Download Problem 47 - Chest Pain

Chest Pain
Focussed history of chest pain
As the patient walks into the consultation room or listening actively over the telephone, discern:
- General appearance/status:
- Confused
- Highly anxious
- Short of breath
- In severe pain and distress
- Pale or sweaty
- Vomiting
ABC & vital signs - if any of the following are present in conjunction with chest pain, treat as an
emergency.
- Respiratory rate is <10 or >29/min
- O2 sats<92%
- Pulse<50 or >120/min
- Systolic BP<90 mmHg
- Glasgow coma score<12
Differential Diagnosis (life threatening in red)
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Cardiac:
o IHD - AMI, angina (stable/unstable)
o Arrhythmias
o Aortic dissection
o Aortic stenosis / Mitral valve disease
o Pericarditis
o Vasospasm secondary to illicit drug use
o HOCM
Respiratory:
o Pneumothorax (tension or otherwise)
o PE
o Pneumonia
o Pleurisy
Chest wall / Musculoskeletal:
o Costochondritis
o Rib pain
o Non-specific musculoskeletal pain
o Bone metastases
o Radicular pain
o Breast disease
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Gastrointestinal:
o Oesophageal rupture
o Oesophageal spasm
o Peptic ulcer disease
o Cholecystitis
o Pancreatitis
o Gastroesophageal reflux / Gastritis
Neurogenic:
o Herpes zoster
o Psychological e.g. panic disorder
Others:
o Sickle cell crisis
o Diabetic mononeuritis
o Tabes dorsalis
Emergency management.
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ABC – remember association of chest pain and CV collapse.
Keep patient on cardiac monitor until CV cause is ruled out.
Observation checked frequently (every 15 mins) until stable
Gain IV access and take bloods for Ix
Consider IV fluids if haemodynamically unstable (cautious if suspect heart failure – use
smaller bolus)
Administer analgesia – diamorphine 5mg slow IV injection and metoclopramide 10mg IV
12 lead ECG
ABG if in respiratory distress or low Sats.
Check temperature for pneumonia/pericarditis.
Describe the basic investigations in a patient presenting with chest pain in the community (CS07).
Within primary care, non-acute chest pain:
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FBC (to exclude anaemia)
U&Es and creatinine
TFTs
Creatinine kinase
CRP
Fasting lipids and glucose
Resting ECG (note, a resting ECG is normal in over 90% patients with recent symptoms of
angina.6 If an urgent ECG is considered necessary on clinical grounds, admission to hospital
is usually required.)
Additional tests if non-cardiac cause suspected e.g. CXR, LFT and amylase, abdominal
ultrasound
Referral to a rapid access chest pain clinic is now usual for exercise ECG and review
With acute chest pain, in a hospital setting:
 Bloods:
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FBC
U&E and creatinine
LFT and amylase
Coagulation screen
Serial myocardial markers7 - Troponin I or T (Creatinine kinase is much less
commonly used now)
 Serial ECG
 CXR
Second line investigations, as indicated, include:
 Echocardiography
 CT
 V/Q scan
 Coronary or pulmonary angiography
 Exercise testing
 Myocardial perfusion scan
EPIDEMIOLOGY
Risk factors for MI
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Age >40
Male or postmenopausal female
Hypertension
Cigarette smoking
Hypercholesterolaemia
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Diabetes mellitus
Ethnicity
Truncal obesity
Family history
Sedentary lifestyle
Cocaine use
Be able to assess a patient's cardiovascular risk factors including use of a JBS risk chart (CS02)
NICE recommends that the Framingham 10-year risk equations (as used in the JBS2 risk calculator)
should be used to assess CVD risk.
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The JBS2 risk calculator is not the only risk calculator in use and tends to be less accurate for
certain population groups, e.g. women, ethnic minority groups, social deprivation.
