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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
293BREATHLESSNESS AND LOWSATS
Spontaneous pneumothorax(E OHAM4 p. 210.)
2
K May occur apparently spontaneously (primary) or in the presence of
underlying lung disease or injury (secondary).
Risk factors Primary Tall, slim, male; Marfan’s; recent central line, pleural
aspiration or chest drain;
Secondary COPD, asthma, infection, trauma,
mechanical ventilation.
SymptomsBreathlessness ±chestpain.
Signs Hyper- resonant and reduced air entry on aected side, tachyp-
noea, may have tracheal deviation or fracturedribs.
Investigations CXRLung markings not extending to the peripheries, line of
pleura seen away from the periphery.
TreatmentSit up and give 5L/ min O
BTS guidelines (E p. 294). In essence, primary pneumothoraces can po-
. Chest drain/ aspiration as directed by
2
tentially be discharged, while secondary pneumothoraces require admission
and either aspiration (E p. 566) or, more usually, drainage (Epp. 558–9).
3Tension pneumothorax
If air trapped in pleural space is under positive pressure (eg following penetrating
trauma or mechanical ventilation) then mediastinal shift may occur, compressing
contralateral lung and reducing venous return. The patient may be hypoten-
sive, tachycardic, tachypnoeic, with unilateral hyper- resonance and reduced
air entry; iJVP and tracheal deviation away from side of pneumothorax.
2This is an emergency, it will rapidly worsen if not treated. Sit up and give
5L/ min O
2nd intercostal space, midclavicular line. Listen for a hiss and leave it in situ;
. Treat prior to CXR. Insert a large cannula (orange/ grey) into
2
insert chest drain on same side. If there is no hiss, leave the cannula in situ
and consider placing a 2nd cannula or alternative diagnoses; a chest drain is
usually still required to prevent a tension pneumothorax accumulating.
Pleural eusion(E OHAM4 p. 220.)
2
K Excessive uid within the pleural space reects an imbalance between
hydrostatic and oncotic pressures within the pleural vasculature, and/ or
disruption to lymphatic drainage.
Causes
Pleural eusion may be divided into those causing
transudates
(where
pleural uid protein <25g/ L— tend to be bilateral); pulmonary oedema, cirrhosis,
nephrotic syndrome, hypothyroidism, intestinal malabsorption/ failure; and
ates
(protein >35g/ L— may be uni- or bilateral); malignancy, infection, vasculit-
ides, rheumatoid; if purulent and pH <7.2, this is
Light’s criteria
These help dierentiate, especially when protein >25g/ L but <35g/
empyema
reecting infection.
exud-
L. Consider the eusion an exudate if pleural protein:serum protein >0.5, pleural
LDH:serum LDH >0.6, or pleural LDH >⅔ of upper limit of normal serumvalue.
Symptoms The patient may be breathless with pleuritic chestpain.
SignsStony dull to percussion with reduced air entry, tachypnoea.
Investigations CXRLoss of costophrenic angle with a meniscus Epp. 610–11.
TreatmentSit up and give targeted O
large, pleural aspiration (E p. 566) may relieve symptoms and aid diagnosis
. Investigate the cause; if the eusion is
2
(draining >.5L/ 24h may cause re- expansion pulmonary oedema).
2
BTS guidelines available at Mhttps://www.brit-thoracic.org.uk/document-library/guidelines/
pleural-disease/bts-pleural-disease-guideline/
294 CHAPTER9 Respiratory
Algorithms forthe treatment ofspontaneous pneumothorax
Fig.9. Treating spontaneous pneumothorax in patients over 50 with no
signicant smoking history or evidence of underlying lung disease. Adapted
by permission from BMJ Publishing Group Ltd, Management of spontaneous
pneumothorax:British Thoracic Society pleural disease guideline 200, MacDu,
A.etal. Thorax 200 65 (Suppl 2):ii8.
295BREATHLESSNESS AND LOWSATS
Fig.9.2 Treating pneumothorax in patients over 50 with signicant smoking
history or evidence of underlying lung disease. Adapted by permission from
BMJ Publishing Group Ltd, Management of spontaneous pneumothorax:British
Thoracic Society pleural disease guideline 200, MacDu, A.etal. Thorax 200 65
(Suppl 2):ii8.
