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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1093_Библиотеки_им_академика_М_И_Перельмана.pdf
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Confusion (MTS ≤8), Urea raised (>7 mmol/l), Raised respiratory rate (>30
breaths/min), BP systolic <90 mmHg, diastolic <60 mmHg, Age >65 years.
COMPLICATIONS
● Empyema, lung abscess, pleural effusion, metastatic abscesses, lung fi brosis,
death.
Empyema/lung abscess
● Empyema: suspect if high spiking temperatures, pleural effusion and no
response is seen to antibiotics. Diagnosis is by pleural aspiration. Treatment:
chest drain and antibiotics.
Lung abscess:
●
Seen with S. aureus and Klebsiella pneumonia, aspiration,
bronchial obstruction, septic emboli (e.g. IE), spread of subphrenic abscess,
pulmonary infarction. Most commonly mixed organisms, frequently Strep.
species with anaerobes. Treat with broad spectrum antibiotics, surgery is rarely
indicated.
3.6. Bronchiectasis
Permanent dilation of the bronchi. Mucus pooling leads to infection usually S. Aureus
or H. influenzae, also Pseudomonas (poorer prognosis), with copious sputum
production. Clinical features: clubbing; inspiratory and expiratory crackles.
Causes of bronchiectasis
❍
Congenital: cystic fibrosis (CF), Kartagener’s syndrome
❍
Acquired: following infection (e.g. TB, measles, pertussis), bronchial
obstruction, gastric aspiration, allergic broncho-pulmonary aspergillosis,
hypogammaglobulinaemia
INVESTIGATIONS
● Sputum MC&S.
● CXR: for cystic areas, fluid levels, thickened bronchial walls; classically ‘cysts
and tram lines’.
CT chest: to establish extent of disease, look for signet ring sign.
●
● Bronchoscopy: if obstruction seen on CT.
● Spirometry: to assess reversibility.
● Establish cause: test for CF, Aspergillus precipitins, cilial function and
immunity, consider gastro-oesophageal refl ux disease.
TREATMENT
● In acute infection, high dose antibiotics for 14 days.
● If Pseudomonas isolated, attempt to eradicate at fi rst isolation.
Regular postural drainage of mucus.
●
● Bronchodilators (if reversible airfl ow obstruction).
● Lobectomy for localised disease.
COMPLICATIONS
● Respiratory: haemoptysis (massive), empyema, abscess, respiratory failure, cor
pulmonale, pneumothorax.
Metastatic abscess formation.
●
● AA amyloid.
44
RESPIRATORY DISEASE
Cystic fi brosis
Common – 1/2500 Caucasian births, carrier rate 1 in 25 (less common in other ethnic
groups)
❍
Genetics: Autosomal recessive, mutation of CF transmembrane conductance
regulator gene, chromosome 7 (ΔF508 in 80%). Cells unable to transport chloride
leading to secretions with low water and high salt content (mucus is viscous –
abnormalities of respiratory tract, pancreas and sweat glands)
❍
Diagnosis: CF sweat test; genotyping. New-born babies are screened
❍
Complications: neonates – meconium ileus; children – failure to thrive, pancreatic
failure (diabetes, steatorrhoea), recurrent infections/bronchiectasis, biliary disease,
infertility
❍
Management: requires a multidisciplinary team approach. Chest: chest physio,
antibiotics. Pancreas: oral pancreatic supplements. Nutritional: advice on diet.
Genetic counselling for parents
3.7. Pulmonary embolism (PE)
Occlusion of one or more branches of the pulmonary artery usually by a blood clot
from a deep vein thrombosis (DVT). Termed ‘massive’ if associated with circulatory
collapse.
ASSESS CLINICAL PROBABILITY OF PE ON FOLLOWING BASIS:
1. Symptoms (SOB, pleuritic chest pain or haemoptysis) and signs (cyanosis, raised
JVP, raised RR, loud P2, pleural rub).
2. Risk factors for PE:
major surgery especially abdominal/pelvic surgery
◗
◗ obstetrics: pregnancy, post-partum
◗ malignancy
◗ reduced mobility, e.g. nursing home, hospitalisation
◗ previous DVT
◗ varicose veins, fracture to lower limb.
3. Alternative explanation can be ruled out, e.g. pneumonia.
RISK ASSESSMENT
● High probability patients: 2 and 3 true.