The JBS2 Guidelines recommend that all adults from above 40 should be considered for an
opportunistic comprehensive CVD risk assessment in primary care
Adults under 40 years with a family history of premature atherosclerotic disease should
also have their cardiovascular risk factors measured.
The American Heart Association guidelines also recommend recording the pulse rate and
rhythm to screen for atrial fibrillation.
The JBS2 cardiovascular risk chart or calculator should be used to estimate total risk of
developing CVD over 10 years based on five risk factors: age, sex, smoking habit, systolic
blood pressure and the ratio of total cholesterol to HDL cholesterol.
Total CVD risk should be estimated for the person's current age. A total CVD risk of over 20%
over 10 years is defined as high risk.
Other risk factors not included in the CVD risk prediction charts should be taken account of in
assessing and managing a person's overall CVD risk:
1. For people originating from the Indian subcontinent it is reasonable to assume that CVD risk
is about 1.4 times higher than predicted from the charts.
2. Abdominal obesity (waist circumference: men > 102 cm, women > 88 cm, and in Asians > 90
cm in men and > 80 cm in women) increases the risk of diabetes and CVD.
3. Impaired fasting glucose and impaired glucose tolerance are both associated with an
increased risk of developing diabetes and CVD.
4. Raised fasting triglyceride (> 1.7 mmol/l) increases the risk of CVD.
5. A family history of premature CVD (men <55 years and women <65 years) in a first degree
relative increases the risk of developing CVD by about 1.3.
6. Women with a premature menopause will also have an increased risk.
7. Risk factors should be monitored at least annually in people on antihypertensive or lipid
lowering therapy.
8. Over the age of 70 years CVD risk is usually greater than 20% over 10 years, especially for
men, but total CVD risk should still be formally estimated using the charts. However, this will
underestimate the true total CVD risk of a person older than 70 years.
ANGINA PECTORIS
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Is due to myocardial ischaemia and presents with central chest pain which can radiate to the
neck and jaw.
Comes on with exercise and relieved by rest
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Associated symptoms; dyspnoea, nausea, sweatiness, faintness
V
• most causes- atherosclerosis, anaemia, tachycardia
I
• arteritis
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D
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TYPES OF ANGINA
o Stable angina
 Induced by effort relieved by rest.
o Unstable angina
 Occurs at rest and with minimal effort. Increasing severity or frequency
o Decubitus angina
 Precipitated by lying flat
o Variant angina
 Due to coronary artery spasm, which can occur in normal coronary arteries, pain
occurs at rest rather than with exercise. ECG whilst having pain shows ST
segment elevation. Pt don’t have the usual risk for atherosclerosis.
 Rx; calcium channel blockers, long acting nitrates, Aspirin- can WORSEN the
attack and beta blockers should be AVOIDED as they can increase vasospasm.
Ix:
o ECG- may show ST depression. Flat or inverted T waves- signs of past MI.
o Exercise ECG
o Coronary angiography
o Echo. Stress echo can detect changes in the wall during ischaemia.
Mx:
o Modify risk factors- stop smoking, diet improvements, alcohol , fat , exercise,
weight loss.
o 75-150mg Aspirin- reduces mortality by 35%
o Beta blockers- atenolol 50-100mg/ 24h- reduce symptoms unless contraindicated
o Nitrates- spray or sublingual nitrates to help relieve symptoms. For long term
prophylaxis give oral nitrates (isosorbide mononitrate 20-40mg PO BD)
o Long acting calcium antagonists- amlodipine 10mg/24h. Diltiazem 90-180mg/12h.
o K+ channel activator- nicorandil 10-30mg/12h po
AORTIC DISSECTION
Suspect in anyone with High BP and Chest Pain.
Instantaneous tearing chest pain to back. If its at the arch of aorta then pain goes to neck and then back.