296 CHAPTER9 Respiratory
Pulmonary oedema(E OHAM4p. 92.)
3
Symptoms Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea,
frothy sputum; coexistent dependent oedema or previous heart disease.
Signs iJVP, tachypnoea, ne inspiratory basal crackles, wheeze, pitting cold
hands and feet; oedema (ankles and/ or sacrum) suggests right heart failure.
Investigations blds (Look specically for anaemia, infection, or MI): FBC,
U+E, CRP, troponin; BNP (normal levels unlikely in cardiac failure);
ABG May
show hypoxia; ECG Exclude arrhythmias and acute STEMI, may show old
infarcts, LV hypertrophy or strain (Epp. 600–2); CXRCardiomegaly (not if
AP projection), signs of pulmonary oedema (Epp. 610–11);
Echo Poor LV
function/ ejection fraction, pulmonary eusions.
Acute treatmentSit up and give 5L/ min O
call an intensivist early as CPAP and ICU may be required. Otherwise
monitor HR, BP, RR, and O
If further treatment is required, be guided by blood pressure:
•
Systolic <00 The patient is in shock, probably cardiogenic. Get senior
sats while giving furosemide 40– 20mg IV.
2
. If the attack is life- threatening
2
help as inotropes are often required. Do not give nitrates
•
Wheezing Treat as for COPD alongside above- mentioned treatment
•
No improvement Give IV furosemide up to 20mg total (more if
chronic renal failure) and consider CPAP (Box 9.4). Insert a urinary
catheter to monitor urine output, ±CVP monitoring. Request senior
help. Consider HDU/ ICU
• Consider GTN infusion with concomitant myocardial ischaemia,
hypertension, or aortic/mitral regurgitation. Requires senior support
and close monitoring in level 2 care.
Once stabilized, the patient will need daily weights ±uid restriction. Document LV function with an echo and optimize treatment of
heart failure (E p. 282). Oral bumetanide may be preferred to oral
furosemide for diuresis since absorption is said to be more predictable
in the presence of bowel oedema, though evidence for this is lacking.
Always monitor U+E during diuresis:The heart- sink patients are those
with simultaneously failing hearts and kidneys who seem fated to spend
their last days alternating between uid overload and AKI— close liaison
with the patient’s GP and palliative care teams is as essential as everhere.
K Box 9.4 Continuous positive airway pressure (CPAP)
Application of positive airway pressure throughout all phases of the
respiratory cycle limits alveolar and small airway collapse, though the
patient must still initiate a breath and have sucient muscular power to
inhale and exhale. Pursed- lip breathing has a similar eect, and is often
observed in patients with chronic lung disease. CPAP is often used in
the acute treatment of pulmonary oedema or the chronic treatment
of sleep apnoea (may use nasalCPAP).
3
NICE guidelines available at Mhttps://www.nice.org.uk/guidance/cg87
SVC obstruction(E OHCM1p. 524.)
K Typically due to intrathoracic malignancy, usually lung cancer.
SymptomsBreathlessness, orthopnoea, facial/ arm swelling, headache.
SignsFacial plethora (redness), facial oedema, engorged veins, stridor.
Pemberton’s test Elevating the arms over the head for min results in in-
creased facial plethora andiJVP.
Investigations CXR/ CT Mediastinal mass, tracheal deviation, venous con-
gestion distal to lesion;
Treatment Seek senior input early. Sit up and give 5L/ min O
OtherSputum cytology for atypicalcells.
Dexamethasone 4mg/ 6h PO/ IV. Consider diuretics to decrease venous
return and relieve SVC pressure (eg furosemide 40mg/ 2h PO).
Otherwise symptomatic treatment while arranging for tissue diagnosis.
Acute respiratory distress syndrome (ARDS)(E OHAM4.p. 204.)
K Acute- onset respiratory failure due to diuse alveolar injury following
a pulmonary insult (eg pneumonia, gastric aspiration) or systemic insult
(shock, pancreatitis, sepsis). Characterized by the acute development of
bilateral pulmonary inltrates and severe hypoxaemia in the absence of
evidence for cardiogenic pulmonary oedema.
