Abdominal Xrays

1. Abdominal Xrays!!!

2. The Abdominal X ray

3. Position of Patient Supine (lying on their back) with the plate (film) underneath them – x rays from front to back Unless otherwise labelled, the film will probably be supine Erect – may be useful if looking for fluid levels Decubitus – taken with the patient in the lateral position – may be useful to detect intraperitoneal gas Prone - patient lying on their front - occasionally used in IVUs

4. Densities of structures on the radiograph Black – gas White – calcified structures Grey – soft tissues Dark grey – fat Intense white – metallic structures

5. Interpreting the AXR

6. Part 1 – Patient Details

7. Part 2- Technical Details Orientation- check the pelvis is at the bottom, the liver is on the left, stomach on the right. Penetration- see the spinous processes of the vertebrae Adequate view – xiphisternum to pubic symphysis with both flanks visible.Orientation- check the pelvis is at the bottom, the liver is on the left, stomach on the right. Penetration- see the spinous processes of the vertebrae Adequate view – xiphisternum to pubic symphysis with both flanks visible.

8. Example of a Normal Radiograph

9. Part 3 – Intraluminal gas Stomach Small intestine (n= 2.5 cm) Colon (n= 5 cm) Caecum (n= 9 cm) Rectum (sometimes visible)

10. Gas in the stomach

11. Clinical Findings- Obstruction

13. “

14. Caecal Volvulus

15. Part 4 – Extraluminal gas

16. Gas under diaphragm

17. Perforation Perforation - When a patient is supine, free intraperitoneal gas doesn’t collect under the diaphragm, but rises to the centre of the abdomen giving rise to a central dark area and peripheral light area Perforation - When a patient is supine, free intraperitoneal gas doesn’t collect under the diaphragm, but rises to the centre of the abdomen giving rise to a central dark area and peripheral light area

18. Part 5 – soft tissue structures Liver Spleen Pancreas Kidneys Ureters Bladder Psoas muscles

19. Clinical Findings

21. Absence of Psoas Muscle Absence of the left psoas muscle-retropritoneal diseaseAbsence of the left psoas muscle-retropritoneal disease

22. Part 6 – Abnormal calcification Aorta Pancreas Cystic Duct Gall bladder Kidneys Ureter Bladder Urethra

23. Bladder calculi

24. Renal Stones

26. Pancreatic Calcification

27. Gallstones

28. Aorta

29. Part 7 – Look at bone structure Fractures – vertebral bodies Metastases Changes in bone density Shape

30. Fracture

31. Bone pathologies

32. Finally- Extra features Foreign objects ECG leads Tubes/stents Surgical clips – aid diagnosis

34. Summary – Presenting Patient Details - easy Technical Details Intraluminal Gas – dilated etc. Extraluminal Gas- preforation Soft tissue Structures- “-megaly” Abnormal Calcification - stones Bony Structures Any Extra Features - objects SUMMARY