As it progresses;
HEMIPLEGIA – carotid artery
UNEQUAL PULSES and BP – subclavian artery
PARAPLEGIA – spinal arteries
ACUTE RENAL FAILURE – renal arteries
ACUTE PERICARDITIS
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A
•myocardial infarction
•viruses (varicella, mumps, HIV, coxsackie, flu epstein-barr)
•Bacteria (pneumonia, rheumatic fever, Tb, staphs, streps, MAI in HIV)
•trauma, surgery
•SLE
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•idiopathic
•malignancy and subsequent radiotherapy
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D
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•drugs (procainamide, hydralazine, penicillin, cromolyn sodium, isoniazid)
Clinical features
o Central chest pain worse on inspiration or lying flat +- relieved by sitting forward.
o Pericardial friction rub
o Evidence of pericardial effusion or cardiac tamponade
Ix:
o ECG classically shows concave (saddle shaped) ST segment elevation
o Bloods- FBC, ESR, UEs, cardiac enzymes. Viral serology, blood cultures, autoantibodies.
TFTs.
o CXR- cardiomegaly
Rx:
o Analgesia
o Treat the cause
o Steroids should be used carefully as they may increase the risk of recurrence.
ACUTE CORONARY SYNDROMES
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ACS includes unstable angina and evolving MI. Sharing a common pathology- plaque rupture,
thrombosis, inflammation
ACS WITH ST SEGMENT ELEVATION- or new onset LBBB, what most of us mean by acute MI.
ACS W/O ST SEGMENT ELEVATION- ECG may show ST depression, T wave inversion, non-specific
changes
RISK FACTORS
o Non modifiable- age, gender, fh,
o Modifiable- smoking, diet, exercise, weight, hyperlipidaemia
o Controversial- stress, type a personality, hyperinsulinaemia, homocysteine levels,
cocaine use.
Incidence- 5/1000
Dx; by  and a  in cardiac markers Trop. Symptoms of ischaemia, ECG changes, development
of pathological q waves, loss of myocardium on imaging.
Symptoms; acute central chest pain, lasting >20mins, associated nausea, vomiting, dyspnoea,
palpitations. May present as silent MI in diabetics and elderly.
Signs: distress, anxiety, pallor, sweatiness, / pulse, / bp, 4th HS, may be signs of heart
failure or a pansystolic murmur. Low grade fever may be present.
Test:
o ECG- hyperacute (tall) T waves, ST elevation, or new LBBB occurs within hours of
infarction. T wave inversion and pathological Q waves occur after hours to days.
o In other ACS- ST depression, T wave inversion, non specific changes or normal.
o NORMAL ECG in 20% of MIs
o CXR- cardiomegaly, pulmonary oedema, widened mediastinum
o BLOODS- FBC, UEs, glucose, lipids
o CARDIAC ENZYMES- Cardiac troponin (T and I)  sensitive markers for myocardial
necrosis. Serum levels increase within 3-12/24 from the onset of chest pain. Peak at 2448/24 and drop to baseline over 5-14days.
 If normal after 6hours and no ECG changes the risk of MI is tiny.
o Creatine kinase- 3 types
 CK-MM- found mainly in skeletal muscles and can be raised due to trauma, afroCaribbean, prolonged exercise, hypothyroidism.
 CK-BB- found predominantly in the brain
 CK-MB- found predominantly in the heart. Levels rise from 3-12/24 and peak at
24 hours and then begin to drop after 48-72h.
Prognosis- 50% of deaths occur within 2hours of chest pain, 7% die before discharge.
MANAGEMENT
o Pre hospital- arrange ambulance. 300mg aspirin chew/sublingual. 5-10mg morphine
and GTN spray. Also give metoclopramide 10mg IV (not IM because of risk of bleeding)
o HOSPITAL- determine if there is ST elevation or not.
o ST segment Elevation- primary angioplasty or thrombolysis if not contraindicated. Beta
blocker atenolol 5mg IV unless CI (asthma). ACE inhibitor- consider starting ACE-i
(lisinopril 2.5mg) in all normotensive evidence of heart failure or echo evidence of LV
dysfunction.
o Consider clopidogrel 300mg loading followed by 75mg/day for 30days.
o NO ST elevation- beta blocker (atenolol 5mg IV). Low molecular weight heparin
(enoxaparin 1mg/kg/12h). Nitrates unless contraindicated. High risk patients require
infusion of GPIIb/IIIa antagonist and urgent angiography. Clopidogrel in addition to
aspirin. Low risk patients can be discharged if repeat troponin is negative.
o SUBSEQUENT MX;
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Bed rest for 48h
Daily examination
Prophylaxis against thromboembolism.
