
Figure 14.41 A 74-year-old man presented with dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea. On echocardiography there was severe hypertrophy of the left ventricle with impaired diastolic filling.
Figure 14.42 A 60-year-old smoker presented with angina on exertion. Coronary angiography showed stenosis of the left anterior descending (LAD) artery. This lesion was further characterised and measured with intravascular ultrasound (IVUS) imaging. The lesion was subsequently treated with a coronary stent
Figure 14.43 A 47-year-old woman with a past history of breast cancer presented with syncope. On examination she was hypotensive at 80/40 mmHg and her pulse rate was 120 bpm. Her JVP was elevated with evident Kussmaul’s sign. There was pulsus paradoxus. Echocardiography revealed a significant pericardial effusion with evidence of cardiac tamponade. Note the large collection of fluid around the left ventricle.
Figure 14.44 A 46-year-old heavy smoker presented with severe retrosternal chest tightness, nausea, vomiting and diaphoresis of 1 hour’s duration. He was hypotensive on assessment. The 12-lead ECG showed ST segment elevation of 2 mm in leads II, III and AVF, confirming the diagnosis of ST elevation myocardial infarction (STEMI) (see figure D). The patient was referred to the interventional cardiology team for primary percutaneous intervention (primary PCI). Angiography revealed an occluded right coronary artery (RCA) which was reopened with balloon angioplasty and stenting.
Figure 14.45 CT coronary angiogram
Figure 14.46 A 52-year-old man with new-onset atrial fibrillation underwent transoesophageal echocardiography (TOE) prior to direct current cardioversion. There was no thrombus seen within the left atrial appendage and the Doppler flow assessment ruled out stasis in the vicinity.
[/level-membership-for-internal-medicine-category][not-level-membership-for-internal-medicine-category]ESSENTIALS OF ELECTROCARDIOGRAM READING
The major components to observe in the interpretation of an ECG are the rhythm, rate, axis and morphology, as shown by the P wave, P-R interval, QRS complex, ST segment, T wave and Q-T interval (see box).
Interpretation of ECG
1. Confirm the name and the date of birth/age of the patient and the date on which the ECG was recorded.
2. Ascertain the number of leads on display (usually 12 leads).
3. Check the calibration: standard paper speed is 25 mm/s (where each small 1 mm square denotes 0.04 s or 40 ms horizontally); vertically each 1 cm square denotes 1 mV.
4. Check the rate.
5. Check the rhythm (regular, irregular): this is best seen in lead II—the rhythm strip.
6. Check the axis (normal axis is between –30° and +120°; if between –90° and –30° it is left-axis deviation and if between +120° and +180° it is right-axis deviation).
7. Analyse the P wave (morphology, regularity and relationship to the QRS complex).
8. Assess the P-R interval (normal is 200 ms).
10. Analyse the ST segment: depression and elevation in relation to the isoelectric line and its significance according to the context.
11. Check the Q-T interval (this is a rate-dependent phenomenon; < 430 ms is normal for the adult male, < 450 ms for the adult female).
12. Study the T wave: height and morphology.
13. Look for special features (e.g. bundle branch block) and possible diagnosis according to the clinical context.
It is not necessary to describe the ECG in the traditional and pedantic way, opening with the rate, rhythm and axis and then going on to describe the rest if they are normal. At the examination this may sound superfluous, and there is no time to waste! Candidates should identify the name of the patient and the date the ECG was done, and immediately start describing the abnormalities with references to the clinical findings. The following is a discussion of the various ECG findings commonly encountered in the long case examination.
Acute (transmural) myocardial infarction
ST elevation of more than 1 mm in two contiguous leads. In anterior infarcts this would be in the chest leads V2–V6. Left heart infarcts show this in leads I, II and aVL. In inferior infarcts it is seen in leads II, III and aVF. Posterior infarctions show up as reciprocal changes in the anterior leads, and the classic findings include R waves, ST segment depression or tall T waves in leads V1 and V2. Acute myocardial infarction can sometimes present as a new bundle branch block.
Q waves are pathological if they are broader than 1 mm or deeper than 2 mm (or > 25% of the height of the following R wave).
Subendocardial ischaemia
ECG changes consistent with subendocardial ischaemia (acute coronary syndrome) are ST segment depression of 1 mm or more, 0.08 seconds after the J point and corresponding T wave changes. The slope of the ST segment may provide some clues to the severity of the ischaemic phenomenon. Upward sloping indicates less severe disease, horizontal sloping indicates more severe disease, while downward sloping is usually considered the most significant and severe. The T wave changes include T wave flattening and T wave inversion.