35. Its practice time!!!!

36. NORMAL

37. Title Air under diaphragmAir under diaphragm

38. Dilated small bowelDilated small bowel

39. Faecal loading and stag horn calculusFaecal loading and stag horn calculus

40. Air in the biliary treeAir in the biliary tree

41. Toxic megacolon of ulcerative colitisToxic megacolon of ulcerative colitis

42. volvulusvolvulus

43. Pancreatic calcificationPancreatic calcification

44. gallstonesgallstones

45. This 67 year-old women presented to the surgical ward with a distended abdomen and vomiting. Answer :Small bowel obstruction Multiple dilated loops of small bowel within the central abdomen. Gas is not seen in the large bowel. No evidence of hernia or gallstone to suggest potential cause of the dilated loops. These findings are in keep with a low small bowel obstruction. I would like to know if the patient has a history of abdominal surgery as the commonest cause is surgical admissions. 3 main causes of small bowel obstruction : Surgical adhesions Herniae Intraluminal mass eg, small bowel lymphoma or gallstone (in gallstone ileus)This 67 year-old women presented to the surgical ward with a distended abdomen and vomiting. Answer :Small bowel obstruction Multiple dilated loops of small bowel within the central abdomen. Gas is not seen in the large bowel. No evidence of hernia or gallstone to suggest potential cause of the dilated loops. These findings are in keep with a low small bowel obstruction. I would like to know if the patient has a history of abdominal surgery as the commonest cause is surgical admissions. 3 main causes of small bowel obstruction : Surgical adhesions Herniae Intraluminal mass eg, small bowel lymphoma or gallstone (in gallstone ileus)

46. This 71 year-old gentleman visits his GP complaining of blood in his urine. He has had a number of UTI’s in recent years. Answer : bladder calculus Two rounded radio-opacities measuring 4cm within the pelvis. Both opacities are smooth in outline, laminated in nature, have the same density as bone and project over the bladder. No other renal tract calcification. Does the patient have a history of neurogenic bladder? Given the size of these stones and history of UTI’s these are bladder calculi. 3 causes : •UTI’s •A neurogenic bladder •Bladder diverticulum This 71 year-old gentleman visits his GP complaining of blood in his urine. He has had a number of UTI’s in recent years. Answer : bladder calculus Two rounded radio-opacities measuring 4cm within the pelvis. Both opacities are smooth in outline, laminated in nature, have the same density as bone and project over the bladder. No other renal tract calcification. Does the patient have a history of neurogenic bladder? Given the size of these stones and history of UTI’s these are bladder calculi. 3 causes : •UTI’s •A neurogenic bladder •Bladder diverticulum

47. This patient was admitted with poor renal function. Answer : kidney stones!! Multiple areas of punctuate calcification project over the renal outlines bilaterally. The calcification is within the medulla of the renal parenchyma. The bones are normal in appearance. These findings are consistent with nephrocalcinosis This patient was admitted with poor renal function. Answer : kidney stones!! Multiple areas of punctuate calcification project over the renal outlines bilaterally. The calcification is within the medulla of the renal parenchyma. The bones are normal in appearance. These findings are consistent with nephrocalcinosis

49. ECG Adeel Iqbal Year 5 Presentation slide for courses, classes, lectures et al. Presentation slide for courses, classes, lectures et al.

51. Rate Abnormalities: Sinus Bradycardia: - Apart from fit, but otherwise normal individuals, there's a long list of situations where sinus bradycardia occurs, including: - hypothermia; - increased vagal tone (due to vagal stimulation or e.g. drugs); - hypothyroidism;

52. - beta blockade; - marked intracranial hypertension; - obstructive jaundice, and even in uraemia; - structural SA node disease, or ischaemia.

53. Sinus tachycardia: - Always consider pain as a possible cause of tachycardia. There's a long list, however: - Any cause of adrenergic stimulation (including pain); - thyrotoxicosis; - hypovolaemia;

54. - vagolytic drugs (e.g. atropine) - anaemia, pregnancy; - vasodilator drugs, including many hypotensive agents; - FEVER myocarditis If the rate is almost exactly 150, always make sure that you are not mistaking atrial flutter with a 2:1 block for sinus tachycardia. A common error.

55. Rhythm Abnormalities: Irregular Supraventricular tachyarrhythmias (SVT): By far the commonest cause of irregular SVT is atrial fibrillation, where the atrial rate is in the region of 450 to 600/min, and the atria really do not contract rhythmically at all.

56. The pathogenesis of AF is that there are multiple re-entrant `wavelets' moving through the atrial muscle, But recent evidence suggests that much AF actually arises from ectopic activity in the muscular cuff surrounding the pulmonary veins where they enter the left atrium.

57. Regular SVT: Atrial flutter is common. The atrial rate is commonly 300/min, and there is usually a 2:1 block, resulting in a ventricular response rate of 150/min. Other ratios are possible, and sometimes the ratio varies. This rhythm is often unstable, and the heart may flip in and out of sinus rhythm, or there may be runs of atrial fibrillation.