Aspirin 75mg, vascular events by 29%
Long term blockade mortality from all causes by 25% in pts who have a
previous MI.
Continue ACE-i in all patients.
Start simvastatin 40mg.
Address modifiable risk factors- smoking, diet, exercise, diabetes.
Exercise ECG.
General advice- discharge after 5-7d. Work after 2/12. Sex after 1/12. Air travel
after 2/12.
Review at 5/52 post MI. And at 3/12
COMPLICATIONS OF MIS
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Cardiac arrest
Cardiogenic shock
Unstable angina- manage along standard lines
Bradycardias or heart block
o Sinus bradycardia- treat with atropine 0.6-1.2mg IV. Consider temporary pacing. bp
which doesn’t respond to atropine in patients with inferior MI may be due to RV
infarction.
 1st degree AV block; most commonly seen in inferior MI. 40% develop more
severe forms of heart block.
 Mobitz type 1 heart block: does not require pacing unless poorly tolerated
 Mobitz type II block: high risk of developing complete block and should be
monitored.
 Complete AV block; usually resolves within a few days. Insert a pacemaker.
 Bundle branch block: MI complicated by trifascicular block or non-adjacent
bifasicular disease should be paced.
Tachyarrhythmias- K+, hypoxia, and acidosis all predispose to arrhythmias and should be
corrected. Sinus tachycardia can  myocardial 02 demand.
o SVT
o AF- can be DC cardioverted, digoxin 0.125-0.25mg/12h + beta blocker. Amiodarone can
also be used
o Flutter- amiodarone.
o Frequent premature ventricular contractions are common post MI.
o VF: 80% occur in first 12h. If after 48h then indicates pump failure or cardiogenic shock.
Rx; DC shock.
Right ventricular failure RVF/infarction- presents with low cardiac output and JVP, Consider a
Swan-Ganz catheter to measure the right sided pressures. If BP remains  give inotropes.
Pericarditis- central chest pain. Relieved by sitting forwards. Saddle shaped ST elevation. Rx;
NSAIDs, Echo to check for effusion.
DVT/PE- pts at risk of developing DVT/ PE, prophylaxis should be given.
Systemic embolism- may arise from LV mural thrombus. Post large anterior MI consider
warfarin
Cardiac tamponade- low cardiac output, pulsus paradoxus, raised JVP, muffled heart sounds,. Dx
based on echo. Rx; pericardial aspiration, surgery.
Mitral regurgitation- may be mild (due to mild papillary muscle dysfunction) or severe (papillary
muscle rupture or ischaemia). Consider valve replacement.
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Ventricular septal defect- pansystolic murmur,  JVP, cardiac failure. Dx: echo. Rx: surgery.
Late malignant ventricular arrhythmias occur 1-3wks post MI. Hypokalaemia is most avoidable
cause.
Dressler’s syndrome- recurrent pericarditis. Pleural effusions, fever, anaemia, and ESR 1-3wks
post MI. Rx: NSAIDs and steroids.
