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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2683_Библиотеки_им_академика_М_И_Перельмана.pdf
Writing in the medical notes
SAMPLE CLERKING
38
Sample clerking
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Writing in the medical notes
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Clinical Presentations
Chapter 4
Chest pain . . . . . . . . . . . . . . . . . . . . . . . 43
Chapter 5
Shortness of breath . . . . . . . . . . . . . . . . . . 47
Chapter 6
Cough and haemoptysis . . . . . . . . . . . . . . . . 53
Chapter 7
Palpitations. . . . . . . . . . . . . . . . . . . . . . .57
Chapter 8
Pyrexia of unknown origin . . . . . . . . . . . . . . . 61
Chapter 9
Abdominal pain. . . . . . . . . . . . . . . . . . . . .65
Chapter 10
Heartburn and indigestion . . . . . . . . . . . . . . .71
Chapter 11
Gastrointestinal bleed . . . . . . . . . . . . . . . . . 75
Chapter 12
Change in bowel habit . . . . . . . . . . . . . . . . . 81
Chapter 13
Weight loss . . . . . . . . . . . . . . . . . . . . . . . 85
Chapter 14
Jaundice . . . . . . . . . . . . . . . . . . . . . . . . 89
Chapter 15
Urinary symptoms and haematuria. . . . . . . . . . . 93
Chapter 16
Headache and facial pain . . . . . . . . . . . . . . 101
Chapter 17
Goitre, thyroid disease and thyroid malignancy . . . 107
Chapter 18
Loss of consciousness . . . . . . . . . . . . . . . . 111
Chapter 19
Confusion and delirium. . . . . . . . . . . . . . . . 117
Chapter 20
Stroke and TIA . . . . . . . . . . . . . . . . . . . . 121
Chapter 21
Lumps . . . . . . . . . . . . . . . . . . . . . . . . 129
Chapter 22
Focal neurological deficits . . . . . . . . . . . . . . 133
Chapter 23
Dizziness and vertigo . . . . . . . . . . . . . . . . 141
Chapter 24
Back pain and joint pain . . . . . . . . . . . . . . . 145
Chapter 25
Skin lesions and rash . . . . . . . . . . . . . . . . . 151
Chapter 26
Excessive bruising and bleeding . . . . . . . . . . . 159
Chest pain
4
INTRODUCTION
Chest pain is a common reason for a patient to present
for care. The causes can range from a simple musculoskeletal strain to a life-threatening myocardial infarction
(Table4.1). Taking a clear history is essential in making the
correct diagnosis.
CLINICAL NOTES
DIFFERENT TYPES OF PAIN AND THEIR
DIFFERENTIAL DIAGNOSIS
Central chest pain
The differential diagnosis of pain in the centre of
the chest includes:
• angina: crushing/tightness;
• acute coronary syndrome: angina-like but
commonly more severe, long-lasting and with
associated symptoms;
• dissecting aortic aneurysm: tearing interscapular
pain;
• oesophagitis: burning;
• oesophageal spasm.
Pleuritic chest pain
This is sharp pain caused by irritation of the
pleura that is worse on deep inspiration,
coughing or movement. The differential diagnosis
includes:
• pneumothorax;
• pneumonia;
• pulmonary embolism;
• pericarditis: retrosternal.
Chest wall tenderness
The differential diagnosis of chest wall tenderness
includes:
• rib fracture;
• shingles (herpes zoster): pain precedes rash;
dermatomal distribution;
• costochondritis (Tietze syndrome).
CLINICAL NOTES
DEFINITION OF ANGINA-TYPE PAIN
The National Institute for Health and Care
Excellence describes angina pain as:
• constricting discomfort in the anterior chest,
neck, shoulders, jaw or arms;
• precipitated by physical exertion;
• relieved by rest or glyceryl trinitrate within 5
minutes.
CLINICAL NOTES
ACUTE CORONARY SYNDROME
• ‘Acute coronary syndrome’ describes a range of
clinical conditions, from ST-segment elevation
myocardial infarction to non-ST-segment
elevation myocardial infarction or unstable angina.
Acute coronary syndrome is almost always due
to rupture of an atherosclerotic plaque with
subsequent thrombosis of the artery which
supplies the infarcted cardiac muscle territory.