SymptomsBreathlessness, often multiorgan failure.
Signs Hypoxic, signs of respiratory distress, and underlying condition.
Investigations CXRBilateral inltrates.
Treatment Sit up and give 5L/ min O
treat underlying cause. Often requires ventilation.
. Refer to HDU/ ICU early and
2
Interstitial lung disease (ILD)
K Can be thought of as a nal common pathway of various conditions
resulting in a typical clinical presentation.
Causes Common causes include idiopathic pulmonary brosis, drugs
(amiodarone, methotrexate), and inammatory conditions (sarcoidosis,
rheumatoid arthritis, scleroderma).
SymptomsBreathlessness, dry cough.
Signs Hypoxia, nger clubbing, stigmata of underlying cause, bilateral in-
spiratory pulmonary crackles (like footsteps in snow).
Investigations CXR Interstitial changes; HRCT Typically demonstrates
honeycombing; PFTS A restrictive picture.
TreatmentSupportive. Smoking cessation is essential. Pulmonary rehabili-
tation. LTOT may be required. New antibrotic agents can be trialled
upon specialist consultation in some subtypes. Some patients may be
eligible for lung transplantation.
297BREATHLESSNESS AND LOWSATS
.
2
298 CHAPTER9 Respiratory
2Stridor ina conscious adult patient
2 Airway
2 Breathing
2 Circulation
Acute stridor— CALL ANAESTHETIST AND ENT URGENTLY
If poor respiratory eort—
If no palpable pulse—
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior anaesthetics and ENT help immediately.
•
Do not attempt to look in the mouth/ examine theneck
• If
choking, follow algorithm in Fig.9.3
• Avoid
disturbing/ upsetting the patient in anyway
• Let the
• Oer
•
•
•
•
• Check
patient sit in whatever position theychoose
supplemental O
Fast bleep senior anaesthetist
Fast bleep seniorENT
Adrenaline (epinephrine) nebs (5mL of :000 withO
Monitor pulse oximeter ±debrillator ECG leads ifunwell
temp
to all patients
2
)
2
• Take brief history from relatives/ ward sta or checknotes
•
Look for swelling, rashes, itching (?anaphylaxis)
• Consider
• Await
• Request urgent portable
serious causes (see ‘Life- threatening causes’)
anaesthetic and ENTinput
CXR
• Call for seniorhelp
•
Reassess, starting with A, B, C…
2Life- threateningcauses
• Infection (epiglottitis, abscess)
• Tumour
• Trauma
• Foreignbody
• Post- op
• Anaphylaxis.
Fig.9.3 Adult choking treatment algorithm, 202 guidelines. Reproduced with
the kind permission of the Resuscitation Council(UK).
Cough
Box 9.5 Causes ofcoughs
URTI, post- viral, post- nasal drip (allergy), pneumonia, LVF, PE
Acute
Asthma, COPD, bronchitis, bronchiectasis, smoking, post- nasal drip,
Chronic
oesophageal reux, pneumonia, TB, parasites, interstitial lung disease,
heart failure, ACEi, lung cancer, sarcoid, sinusitis, cystic brosis, habitual
Massive bronchiectasis, lung cancer, infection (including TB and
Bloody
aspergilloma), trauma, AV malformations
Other Bronchitis, PE, LVF, mitral stenosis, aortic aneurysm,
vasculitides, parasites
Usually, the cause of coughing is obvious (Box 9.5). Chronic (>8wk), unexplained coughing with a normal CXR and the absence of infective features requires a considered approach. Is there diurnal or seasonal variation
in coughing (cough- variant asthma; do PEFR diary, lung function testing, and a
trial of inhaled steroids)? Is there a history suggestive of gastro- oesophageal
reux (trial of PPI)? Does the onset of a dry cough follow the introduction
of an ACEi (consider an AT II receptor blocker)? Or is there a sensation
of mucus accumulation at the back of the throat (consider chronic/ allergic
rhinitis and ‘post- nasal drip’ and a trial of nasal steroids or antihistamines)?