Left ventricular hypertrophy
Left ventricular hypertrophy is described according to voltage criteria and strain/repolar-isation criteria.
Voltage criteria
1. Length of the deepest S wave in leads V1 or V2, or height of the tallest R wave of lead V5 or V6 > 25 mm
2. Sum of the lengths of the S wave of V1 and the R wave of either V5 or V6 > 35 mm
3. Height of the R wave in aVL > 12 mm and height of the R wave in aVF > 20 mm
4. Sum of the lengths of the S wave in lead III and R wave of lead I > 25 mm
Right ventricular hypertrophy
This may be associated with pulmonary stenosis or pulmonary hypertension.
Right atrial hypertrophy/strain
This is associated with right atrial overload, as in pulmonary hypertension and right heart failure.
Right bundle branch block
This is seen in right heart strain associated with pulmonary hypertension, chronic lung disease, pulmonary emboli and mitral valve pathology. Some people may have non-pathological right bundle branch block, which is of no significance.
Left bundle branch block
This is seen in ischaemic heart disease, hypertension, aortic stenosis and cardio-myopathy. Features to notice:
Left anterior hemiblock
This is the most common cause of left-axis deviation. There is marginal prolongation of the QRS complex with left-axis deviation. Also notice terminal R waves in leads aVR and aVL, deep S wave in lead II, and RSR pattern in leads II, III and aVF. This feature is commonly seen in anterolateral or inferior myocardial infarcts.
Left posterior hemiblock
This abnormality is associated with right-axis deviation of about 120°, Q waves in leads II, III and aVF, R waves in leads I and aVL. When left posterior hemiblock is present it is almost always associated with right bundle branch block. This combination has a poor prognosis, and progression to complete heart block needing a pacemaker is the likely eventuality.
Bifascicular block
Right bundle branch block in combination with a left-sided hemiblock or left bundle branch block. There is a high likelihood of progression to complete heart block requiring a permanent pacemaker.
First-degree heart block
The rate is usually normal and the main abnormality is a prolonged P-R interval (> 200 msec or 5 mm).
Second-degree heart block
Type I (Wenckebach phenomenon)
The sinus rate is normal but the ventricular rate is slower than normal. The main abnormality is the gradual prolongation of the P-R interval until one P wave is not conducted to the ventricles. A new cardiac cycle begins following the non-conducted P wave. Rhythm is usually irregular. This pattern has an association with inferior myocardial infarctions.
Type II
The sinus rate is normal but the ventricular rate is a definite fraction of the sinus rate. There are more P waves than QRS complexes, as only one P wave is conducted for several subsequent P waves. Note the block, which is 2:1, 3:1 or more. This condition is usually associated with anterior myocardial infarctions.
Complete heart block
The sinus rate is normal but the ventricular rate is much slower. The ventricular rate is dependent on the site of the escape pacemaker (if it is in the AV junction, the rate would be around 40–60 bpm; if ventricular, the rate would be < 30 bpm). The P-R interval changes constantly and the P wave has no relationship to the QRS complex (AV dissociation).
Tachyarrhythmias
Ventricular tachycardia
A broad complex tachycardia with a rate exceeding 100 bpm. In practice, however, it is common to see the rate at 140–200. The rhythm is regular. It is called sustained ventricular tachycardia if it persists beyond 30 seconds. The QRS complex is longer than 140 milliseconds. There is evidence of AV dissociation, fusion beats and variable retrograde conduction. QRS pattern of all precordial leads should be in concordance. There may be features of left-axis deviation in the presence of right bundle branch block. A broad complex ventricular rhythm at a rate of less than 100 bpm is called accelerated idioventricular rhythm.
Atrial tachycardia
The rhythm is regular and the rate is 140–280 bpm. QRS complex follows each P wave, but the P wave may also be buried in the QRS complex or the T wave and not be visible.
Atrial flutter
The rhythm is most often regular but may vary if the degree of AV nodal block changes. Ventricular rate may vary between 60 and 150, again depending on the block. There are characteristic atrial oscillations described as ‘sawtooth’-shaped flutter waves. These flutter waves occur regularly at a rate of 250–300 per minute. Depending on the block, the rhythm should be described as atrial flutter with 2:1, 3:2 or 4:1 block.
Junctional tachycardia (AV nodal re-entry tachycardia)
The rhythm is regular and the rate is 100–200 bpm. The P wave appears inverted and is located immediately before or after the QRS complex due to retrograde conduction.