58. In the above ECG the clue is the rate. A rate of 150 should always engender the suspicion of atrial flutter with 2:1 block.

59. Accessory pathways Abnormal, congenital extra pathways between the atria and ventricles are common, and can perforate the electrically insulating fibrous ring that normally separates the atrial `chamber' and the ventricular one. The most well-characterised is the Wolff-Parkinson-White syndrome. Reasonable (WHO) criteria for the WPW pattern on ECG are:

60. PR interval under 0.12s A delta wave QRS duration of 0.12s (or more) A normal P-wave axis

61. The WPW syndrome is a combination of the WPW pattern, and tachycardias. The ventricle may be driven at rates in excess of 200/min, causing collapse or even death.

62. Ventricular fibrillation This is a chaotic ventricular rhythm that rapidly results in death. It is often precipitated by a critically timed extrasystole, that occurs during the relative refractory period of the myocardial fibres. Conventional wisdom has it that this results in chaotic, unco-ordinated wavelets of depolarisation moving through the ventricular mass.

63. VF is a dire emergency. If unsynchronised DC countershock is applied within 30s of the onset of VF, there is an approximately 97% chance that sinus rhythm will be restored, and the person will survive. Survival decreases exponentially thereafter, with every minute of delay.

64. AV nodal blocks There are three "degrees" of AV nodal block: 1- First degree block: simply slowed conduction. This is manifest by a prolonged PR interval;

65. 2- Second degree block: Conduction intermittently fails completely. This may be in a constant ratio (more ominous, Type II second degree block) Progressive (The Wenckebach phenomenon, characterised by progressively increasing PR interval culminating in a dropped beat --- this is otherwise known as Mobitz Type I second degree heart block).

67. 3- Third degree block: There is complete dissociation of atria and ventricles.

68. Bundle branch blocks: A broadened QRS complex suggests a bundle branch block, although there are other causes: 1- RBBB: - Diagnostic criteria for right bundle branch block are somewhat empiric, but useful. Here they are: 1- Tall R' in V1; 2- QRS duration 0.12s or greater (some would say, >= 0.14); - In addition, there is usually a prominent S in the lateral leads (I, V5, V6).

69. RBBB is sometimes seen in normal people, or may reflect congenital heart disease (e.g. atrial septal defect), ischaemic heart disease, cardiomyopathy, or even acute right heart strain.

70. 2- LBBB: Diagnose this as follows: - No RBBB can be present; - QRS duration is 0.12s or more; - There must be evidence of abnormal septal depolarization. The tiny q waves normally seen in the left-sided leads are absent. (And likewise for the normal tiny r in V1). In addition, the VAT is prolonged, and tall, notched R waves are seen in the lateral leads (RR' waves). There is usually a notched QS complex in V1 and V2.

71. Ischaemic heart disease - ST changes: One should always remember that more than a quarter of people presenting with an acute myocardial infarction will have no ECG evidence of ischaemia or infarction! The ECG on its own is a blunt-edged tool in the detection of coronary artery disease. Exercise testing to elicit ischaemia is also not very sensitive in detecting this common disease.

72. 1- Acute myocardial infarction --- the `hyperacute phase' - There are four main features of early myocardial infarction increased VAT increased R wave amplitude (!) ST elevation which is sloped upwards! Tall, widened T waves (The ST segment often merges with these)

73. Note that Q waves are not seen early on.

74. Established acute myocardial infarction We now lay great emphasis on ST segment elevation in diagnosing acute MI (In the past, Q waves were remarked on, but as noted above, these are often absent, early on). The features of `full blown' MI may be: 1-prominent Q waves; 2-elevated ST segments; 3-Inverted `arrowhead' T waves. Remember our previous warning, that a significant proportion of people having an acute MI will have a normal ECG, so do not rely on any of these features to exclude MI.