Table4.1 Differential diagnosis in chest pain
Cardiovascular Respiratory Gastrointestinal Musculoskeletal
Angina Pneumonia Gastritis Rib fracture
Myocardial infarction Pulmonary embolism Pancreatitis Varicella zoster
Pericarditis Pneumothorax Gastro-oesophageal reflux
disease and spasm
Dissecting aortic aneurysm Biliary colic/cholecystitis Vertebral
Costochondritis
43
Chest pain
HISTORY AND EXAMINATION FINDINGS
History
Generally, a carefully taken history will lead to the most
likely underlying diagnosis and determine whether
the chest pain is of cardiac origin. Once this has been
established, enquire about the presence of cardiovascular risk factors, previous investigations for chest pain
and history of coronary heart disease and any previous
treatment.
Type of chest pain
Onset and progression
Cardiac ischaemic pain typically builds up over a few minutes and may be brought on by exercise, emotion or cold
weather. In angina, the pain resolves on resting or with use
of glyceryl trinitrate. It is often reproducible with consistent
effort. Spontaneous pneumothorax and pulmonary embolism (PE) usually cause sudden onset of pleuritic pain and
dyspnoea.
CLINICAL NOTES
National Institute for Health and Care Excellence
advises that the following symptoms may indicate
acute coronary syndrome:
• pain in the chest and/or other areas (the arms,
back or jaw) that lasts more than 15 minutes;
• chest pain associated with nausea and
vomiting, marked sweating, breathlessness, or a
combination of these;
• chest pain associated with haemodynamic
instability;
• new-onset chest pain, or abrupt deterioration in
previously stable angina, with frequent recurrent
episodes that last more than 15 minutes and are
brought on by little or no exertion.
Site and radiation
Cardiac ischaemia and pericarditis cause retrosternal pain.
With ischaemia, the pain is tight and ‘crushing’, band-like,
etc., often radiating to the neck, jaw or arms. Pericarditis
produces pleuritic chest pain; it is classically worse on lying flat and is relieved by sitting up and leaning forward.
A dissecting aortic aneurysm causes tearing pain radiating
through to the back. Pulmonary disease may cause unilateral pain, which the patient can often localize specifically.
Oesophageal disease can also cause retrosternal pain, and
may mimic cardiac pain. Referred pain from vertebral collapse or shingles will follow a dermatomal pattern.
Nature of pain
The precise nature of the pain gives important clues as to
the underlying diagnosis. Most commonly the pain is dull/
tight or sharp/stabbing.
Associated symptoms
Important associated symptoms include:
• Dyspnoea: PE, pneumonia, pneumothorax, pulmonary
oedema, hyperventilation in anxiety (these patients
will often report dizziness and tingling in their lips and
extremities which is due to respiratory alkalosis).
• Cough: purulent sputum in pneumonia, haemoptysis
in PE, frothy pink sputum in pulmonary oedema.
• Rigors: pneumonia (particularly lobar pneumococcal
pneumonia).
• Palpitations: arrhythmia (e.g. new-onset atrial
fibrillation) can cause angina or result from cardiac
ischaemia, PE or pneumonia.
• Clamminess, nausea, vomiting and sweating are
features of myocardial infarction or massive PE.
CLINICAL NOTES
PRESENCE OF RISK FACTORS
Important risk factors include:
• Coronary heart disease: smoking, family history,
hypercholesterolaemia, hypertension, diabetes.
• Pulmonary embolism: recent travel, immobility,
surgery, family history, pregnancy, malignancy,
oral contraceptive pill use.
• Pneumothorax: spontaneous (young, thin men,
more commonly smokers), trauma, emphysema,
asthma, malignancy.
Examination
The examination should focus on determining the cause of
the pain, then looking for risk factors and consequences of the
underlying problem. A schematic guide to examining the patient with chest pain is given in Fig.4.1. Remember to assess
the patient for the presence of complications of acute coronary
syndrome (ACS; e.g. pulmonary oedema, cardiogenic shock).
Pay attention to:
• Pale cold and clammy skin.
• Pulse: tachycardia/bradycardia or arrhythmia.
• Blood pressure: discrepancy between left and right
arms in aortic dissection (the pulse volumes may also
be unequal). Shock in tension pneumothorax, massive
PE, myocardial infarction.