Wolff-Parkinson-White syndrome
This conduction defect occurs due to ventricular pre-excitation due to the presence of an accessory AV conduction pathway. The P-R interval is shorter than 110 milli-seconds and the QRS complex has a slurred upstroke (delta wave). The patient may be in atrial fibrillation. A negative delta wave in lead V1 suggests a right-sided bypass tract.
Hypertrophic obstructive cardiomyopathy
Patients with hypertrophic obstructive cardiomyopathy may show non-specific ECG features. Evidence of left ventricular hypertrophy and diffuse, widespread, deep and broad Q waves are some commonly seen abnormalities.
HAEMATOLOGICAL STUDIES
Blood test results encountered in the examination include the full blood count, electrolyte profile, renal function indices, liver function studies, endocrine studies and serology. Serological tests can be either infective or autoimmune serology.
Full blood count
Here the focus should be on haemoglobin level, haematocrit, mean cell volume, mean cell haemoglobin concentration, and white cell count with differential and platelet count.
Candidates should know the normal values of all the above so that an abnormal value can be spotted immediately and interpreted accurately. When an abnormality in the blood count is present, ask for the report of the blood film for further clarification and, if appropriate, ask for other tests such as the results of the bone marrow biopsy, haemolytic screen, iron studies and vitamin B12 and folate levels in anaemia, results of the blood culture in the setting of significant leucocytosis and febrile illness, and antiplatelet antibodies in idiopathic thrombocytopenia.
Figure 14.1 ECG showing atrial and ventricular paced rhythm with pacing spikes clearly visible before each atrial and ventricular complex. Also note the left bundle branch block (LBBB) pattern due to the early stimulation of the right ventricle by the pacing lead located there.
Figure 14.3 ECG showing Wolff-Parkinson-White (WPW) syndrome. Notice the short P-R interval and the delta wave visible in most QRS complexes.
Figure 14.5 ECG showing supraventricular bigeminy and left axis deviation
Figure 14.7 ECG showing left bundle branch block (LBBB)
Figure 14.9 ECG showing atrial fibrillation
Figure 14.10 ECG showing supraventricular tachycardia with aberrancy
Neutrophilia
Neutrophilia is diagnosed when the neutrophil count is elevated above 7.5 × 109/L. The possible causes are:
Lymphocytosis
Lymphocytosis is diagnosed when the lymphocyte count is elevated above 4 × 109/L. The possible causes are:
Eosinophilia
Eosinophilia is diagnosed when the eosinophil count is elevated above 0.5 × 109/L. The possible causes are:
Basophilia
Basophilia is diagnosed when the basophil count is elevated above 0.1 × 109/L. The possible causes are:
Leucopenia
Leucopenia is diagnosed when the white cell count is less than 4 × 109/L. The possible causes are:
Microangiopathic haemolytic anaemia (MAHA) should be suspected in an anaemic and coagulopathic patient if the blood film report shows fragment cells, helmet cells, polychromasia and reticulocytosis. The possible causes include:
Thrombophilic screen
This should be performed in cases of thromboembolic disease with a strong family history or recurrent spontaneous venous thrombosis in any patient, arterial throm-bosis in a patient aged under 30 years, and venous thrombosis in a patient aged under 40 years without a predisposing condition.
Thrombophilic screen involves testing for the following:
Electrolyte profile
Look at the sodium level, potassium level, chloride level, bicarbonate level and the renal function indices. If any abnormality is noticed, try interpreting it in the context of the clinical setting or a causative medication.
Sodium
The normal serum sodium level is 136–144 mmol/L.
Hypernatraemia
This can be caused by hypovolaemia and dehydration as well as primary hyperaldosteronism, Cushing’s syndrome and excess salt intake. Patients present with lethargy, irritability, fever, nausea, vomiting and confusion. Management is with controlled hydration using 4% dextrose with 1/5 normal saline or 5% dextrose solution together with judicious diuretic therapy.
Hyponatraemia
This can be caused by inappropriate secretion of antidiuretic hormone (SIADH), congestive cardiac failure, severe hepatic failure, Addison’s disease, aldosterone insufficiency, hypothyroidism, diuretic therapy, salt-losing nephropathy, renal tubular disorders and water retention.
SIADH can be due to small cell lung cancer, central nervous system disorders such as meningitis and subarachnoid haemorrhage, lung disease such as asthma, pneu-monia and tuberculosis, and drug therapy with tricyclic antidepressants, carbamazepine and monoamine oxidase inhibitors. The phenomenon of pseudohyponatraemia occurs in hyperglycaemia, alcohol excess and hyperuricaemia. Significant hyponatraemia (serum sodium of < 125 mmol/L) presents with lethargy, confusion, convulsions and coma. Management of severe symptomatic hyponatraemia uses controlled infusion (1–3 mL/kg/h) of hypertonic saline (3% NaCl) with judicious diuretic therapy. Chronic, asymptomatic hyponatraemia can be well managed with fluid restriction to 1 L/day. Resistant hyponatraemia due to SIADH can also be treated with regular oral demeclocycline.