DYSPEPSIA
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A group of non specific symptoms related to upper GI tract.
o Epigastric pain with various associations such as hunger, time of day, eating
o Bloating
o Fullness after meals
o Heartburn
o ALARM Symptoms
 Anaemia
 Loss of weight
 Anorexia
 Recent onset of progressive symptoms
 Melaena
 Swallowing difficulty
Signs
o Tender epigastrium
o Abdominal mass may be felt
o Supraclavicular nodes
Mx of new dyspepsia
o If <55 yrs test for H.pylori and treat if +ve
 PPI are better than H2 agonists at treating dyspepsia
 Most effective test is the CLO test for H.pylori
o If >55 yrs and new dyspepsia not accounted for by NSAID use or ALARM-Symptoms refer
for urgent endoscopy
 If no ALARM symptoms Stop drugs causing dyspepsia eg NSAIDs
 Lifestyle changes
 Over the counter antacids eg magnesium trisilicate 10ml/8h PO
 Review after 4 weeks
 If not improvement test for H.pylori.
 See flow chart on page 243 OHCM
GALLSTONES
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Bile contains cholesterol, bile pigments and phospholipids
Varying concentrations form different stones
Pigment stones  small, friable, irregular- caused by haemolysis
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Cholesterol stones  large, solitary stones- causes- female, age, obesity
Mixed stones  faceted (calcium salts, pigment and cholesterol)
Gall stone prevalence  8% of those over 40yrs. 90% remain asymptomatic.
ACUTE CHOLECYSTITIS
o Impaction of stone in the neck of the gallbladder.
o May cause continuous epigastric pain or RUQ pain (ref to right shoulder)
o Vomiting, nausea, fever, local peritonism, GB mass
o Causes local peritonism, fever and WCC
o If stone moves to the common bile duct then there is jaundice and cholangitis
o Murphys sign- 2 finger over the ruq and then ask patient to breath in. This should elicit
the pain.
o Ix
 Bloods
 FBC- WCC
 US- thick walled, shrunken gallbladder.
o Rx
 NBM, pain relief
 Abx- cefuroxime 1.5mg/8h IV
 Cholecystomtomy- open or lap
CHRONIC CHOLECYSTITIS
o Chronic inflammation and colic
o Flatulent dyspepsia, vague abdominal discomfort. Distension, nausea, flatulence and fat
intolerance
o US to image stones
o Rx
 Cholecystectomy
 ERCP
 Lithotripsy?
BILIARY COLIC
o Gallstones are symptomatic with cystic duct obstruction or bypassing into the CBD.
o RUQ pain  radiates to back +- jaundice
o Rx;
 Analgesia
 Rehydrate
 NBM
 Elective cholecystectomy
PNEUMONIA
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An acute lower respiratory tract illness associated with fever, symptoms, and signs in the chest
and abnormalities in the CXR
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5-11/1000 (young and elderly)
~10% hospital mortality. ~30% if admitted to ITU
Classification and causes
o Community acquired pneumonia (CAP)
 May be primary or secondary to underlying disease
 Strep pneumonia is the commonest cause followed by H. Influenza, Mycoplasma
Pneumoniae.
 Staph aureus, Legionella, Moraxella catarrhalis and Chlamydia account for the
remaining.
 Viruses account for 15%
 Flu might be complicated by community acquired MRSA pneumonia
o Hospital acquired pneumonia
 Most commonly Gram -ve enterobacteria or Staph aureus.
 Also pseudomonas, Klebsiella, Bacterioides, Clostridia
o Aspiration
 Those with stroke, myasthenia, bulbar palsies, consciousness, oesophageal
disease or with poor dental hygiene risk aspiration
o Immunocompromised patient
 Strep pneumonia, H. Infleunzae, Staph aureus, M Catarrhalis, M pneumonia,
Gram -ve bacilli, Pneumocystis jiroveci (P. carinii)
 Other fungi and viruses (CMV, HSV) and mycobacteria
Clinical features
o Symptoms
 Fever
 Rigours
 Dyspnoea
 Anorexia
 Malaise
 Cough
 Purulent sputum
 Haemoptysis
 Pleuritic chest pain
o Signs
 Fever
 Cyanosis
 Confusion
 Tachypnoea
 Tachycardia
 Hypotension
 Signs of consolidation dull to percussion, reduced expansion, tactile/vocal
fremitus, bronchial breathing
 Pleural rub
Ix
o O2 sats
o CXR- lobar or multilobar infiltrates
o Cavitation or pleural effusion
o Bloods
 FBC, U+E, LFT, CRP, blood cultures
o Sputum microscopy
o Pleural fluid may be aspirated for culture.
o Bronchoscopy and bronchoalveolar lavage may also be used
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Severity- assessed using CURB-65 Confusion (mini mental <8), Urea >7mmol/L, Respiratory rate
>30/min, BP <90 systolic and or 60 diastolic, 65 years old.