Intermediate probability patients: 2 or 3 true.
●
Low probability patients: neither 2 nor 3 true.
●
INVESTIGATIONS
● CXR: oligaemic lung fields; wedge-shaped infarct; often normal.
● ECG: sinus tachycardia; AF; right atrial dilatation, right heart strain, RBBB;
rarely SI, QIII, TIII.
ABG: hypoxia, type 1 respiratory failure.
●
● D-dimers: should not be used in patients with high probability of PE. Use in
low/intermediate risk depending on local hospital recommendations.
Computed tomography pulmonary angiography: for non-massive or massive
●
PE.
Echocardiography is an alternative investigation for massive PE.
●
● V/Q scan – only if CXR normal and no concurrent pulmonary disease.
● Look for occult malignancy – only if indicated clinically, on CXR or on routine
blood tests.
Consider thrombophilia screen if <50 years with recurrent PE, or strong family
●
history.
45
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
MANAGEMENT Initiate treatment if high/intermediate probability before diagnosis
is confi rmed
General measures: oxygen therapy, analgesia, cardiac monitor if unwell.
●
● Anticoagulation:
◗ in massive PE: thrombolysis
◗ in non-massive PE: low molecular weight (LMW) heparin
◗ warfarin once PE is confirmed: three months for temporary risk factors; six
months for first idiopathic PE.
PROPHYLAXIS Consider TEDS and prophylactic dose LMW heparin in at-risk
patients, e.g. peri-operative patients.
3.8. Pneumothorax
Definition: ‘Air within the pleural space’.
Primary: occurring spontaneously in otherwise healthy people; often tall and
●
slim.
Secondary:
●
CLINICAL FEATURES
● Symptoms: SOB, chest pain (classically worse on inspiration).
● Signs: raised RR, reduced chest expansion, hyper-resonant percussion note,
occurring in patients with underlying lung disease.
reduced breath sounds on affected side; check trachea is central: if deviated
suspect tension pneumothorax (this is a medical emergency).
INVESTIGATIONS CXR to confirm diagnosis (not if tension pneumothorax –a
medical emergency).
TREATMENT Primary pneumothorax
No intervention if not SOB and rim of air <2 cm on CXR.
●
● If SOB and >2 cm rim of air: attempt simple aspiration.
● If aspiration unsuccessful, proceed to repeat aspiration or intercostal drain.
● If still unsuccessful, refer to respiratory physician within 48 hours or
cardiothoracic surgeons after five days for consideration of pleuradhesis.
On discharge, give advice regarding flying (not for six weeks and risk remains
●
for up to one year) and diving (should be avoided).
Secondary pneumothorax
If >50 years + >2 cm rim of air on CXR proceed straight to intercostal drain,
●
otherwise attempt aspiration.
If intercostal drain unsuccessful, then contact respiratory team within 48 hours
●
or cardiothoracic surgeons after three days for consideration of pleuradhesis.
On discharge, give advise regarding flying and diving (as above).
●
Tension pneumothorax – medical emergency
❍
Mediastinal shift with tracheal deviation to the contralateral side occurs;
cardiorespiratory arrest is imminent
❍
Patient shows signs of respiratory distress, tachypnoea, tachycardia, shock;
tracheal deviation to the contralateral side; reduced breath sounds; hyperresonance on the affected side
❍
Initial management: immediate insertion of a large-bore needle into the second
intercostal space, in the mid-clavicular line; this buys time for placement of a chest
drain (in the 5th intercostal space, anterior mid-axillary line)
46
RESPIRATORY DISEASE
3.9. Interstitial lung disease/pulmonary fi brosis
Idiopathic interstitial pneumonias
Cause often unknown: ‘idiopathic pulmonary fibrosis’ (IPF). Other interstitial
pneumonias associated with connective tissue disease (rheumatoid arthritis,
SLE, etc.), chronic active hepatitis, ulcerative colitis, lymphoma. IPF has poor
prognosis with a mean life expectancy of three years and responds poorly to
immunosuppression. The other interstitial pneumonias have variable but better
prognosis than IPF.
CLINICAL FEATURES Patients suffer worsening SOB with respiratory failure, dry
cough and weight loss. Signs include clubbing and fine, end-inspiratory crackles.