HaemoptysisCoughing up blood, >500mL over 24h is massive.
Management ABC, establish patent airway; FBC, U+E, LFT, clotting, G+S,
sputum C+S and cytology, ABG, ECG, CXR. Sit up, 5L/ min O
Codeine 60mg PO (may dcough);
monitor HR and BP, immediate referral to respiratory team for urgent
bronchoscopy ±CT thorax.
Bronchiectasis(E OHCM1 p. 80.)
K Abnormal and permanently damaged and dilated bronchi caused by
destruction of the elastic tissue of the bronchialwalls.
Causes Cystic brosis, infection (pneumonia, TB, HIV), tumours, im-
munodeciency, allergic bronchopulmonary aspergillosis, foreign bodies,
aspiration, asthma, rheumatoid arthritis, idiopathic.
SymptomsChronic cough with purulent sputum ±haemoptysis, halitosis.
SignsClubbing, coarse inspiratory crepitations ±wheeze.
Investigations FBC, immunoglobulins, aspergillus serology; blood or sweat
test (forCF);
SputumC+S; CXR Thickened bronchial outline (tramline and
ring shadows) ±brotic changes; CT
dilatation; spirometry;
Acute treatment O
±BIPAP. Typical recurrent infections include Pseudomonas (consult local
Bronchoscopyfor other diagnoses.
as required, ±bronchodilators ±corticosteroids,
2
antibiotic guidelines). Chest physiotherapy to mobilize secretions.
Chronic treatmentChest physio, inhaled/ nebulized bronchodilators, anti-
biotics (consider prophylactic on specialist advice), mucoactive agents.
NIV and surgery may be considered where medical managementfails.
Complications Recurrent pneumonia, pseudomonal infection, massive
haemoptysis, cor pulmonale.
4
British Thoracic Society guidelines available at Mhttps://www.brit-thoracic.org.uk/
If massive Good IV access (≥green),
4
thorax(‘high- resolution CT’) Bronchial
299COUGH
.
2
Chapter0
Gastroenterology
2Abdominal pain emergency 302
Abdominal pain 303
2GI bleeding emergency 32
Acute upper GI bleeds 33
Acute lower GI bleeds 35
Nausea and vomiting 38
Diarrhoea 320
Constipation 324
2Liver failure emergency 326
Liver failure 327
Jaundice 332
301
302 CHAPTER0 Gastroenterology
2Abdominal pain emergency
2 Airway
2 Breathing
2 Circulation
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early if patient deteriorating.
5L/ min O
•
Monitor BP, pulse oximeter, debrillator ECG leads ifunwell
•
• Obtain a full set of
• Take brief
Examine patient:condensed RS, CVS, abdo, ±woundexam
•
• Consider
• Initiate
Venous access, take bloods:
•
•
• Give IV
Analgesia as appropriate
•
Arterial blood gas, but don’t leave the patientalone
•
Erect CXR (portable if unwell) and consider plainAXR
•
if SOB or sats<94%
2
observations, are they haemodynamically stable?
history if possible/ check notes/ ask wardsta
serious causes (Box 0.) and treat if present
further treatment Epp. 303–5
FBC, U+E, LFT, amylase, CRP, clotting, X- match 4units, bld cultures
uids if hypovolaemic or shocked (Ep. 480)
• ECG
• Urine dipstick and β- hCG (all pre- menopausal women), ±catheter
• Keep patient
• Call for
NBM if likely to need theatre
seniorhelp
• Reassess, starting with A, B, C…
Box 0. Life- threateningcauses of abdominal pain
• Perforation E p. 305
• Bowel infarction/ ischaemia E p. 307
• Bowel obstruction E p. 306
• Acute pancreatitis E p. 310
• Acute cholangitis E p. 333
• Appendicitis E p. 307
• Leaking abdominal aortic aneurysm (AAA) E p. 477
• Strangulatedhernia E p. 521
• Testicular or ovarian torsion E p. 520, p. 530
• Ruptured ectopic pregnancy E p. 500
• Referred pain (MI, aortic dissection) E pp. 258–61