Mx
o Antibiotics orally if not severe and not vomiting, severe give IV abx.
o Oxygen keep PaO2 >8.0 kPa and sats >94%
o IV fluids
o Analgesia- if pleurisy eg paracetamol
o Antibiotics
 Mild not previously Rx
 Strep pneumoniae and H. Influenza  oral amoxicillin 500mg-1g/8h or
clarithromycin 500mg/12h or doxycycline 200mg loading then
100mg/12h
 Moderate
 Strep pneumoniae, H. Influenza, M. Pneumoniae  oral amoxicillin
500mg-1g/8h + clarithromycin 500mg/12h or doxycycline 200mg loading
then 100mg/12h. If IV required amoxicillin 500mg/8h + clarithromycin
500mg/12h
 Severe
  co-amoxiclav 1.2g/8h IV or cephalosporin IV eg cefuroxime 1.5g/8h
IV AND Clarithromycin 500mg/12h IV. Add flucloxacillin if staph
suspected; vancomycin if MRSA suspected
 See ohcm for more abx
Complications
o Pleural effusion
o Empyema
o Lung abscess
o Respiratory failure
o Septicaemia
o Brain abscess
o Pericarditis
o Myocarditis
o Cholestatic jaundice
Pneumococcal vaccine
o Give to at risk groups.
o Patients with heart failure, >65, DM, immunosuppressed
SPECIFIC PNEUMONIAS
PNEUMOCOCCAL PNEUMONIA
 Is the commonest bacterial pneumonia
 Affects all ages, commoner in elderly, alcoholics, post splenectomy, immuno-suppressed,
patients with chronic heart failure.
 Clinical features
o Fever
o Cough
o Sputum
o Pleurisy
o Herpes labialis
o CXR shows lobar consolidation
 Rx- amoxicillin, benzylpenicillin or cephalosporin
STAPHYLOCOCCAL PNEUMONIA
 May complicate influenza infection or occur in the young, elderly or IV drug users or patients
with underlying disease.
 Causes a bilateral cavitating bronchopneumonia
 Rx; flucloxacillin. MRSA- vancomycin
KLEBSIELLA PNEUMONIA
 Rare occurs in diabetics elderly and alcoholics.
 Causes a cavitating pneumonia of usually the upper lobes.
 Rx; cefotaxime or imipenem
PSEUDOMONAS
 A common pathogen in bronchiectasis and CF
 Also causes hospital acquired infections
 Rx- anti pseudomonal penicillin, ceftazidime, meropenem or ciprofloxacin +aminoglycoside.
MYCOPLASMA PNEUMONIA
 Occurs in epidemics
 Pts present with myalgia, headache, arthralgia followed by a dry cough
 CXR- shows reticular nodular shadowing or patchy consolidation of 1 lower lobe, & often worse
than XR suggests
 DX: mycoplasma serology
 Complications; erythema multiforme (rash), Stevens-Johnson syndrome, menigoencephalitis,
Gullain Barre syndrome.
 Rx; clarithromycin or tetracycline or fluroquinolone.
LEGIONELLA PNEUMOPHILLIA
 Colonises water tanks which are kept under 60 degrees c
 Pts start off with flu like symptoms (fever, malaise, myalgia)and then proceed to develop a dry
cough and dyspnoea
 Extra pulmonary features
o Anorexia, D+V, hepatitis, renal failure, confusion, hyponatraemia and deranged LFTs.