44
History and examination findings
Heart
—Pericardial rub
—Mitral regurgitation
—Ventriculoseptal defect
—Aortic regurgitation
—3rd and 4th heart
sounds
Pulse
—Tachycardia
—Arrhythmia
—Character of the pulse
Hands
—Cigarette-stained fingers
—Tendon xanthomata
—Disparity between arms
Legs
—Deep vein thrombosis
Chest
—Wall tenderness
—Pneumothorax
—Consolidation
—Pleural rub
—Pulmonary oedema
Blood pressure
—Hypotension
—Hypertension
—Pulsus paradoxus
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Fig.4.1 Examining the patient with chest pain.
• Chest wall tenderness: rib fracture, costochondritis,
shingles.
• Chest examination: pneumothorax (absent breath
sounds over the pneumothorax), consolidation
(crackles on auscultation), pleural rub, pulmonary
oedema (bibasal crackles, raised jugular venous
pressure), third heart sound.
• Cardiac examination: rub (pericarditis), murmur of
aortic regurgitation in aortic dissection.
The following risk factors may be present:
• Abnormal levels of lipids: xanthelasmata, tendon
xanthoma.
• Tar-stained fingers: predisposition to coronary heart
disease.
• Hot, oedematous, tender calf suggesting deep vein
thrombosis.
• Hypertension, features of Marfan syndrome or features
of diabetes.
HINTS AND TIPS
Patients who have a median sternotomy scar
are common in final examinations. Always check
the legs for vein harvesting scars and listen for a
metallic valve sound.
Investigations
Consider the following investigations in a patient presenting with chest pain:
• Resting 12-lead ECG: regional ST-segment elevation
or presumed new left bundle branch block (LBBB)
should be treated as ACS until proven otherwise
(Table4.2). Regional ST-segment depression or deep
T-wave inversion suggests a non-ST-segment elevation
General
—Xanthalasmata
—Marfanoid appearance
—Pyrexia
45
Chest pain
Table4.2 Causes of ST-segment elevation on ECG
Cause
Myocardial infarction Inferior aVF, II, III
Pericarditis Across all leads (saddle-shaped
Prinzmetal angina Leads of affected coronary artery
Aortic dissection Only if coronary artery involved
Left ventricular
aneurysm
Distribution of ST-segment
elevation
Anteroseptal V
Lateral I, aVL, V
ST change)
(spasm)
Persistent elevation for 6months
following infarct
1-4
4-6
myocardial infarction or unstable angina. A normal
ECG does not exclude ACS, and serial ECGs are
often helpful. Changes suggestive of PE are listed in
the Clinical Notes box later. Arrhythmia may also be
detected on ECG.
• Chest X-ray: look for pneumothorax, consolidation
(pneumonia), widened mediastinum (aortic
dissection), pulmonary oedema, wedge infarct (PE),
fractured ribs.
• Full blood count, urea and electrolytes, glucose: look
for anaemia, leucocytosis, electrolyte disturbances and
hyperglycaemia.
• Cardiac markers: troponin I and troponin T are
biological markers of cardiac muscle death, and
measurement of their levels can be used to signify the
occurrence of myocardial ischaemia. Troponin levels
are classically measured at 4 hours and 10–12 hours
after the onset of pain. Serial measurements are useful.
• Arterial blood gas: hypoxaemia in PE, pneumonia or
pulmonary oedema. In hyperventilation related to
anxiety, P2 may be mildly elevated, and there will be
hypocapnia and a respiratory alkalosis.
• Echocardiography: can be used acutely to demonstrate
cardiac dysfunction, valvular pathology, pericardial
effusion and aortic dissection (particularly
transoesophageal echocardiography, see Chapter27).
• Percutaneous coronary intervention: angioplasty
and coronary artery stenting can be used to reopen
occluded arteries in acute myocardial infarction.
Coronary angiography allows direct visualization of the
coronary arterial anatomy (see Chapter27).
• Other tests to exclude alternative diagnosis including
PE (see Chapter5) and gastro-oesophageal reflux
disease (see Chapter10).