Potassium
The normal serum potassium level is 3.5–5.0 mmol/L.
Hyperkalaemia
This can be caused by ACE inhibitor therapy, potassium-sparing diuretics, inadvertent potassium supplementation, acidosis, blood transfusion, haemolysis, severe renal failure, rhabdomyolysis and hypoaldosteronism.
Patients present with severe muscular weakness, paralytic ileus, symptomatic brady-cardia and heart block. Management of hyperkalaemia includes administration of 10 mL 10% calcium gluconate if there are electrocardiographic changes of hyperkalaemia (peaked T waves, small P waves and wide QRS complexes). Rapid reversal of potassium levels can be achieved by giving 50% glucose with insulin infusion, but the levels may rise again in a few hours. Concurrently administer oral or per rectum resonium 15–30 g and repeat administration as guided by subsequently measured serum potassium levels. Hyperkalaemia of severe renal failure needs haemodialysis.
Hypokalaemia
Causes of hypokalaemia include loop diuretic therapy, primary hyperaldosteronism, Cushing’s syndrome, renal tubular disease, alkalosis and hyperthyroidism. Therapy with drugs such as verapamil, beta-agonists and amiodarone should be excluded.
Hypokalaemia presents with muscle weakness or tetany. Significant hypokalaemia can lead to rhabdomyolysis. To manage hypokalaemia, usually oral supplementation alone will suffice. If the level is < 2.9 mmol/L, parenteral supplementation with KCl 10 mmol/L over an hour through a central venous line is indicated. The patient’s cardiac function should be monitored during this infusion. It should be repeated as guided by the subsequently performed serum potassium levels.
Calcium
The normal serum calcium level is 2.2–2.5 mmol/L. The serum calcium level varies with the serum albumin level, and the correction can be made using the following formula:
Hypercalcaemia
This can be caused by primary hyperparathyroidism, squamous cell carcinoma of the lung, cancer with bony metastases, multiple myeloma, sarcoidosis, vitamin D intoxi-cation, milk-alkali syndrome and thiazide diuretics.
Significant hypercalcaemia presents with anorexia, nausea, vomiting, constipation, polyuria, severe weakness, stupor and eventually coma.
Steps in the management of hypercalcaemia include, first, hydration with adequate amounts of normal saline, together with loop diuretic therapy. More severe hypercalcaemia needs treatment with a bisphosphonate such as etidronate or pamidronate. Calcitonin injected subcutaneously or intravenously (200 units, 6-hourly) has a short-lived effect. Hypercalcaemia due to multiple myeloma, sarcoidosis or vitamin D toxicity can be treated also with glucocorticoids. Oral phosphate is useful when there is hypercalcaemia together with hypophosphataemia.
Hypocalcaemia
Causes of hypocalcaemia include hypoparathyroidism, vitamin D deficiency, osteomalacia, acute pancreatitis, chronic renal failure, malignancy with osteoblastic metastases, and pseudohypoparathyroidism.
Patients present with circumoral and distal limb paraesthesias, painful muscle cramps, tetany and seizures. Patients may also have Chvostek’s sign and Trousseau’s sign.
Symptomatic hypocalcaemia and corrected serum levels of < 1.88 mmol/L should be treated with parenteral calcium in the form of 10% calcium gluconate.
Acid–base status
Metabolic acidosis
This diagnosis should be suspected when plasma bicarbonate (HCO3) is less than 10 mmol/L and PaCO2 is low with a low pH (a low HCO3 value can be seen in respiratory alkalosis as well as in metabolic acidosis). The anion gap helps the interpretation of metabolic acidosis in more detail, and is calculated as follows:
The normal value is 10–14 mmol/L. Metabolic acidosis could be with a normal or increased anion gap.
Metabolic acidosis with a normal anion gap is due to an associated loss of HCO3 molecules from the body. The possible causes are:
1. HCO3 loss from the gut due to diarrhoea, ureterosigmoidostomy, ileal conduit, pancreatic drainage or biliary drainage
2. HCO3 loss from the kidney due to the use of carbonic anhydrase inhibitor, urinary diversion, renal tubular acidosis (proximal or distal), early renal failure or interstitial nephritis.
This condition is managed with volume repletion and correction of associated hypokalaemia with potassium supplementation.
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