?haematuria
 Rx- clarithromycin and Rifampicin (300-600mg/12h)
CHLAMYDIA PNEUMOPHILLIA
 Commonest Chlamydia- spreads by person to person contact which then causes a biphasic
illness, pharyngitis, hoarseness, otitis followed by pneumonia.
 Dx; chlamydophillia serology
 Rx; tetracycline and clarithromycin
PNEUMOCYSTIS PNEUMONIA
 Pneumocystis jiroveci
 Presents with a simple dry cough, exertional dyspnoea, fever, bilateral crepitations,
 CXR may be normal or show bilateral perihilar interstitial shadowing.
 Dx: visualisation of organism in induced sputum.
 Rx: high dose co-trimoxazole pr pentamidine by slow IVI for 2-3 weeks. Steroids are beneficial
 Prophylaxis is indicated if CD4 count <200 x 106/L
COMPLICATIONS OF PNEUMONIA
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Respiratory failure
o Type I
 PaO2 <8kPa
 Rx with high flow oxygen
 Transfer the patient to ITU if hypoxia does not improve with O2 therapy. Or
PaCO2 rises to >6kPa. Aim to keep SaO2 at 90-94%
Hypotension
o Due to a combination of dehydration and vasoconstriction due to sepsis
o If systolic BP is <90 give a 250ml fluid challenge over 15mins checking lung bases for
pleural effusion? upto 2L??
o If the BP still drops set up a central venous line and give fluid therapy.
o If central line with fluids does not increase the blood pressure, contact ITU for inotropic
therapy such as adrenaline or noradrenaline.
Atrial fibrillation
o Commonly caused by pneumonia.
o Resolves with Rx
o Digoxin or beta blocker may be required to slow ventricular response rate in short term.
Pleural effusion
o Inflammation of pleura by adjacent pneumonia may cause fluid exudation into the
pleural space.
o If it accumulates faster than it is absorbed then an effusion forms
o If it is small no Rx is needed but if it is large then it should be drained
Empyema
o An infected pleural effusion therefore full of pus.
o Should be suspected if pt is getting better then they have a recurrent fever
o CXR indicates a pleural effusion
o When aspirated the effusion liquid is yellow and turbid with a pH <7.2 and glucose ,
LDH
o Rx; drainage under XR guidance
Lung abscess
o Cavitating area of localised suppurative infection within the lung.
o Causes
 Inadequately treated pneumonia
 Aspiration
 Bronchial obstruction
 Pulmonary infarction
 Septic emboli (septicaemia, right heart endocarditis, IV drug users)
 Subphrenic or hepatic abscess
o Clinical features
 Swinging fever
 Cough - with purulent foul smelling sputum
 Haemoptysis
 Weight loss
 Malaise
o Ix
 Blood
 FBC, ESR, CRP, blood cultures
 Sputum -microscopy, culture and cytology.
 CXR- walled cavity, often with fluid level. Consider CT scan to exclude
obstruction and bronchoscopy.
o Rx
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 Abx according to sensitivity
Septicaemia
o Due to spread of bacteria from lung parenchyma into blood
o May cause infective endocarditis, meningitis
MASSIVE PULMONARY EMBOLUS
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Symptoms; pleuritic chest pain, haemoptysis, chest pain, palpitations, tachypnoea,
sob,syncope,
Signs; tachycardia, tachypnoea, gallop rhythm, increased JVP, loud p2, cyanosis
Ix; U&E, FBC, LFT, clotting, d-dimer, ecg; (tachycardia, s1, q3, t3. Deep s waves in 1, q waves
in 3 and inverted t waves in 3)
CXR; wedged shape area of infarction
ABG low O2 and low CO2, high pH
CTPA
Treat with low molecular weight heparin and warfarin in combination and then follow
protocol dependent on risk factors. if acute cause, six weeks treatment on warfarin
normally ok