75. Elements of the trace

76. Leads and what they tell you Each lead can be thought of as ‘looking at’ an area of myocardium Chest leads V1 to V6 ‘look’ at the heart on the transverse plain V1 and 2 look at the anterior of the heart and R ventricle V3 and 4 = anterior and septal V5 and 6 = lateral and left ventricle

77. Interpreting the ECG Check Name DoB Time and date Indication e.g. “chest pain” or “routine pre-op” Any previous or subsequent ECGs Is it part of a serial ECG sequence? In which case it may be numbered Calibration Rate Rhythm Axis Elements of the tracing in each lead

78. Calibration Check that your ECG is calibrated correctly Height 10mm = 1mV Look for a reference pulse which should be the rectangular looking wave somewhere near the left of the paper. It should be 10mm (10 small squares) tall Paper speed 25mm/s 25 mm (25 small squares / 5 large squares) equals one second

79. Rate If the heart rate is regular Count the number of large squares between R waves i.e. the RR interval in large squares Rate = 300 RR e.g. RR = 4 large squares 300/4 = 75 beats per minute

80. Axis The axis can be though of as the overall direction of the cardiac impulse or wave of depolarisation of the heart An abnormal axis (axis deviation) can give a clue to possible pathology

81. Axis

82. Axis deviation - Causes Wolff-Parkinson-White syndrome can cause both Left and Right axis deviation A useful mnemonic: “RAD RALPH the LAD from VILLA” Right Axis Deviation Right ventricular hypertrophy Anterolateral MI Left Posterior Hemiblock Left Axis Deviation Ventricular tachycardia Inferior MI Left ventricular hypertrophy Left Anterior hemiblock

83. The P wave The P wave represents atrial depolarisation It can be thought of as being made up of two separate waves due to right atrial depolarisation and left atrial depolarisation. Which occurs first? Right atrial depolarisation

84. The P wave Dimensions No hard and fast rules Height a P wave over 2.5mm should arouse suspicion Length a P wave longer than 0.08s (2 small squares) should arouse suspicion

85. The P wave Height A tall P wave (over 2.5mm) can be called P pulmonale Occurs due to R atrial hypertrophy Causes include: pulmonary hypertension, pulmonary stenosis tricuspid stenosis

86. The P wave Length A P wave with a length >0.08 seconds (2 small squares) and a bifid shape is called P mitrale It is caused by left atrial hypertrophy and delayed left atrial depolarisation Causes include: Mitral valve disease LVH

87. The PR interval The PR interval is measured between the start of the P wave to the start of the QRS complex (therefore if there is a Q wave before the R wave the PR interval is measured from the start of the P wave to the start of the Q wave, not the start of the R wave)

88. The PR interval If the PR interval is short (less than 3 small squares) it may signify that there is an accessory electrical pathway between the atria and the ventricles, hence the ventricles depolarise early giving a short PR interval. One example of this is Wolff-Parkinson-White syndrome where the accessory pathway is called the bundle of Kent. See next slide for an animation to explain this

89. The PR interval If the PR interval is long (>5 small squares or 0.2s): If there is a constant long PR interval 1st degree heart block is present First degree heart block is a longer than normal delay in conduction at the AV node

90. The PR interval If the PR interval looks as though it is widening every beat and then a QRS complex is missing, there is 2nd degree heart block, Mobitz type I. The lengthening of the PR interval in subsequent beats is known as the Wenckebach phenomenon (remember (w)one, Wenckebach, widens) If the PR interval is constant but then there is a missed QRS complex then there is 2nd degree heart block, Mobitz type II

91. The PR interval If there is no discernable relationship between the P waves and the QRS complexes, then 3rd degree heart block is present