INVESTIGATIONS
● CXR reveals fibrosis at bases.
● Spirometry: restrictive defect is seen.
● Blood tests: inflammatory markers may be raised, positive autoantibodies in
some cases.
High resolution CT useful for diagnosis.
●
● Lung biopsy may be indicated.
Occupational lung disease
Asbestos exposure: linked to the shipping industry, builders, factory workers.
CLINICAL PRESENTATION
● Pleural plaques: can develop >20 years post-exposure, a mild restrictive defect
only is seen.
Diffuse pleural thickening: associated with exertional SOB and a restrictive
●
defect.
Asbestosis: fibrosis in the lower lobes causing dyspnoea; associated risk of
●
developing lung cancer. Compensation is available.
Lung carcinoma, mesothelioma.
●
Coal worker’s pneumoconiosis: dust particles lodge in small airways, causing small
round opacities on CXR, focal emphysema. ‘Simple pneumoconiosis’ may develop
into ‘progressive massive fi brosis’.
Occupational asthma: a number of occupational substances have been identifi ed as
causing asthma, which may or may not be reversible. Compensation is available.
Hypersensitivity pneumonitis: inhalation of substances, usually spores or avian
proteins (farmer’s lung, bird fancier’s lung), causes a hypersensitivity pneumonitis
(type III or IV reaction). Acutely, patients have fever and SOB. Histologically, fi brosis
occurs.
Silicosis berylliosis
Other causes of pulmonary fi brosis
● Infections such as TB.
● Sarcoidosis (see below).
Drugs (e.g. amiodarone, methotrexate).
●
● Radiation.
● Ankylosing spondylitis.
● Allergic bronchopulmonary aspergillosis.
47
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
3.10. Sarcoidosis
Cause unknown, multiple systems affected. Incidence: young > old, blacks > whites.
Prevalence 30/100,000. Characteristic lesion is the non-caseating granuloma.
Presentation: normally insidious onset – asymptomatic, respiratory or systemic
symptoms.
DIAGNOSIS Relies on compatible clinical, radiological and histological fi ndings.
Bilateral hilar lymphadenopathy (BHL) and erythema nodosum (EN) in the young
is strongly suggestive of sarcoid.
INVESTIGATIONS
● CT may be helpful for diagnosis.
● Transbronchial biopsies useful in select cases.
● Biochemical tests include inflammatory markers, serum ACE (raised in 75%
but not diagnostic) and Ca
2+
(increased vitamin D synthesis). Spirometry
reveals a restrictive defect.
Extrapulmonary involvement
❍
Skin: Lupus pernio, EN, nodules
❍
Lymphadenopathy
❍
Liver: biopsy may help clinch diagnosis
❍
Splenomegaly
❍
Bone/joints: arthritis + bone cysts hands/feet
❍
Uveitis
❍
Renal: calculi, nephropathy
❍
Cardiac: cardiomyopathy, effusion or conduction defects
❍
Neurological: cranial nerve palsies, meningitis, space occupying lesion, diabetes
insipidus (infiltration of pituitary)
❍
Parotid gland enlargement
MANAGEMENT Disease progression/regression is monitored via symptoms and
serial CXRs, spirometry, serum ACE and Ca
2+
levels.
Chronic sarcoid may be treated with immunosuppression depending on the
organ affected and severity of disease. Pulmonary sarcoid eventually remits in twothirds, unless extrathoracic disease present.
Acute sarcoidosis or Löfgren’s syndrome: fever, arthralgia, EN, BHL on CXR.
May resolve with no specific treatment. Prognosis better for acute presentation of
sarcoidosis
Differential diagnosis for bilateral hilar lymphadenopathy
❍
TB
❍
Lymphoma
❍
Sarcoid
❍
Cancer
3.11. Lung cancer
Types (commonest fi rst)
● Squamous cell carcinoma (SCC).
● Small cell lung carcinoma (SCLC): usually metastasised at diagnosis.
● Adenocarcinoma: not linked to smoking, peripheral usually, occurs in sites of
fibrosis or scarring (‘scar tumour’).
Undifferentiated.
●
48
RESPIRATORY DISEASE
Pancoast’s tumour is the name given to an apical tumour causing compression of the C8/
T1 nerve roots and pain radiating down the arm. The sympathetic chain is also affected
causing Horner’s syndrome.