CLINICAL NOTES
ECG CHANGES ASSOCIATED WITH
PULMONARY EMBOLISM
• Sinus tachycardia
• Atrial arrhythmia (e.g. atrial fibrillation)
• Right-sided heart strain
• Right axis deviation
• Right bundle branch block
• S1Q3T3 (i.e. deep S wave in lead I, Q wave in
lead III, T-wave inversion in lead III)
HINTS AND TIPS
Although troponin is a useful enzyme to investigate
potential myocardial ischaemia, its level may also be
raised in renal impairment, heart failure, sepsis, PE,
acute pericarditis, myocarditis and aortic dissection.
HINTS AND TIPS
Although not always possible, it is very useful to
compare the ECG done in the acute setting with
an old ECG. Changes such as left bundle branch
block and T-wave inversion may indeed be longstanding, which would alter your management.
Chapter Summary
• There are numerous underlying diseases that can present as chest pain.
• In patients presenting with a history of chest pain suggestive of a cardiac origin, acute
coronary syndrome (ACS) should be excluded.
• Troponin is a cardiac biomarker that is usually measured at 4 hours and 10–12 hours from
the onset of pain.
• Patients presenting with ST-segment elevation myocardial infarction should be urgently
assessed for percutaneous coronary intervention.
• New left bundle branch block should be treated as acute coronary syndrome until proven
otherwise.
46
Shortness of breath
5
INTRODUCTION
Shortness of breath (dyspnoea) is the subjective sensation of
breathlessness which is excessive for a given level of activity.
Dyspnoea may be due to any of the following:
• pulmonary disease: disorders of the airways, lung
parenchyma, pleura, pulmonary vasculature,
respiratory muscles or chest wall;
• cardiac disease: right ventricular dysfunction, left
ventricular dysfunction, arrhythmias, ischaemic heart
disease;
• systemic disease (e.g. anaemia, thyrotoxicosis or
ketoacidosis);
• nonorganic causes (e.g. anxiety or chronic
hyperventilation syndrome).
HISTORY AND EXAMINATION FINDINGS
History
Onset
The onset of breathlessness and rate of decline give clues to
its cause:
• Acute onset may indicate a sudden new change
such as aspiration of a foreign body, pneumothorax,
pulmonary embolism, acute asthma or acute
pulmonary oedema.
• Subacute onset is more suggestive of parenchymal
disease, pleural effusion, pneumonia or carcinoma.
• Chronic onset and progressive decline is associated
with chronic obstructive pulmonary disease (COPD),
interstitial lung disease and some nonrespiratory causes
(e.g. heart failure).
Severity
Exercise tolerance is a good measure of how severe the
shortness of breath is (e.g. distance walked on the flat or on
hills, while dressing or climbing stairs). Has this changed in
recent times? Does it affect daily activities?
Precipitating and aggravating factors
• Precipitating factors: exercise increases the demand
for oxygen, and as such many pulmonary and cardiac
causes of dyspnoea are aggravated by exercise. Cold
and airborne material (such as pollen) can irritate
the airways and can cause dyspnoea in the context
of bronchoconstriction. Dyspnoea that improves at
weekends or on holiday may imply an environmental
cause.
• Aggravating factors: position can affect dyspnoea;
‘orthopnoea’ is the term used for shortness of breath
on lying flat, and often indicates underlying cardiac
dysfunction. Paroxysmal nocturnal dyspnoea is
breathlessness that wakes the patient from sleep and,
again, is generally a symptom of cardiac disease.
COMMUNICATION
When you are clarifying the duration of symptoms,
asking your patient ‘When were you last well?’ and
then ‘Take me through what has happened since’
often opens the consultation better than the more
direct ‘How long has this been going on?’
COMMUNICATION
Asking the patient how many pillows they sleep
on is a good way of quantifying the level of
orthopnoea, and if this has changed, it helps to
assess the severity.
Associated features
• Cough: a chronic persistent cough has many causes;
for example, underlying lung disease, asthma,
gastro-oesophageal reflux, postnasal drip or drugs
(especially angiotensin-converting enzyme inhibitors,
where patients may have a dry cough). How long has
the cough been present? Is the cough worse at any
particular time of day?
• Sputum: how much does the patient produce? What
does it look like?
• Haemoptysis: This is coughing up blood, either
frank blood or blood-tinged sputum. It needs to be
distinguished from haematemesis and nasopharyngeal
bleeding (see Chapter6).
• Stridor: a harsh sound caused by turbulent airflow
through a narrowed airway. Inspiratory stridor suggests
47