92. Heart block (AV node block) Summary 1st degree constant PR, >0.2 seconds 2nd degree type 1 (Wenckebach) PR widens over subsequent beats then a QRS is dropped 2nd degree type 2 PR is constant then a QRS is dropped 3rd degree No discernable relationship between p waves and QRS complexes

93. The Q wave Are there any pathological Q waves? A Q wave can be pathological if it is: Deeper than 2 small squares (0.2mV) and/or Wider than 1 small square (0.04s) and/or In a lead other than III or one of the leads that look at the heart from the left (I, II, aVL, V5 and V6) where small Qs (i.e. not meeting the criteria above) can be normal

94. The QRS height If the complexes in the chest leads look very tall, consider left ventricular hypertrophy (LVH) If the depth of the S wave in V1 added to the height of the R wave in V6 comes to more than 35mm, LVH is present

95. QRS width The width of the QRS complex should be less than 0.12 seconds (3 small squares) Some texts say less than 0.10 seconds (2.5 small squares) If the QRS is wider than this, it suggests a ventricular conduction problem – usually right or left bundle branch block (RBBB or LBBB)

96. QRS width It is then useful to look at leads V1 and V6 If left bundle branch block is present, the QRS complex may look like a ‘W’ in V1 and/or an ‘M’ shape in V6 If right bundle branch block is present, there may be an ‘M’ in V1 and/or a ‘W’ in V6 This can be remembered by the mnemonic: WiLLiaM MaRRoW

97. QRS width If LBBB is present, it is very difficult to interpret the following ST segment If there is new onset LBBB, it may represent an MI Bundle branch block is caused either by infarction or fibrosis (related to the ageing process)

98. The ST segment The ST segment should sit on the isoelectric line It is abnormal if there is planar (i.e. flat) elevation or depression of the ST segment Planar ST elevation can represent an MI or Prinzmetal’s (vasospastic) angina Planar ST depression can represent ischaemia

99. The ST segment If the ST segment is elevated but slanted, it may not be significant If there are raised ST segments in most of the leads, it may indicate pericarditis – especially if the ST segments are saddle shaped. There can also be PR segment depression

100. Myocardial infarction Within hours: T wave may become peaked ST segment may begin to rise Within 24 hours: T wave inverts (may or may not persist) ST elevation begins to resolve If a left ventricular aneurysm forms, ST elevation may persist Within a few days: pathological Q waves can form and usually persist

101. Myocardial infarction The leads affected determine the site of the infarct Inferior II, III, aVF Anteroseptal V1-V4 Anterolateral V4-V6, I, aVL Posterior Tall wide R and ST? in V1 and V2

102. Inferior MI

103. The T wave Are the T waves too tall? No definite rule for height T wave generally shouldn’t be taller than half the size of the preceding QRS Causes: Hyperkalaemia Acute myocardial infarction

104. The T wave If the T wave is flat, it may indicate hypokalaemia If the T wave is inverted it may indicate ischaemia

105. The QT interval The QT interval is measured from the start of the QRS complex to the end of the T wave. The QT interval varies with heart rate As the heart rate gets faster, the QT interval gets shorter It is possible to correct the QT interval with respect to rate by using the following formula: QTc = QT/vRR (QTc = corrected QT)

106. The U wave U waves occur after the T wave and are often difficult to see The are thought to be due to repolarisation of the atrial septum Prominent U waves can be a sign of hypokalaemia, hyperthyroidism

107. Supraventricular tachycardias These are tachycardias where the impulse is initiated in the atria (sinoatrial node, atrial wall or atrioventricular node) If there is a normal conduction pathway when the impulse reaches the ventricles, a narrow QRS complex is formed, hence they are narrow complex tachycardias However if there is a conduction problem in the ventricles such as LBBB, then a broad QRS complex is formed. This would result in a form of broad complex tachycardia

108. Final Reminders Please email feedback to rashad.jurangpathy06@imperial.ac.uk Remember to purchase MM membership for priority for MM OSCE All slides are available online Year 3 OSCE guide is now available online