RISK FACTORS
● Unmodifiable: age, male sex.
● Modifiable: smoking, asbestos exposure, pollution (higher rates in urban areas),
radiation exposure.
CLINICAL FEATURES
● Respiratory: cough, haemoptysis, SOB, chest pain, wheeze, pleural effusion.
● Systemic: weight loss, lethargy, lymphadenopathy, cachexia.
● Paraneoplastic: e.g. clubbing.
● Horner’s syndrome (ptosis, anhydrosis and miosis).
COMPLICATIONS
● Local: pleural effusion, pericarditis, dysphagia (compression from tumour),
erosion into rib, phrenic/recurrent laryngeal nerve palsy, Horner’s syndrome,
superior vena caval (SVC) obstruction, pneumothorax.
Metastases: to bone, brain, liver, adrenal glands.
●
● Paraneoplastic: hypertrophic pulmonary osteoarthropathy (HPOA), SIADH,
increased ACTH, increased TSH, increased PTH, Eaton-Lambert syndrome.
DIAGNOSIS
● Sputum cytology.
● CXR.
● Staging CT scan.
● Biopsy: transthoracic (CT-guided), bronchoscopy.
● Consider PET scan/bone scan.
STAGING
● SCLC: limited stage disease (i.e. all of the tumour can be treated within a
tolerable radiotherapy port); extensive stage disease (metastases in contralateral
lung/elsewhere).
Non-small-cell lung carcinoma (NSCLC): TNM classifi cation.
●
TREATMENT
● Multidisciplinary approach: involve specialist nurse early.
● SCLC
◗ All patients offered multidrug platinum-based chemotherapy.
◗ In limited disease: consider radiotherapy as well as chemotherapy +/–
prophylactic cranial irradiation if tumour responds to initial treatment.
NCSLC
●
◗ Stage I and II: offer surgery, if not medically fit offer radical radiotherapy.
◗ Stage III and IV: chemotherapy.
◗ Stage III can be amenable to surgery or radical radiotherapy.
● Palliation
◗ Radiotherapy/chemotherapy may be appropriate to alleviate certain
symptoms, e.g. SOB.
Dexamethasone for brain metastases.
◗
◗ Spinal cord compression: corticosteroids, radiotherapy, surgery where
appropriate.
49
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
◗ Radiotherapy/chemotherapy/stenting for SVC obstruction.
◗ Symptom control: palliative care input, hospice.
PROGNOSIS Generally poor. SCLC has the worst prognosis, with survival of
months
Other types of tumour
● Carcinoid – clinical features: wheeze, flushing, diarrhoea. Investigations: 24-
hour urine collection for 5-HIAA (5-hydroxy-indolacetic acid) aids diagnosis.
Management: curative surgery often possible.
Mesotheliomna
●
– malignancy of the pleura. Poor prognosis.
3.12. Cor pulmonale
Cor pulmonale is right-sided heart failure caused by pulmonary hypertension.
CAUSES
● Chronic hypoxia leading to raised vascular resistance, e.g. COPD, PE.
● High pulmonary blood flow, e.g. left to right shunt.
● Heart disease: e.g. mitral valve disease, HOCM.
DIAGNOSIS
● Based on history of chronic lung disease and history/examination fi ndings of
right heart failure.
CXR shows enlarged right cardiac silhouette and prominent pulmonary artery.
●
● ECG reveals P-pulmonale, right atrial dilatation, right ventricular strain.
MANAGEMENT
● Treat the underlying condition.
● Long-term oxygen therapy.
● Symptom control: fluid restriction, avoidance of NSAIDs, diuretics.
● Treatment of heart failure (see section on Heart Failure).
Surgery: consider heart-lung transplantation.
●
Primary pulmonary hypertension is a rare condition usually affecting young
patients; the patient presents with pulmonary hypertension but no cause is found.
Management: refer to a specialist centre for further investigation.
3.13. Respiratory emergencies
See sections on Asthma, COPD, PE and Pneumothorax.
Acute respiratory distress syndrome
Can occur secondary to a multitude of severe insults, including severe sepsis and
trauma. The resulting pulmonary oedema is non-cardiac. Management: requires
treatment of the underlying cause and supportive care (airway management,
circulatory support etc).
50
3.14. Investigations
Arterial blood gases
RESPIRATORY DISEASE
pH 7.35–7.45 = normal <7.35 = acidosis
>7.45 = alkalosis
serum Bicarbonate (HCO
Base Excess (BE) +/–2 = normal
pO
2
pCO
2
Type 1 respiratory failure: pO
Type 2 respiratory failure: pO
) 22–26 = normal
3
>10.6 KPa = normal Respiratory failure if pO2 <8 KPa
4.7–6 KPa = normal
<8 KPa and pCO2 <4.7
2
<8 KPa and pCO2 >6
2
Causes of type 1 respiratory failure: any cause of a ventilation-perfusion (V/Q) mismatch,
e.g. PE, pneumonia, COPD, asthma.
Causes of type 2 respiratory failure: any cause of type 1 failure plus any cause of
hypoventilation such as:
1 neuromuscular conditions – causing weakness of the respiratory muscles, e.g.
myasthenia gravis;
2 reduced respiratory drive, e.g. opiates, CNS tumours;
3 thoracic wall defects, e.g. kyphoscoliosis.
normal
Expiratory
flow
extrathoracic obstruction: both
inspiratory and expiratory loops
flattened
COPD: expiratory flow is impeded
Inspiratory
flow
FIGURE 3.1
TLC RV
Flow volume loops.
51
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Peak expiratory flow rate (PEFR) and spirometry
PEFR is a measure of the severity of obstructive airways disease and should be
recorded on all patients with asthma and COPD who are admitted with an exacerba tion of their condition. Always ensure that the patient’s technique is adequate and
compare the results to patient’s best (if patient knows) or predicted PEFR.
Formal spirometry.
FEV1 = volume of gas expired in first second of forced expiration (related to
●
PEFR).
FVC = total volume of gas expired with forced expiration.
●
● FEV1/FVC <70% = Obstruction.
● FEV1/FVC >70% = Restriction (actual FEV1 and FVC must also be lower than
predicted; patients with normal spirometry will have FEV1/FVC >70% also).
Flow-volume loops
Patient inspires rapidly to maximum volume from expiration, then forced expiration
is carried out. This produces a fl ow-volume loop.
Bronchoscopy
Indicated for further investigation of cough, haemoptysis, unusual presentation
of chest infection (e.g. if you suspect PCP), for bronchial washings, and to further
investigate a lesion resting in the bronchial tree when an endobronchial biopsy is
also required. In order to perform, pO
CT guided lung biopsy
needs to be >8k KPa.
2
The procedure of choice if there is a peripheral lesion not amenable to biopsy by
bronchoscopy. Risk of pneumothorax ≈ 20%, 3% require chest drain.
52
4
Gastroenterology
4.1. Disorders of the oesophagus
4.2. Disorders of the stomach
4.3. Upper gastrointestinal bleed
4.4. Coeliac disease
4.5. Malabsorption
4.6. Diarrhoea
4.7. Constipation
4.8. Inflammatory bowel disease
4.9. Jaundice
4.10. Ascites
4.11. Cirrhosis
4.12. Chronic hepatitis
4.13. Alcoholic liver disease
4.14. Autoimmune hepatitis
4.15. Metabolic liver disease
4.16. Other liver disease
4.17. Hepatosplenomegaly
4.18. Acute liver failure
4.1. Disorders of the oesophagus
Dysphagia
Diffi culty swallowing: classically affects solids more than fl uids if obstructive, but
early involvement of fluids if neurogenic or a motility problem, e.g. achalasia.
Causes of dysphagia
❍
In the lumen: foreign body
❍
In the oesophageal wall: carcinoma, achalasia, web, stricture, pharyngeal pouch
❍
Outside the wall: mediastinal tumours, retrosternal goitre, left atrial enlargement
❍
Neurogenic: can be broadly classified into cortical causes (e.g. stroke, dementia)
and ‘peripheral’ disorders affecting the anterior horn cell (bulbar palsy in MND,
polio), neuromuscular junction (myasthenia gravis) and muscle
Oesophageal carcinoma
Incidence increases with increasing age (peak incidence 50–70 years) and more
common in males (3:1). Majority are squamous cell carcinomas (≈ 85%) and the
rest are mainly remainder adenocarcinomas which typically arise from the lower ¹⁄
from a Barrett’s oesophagus.
³
53