Respiratory Flashcards
PE in pregnancy
Risk of PE in pregnancy
*estimated incidence
-0.06% - 8%
-5-10% if previous VTE during pregnancy
*five times increased risk during pregnancy and post-partum
-risk of DVT three times that of PE
-probably an increased risk of pelvic DVT in pregnancy
*risk increased equally in all trimesters
-50% occur prior to 20 weeks gestation
*frequency of VTE
-about 4 times higher in the first six weeks of the postpartum period compared to antepartum
-80% of VTE’s occur in first 3 weeks post partum
-about two times higher from 7-12 weeks
-returns to non-pregnant levels after 12 weeks postpartum
Contributing factors:
* Hyperemesis
* Venous stasis
* Hypercoagulability
* Decreased fibrinolysis
* Bed rest
Pregnancy related risk factors
* Assisted reproduction
* PPH or infection
* Pre-eclampsia
* Caesarean section
Important points
No specific clinical decision rules not yet developed
Risk factors for PE in pregnancy differ from those in the non-pregnant population
Strong left leg predominance of DVT is unique to pregnancy
65% of thrombi involve iliofemoral vessels => higher risk of embolisation
Isolated pelvic vein thrombosis occurs in 10% (< 1% in general population)
Symptoms of DVT / PE may mimic physiological events of pregnancy (e.g. dyspnoea, tachycardia, leg oedema)
Investigation
*non invasive diagnostic methods without imaging are ideal
*false negative results of investigations
-risk (mortality) of untreated PE is high
*false positive results of investigations
-result in unnecessary anti-coagulation
*outcome of investigation may influence delivery, future contraception and need for PE prophylaxis
D-dimer
*concentration rises gradually during pregnancy
*level drops rapidly in the first 3 days postpartum
-reaches normal levels > 4–6 weeks postpartum
*specificity of D-dimer testing in pregnancy and the postpartum period is lower than normal
-D dimer < 0.5microg/mL without thrombosis
-50% in first trimester
-20% in second trimester
-0% in third trimester
-70% in post partum period
*upper limit of normal (95th percentile) (microg/mL)
-first trimester - 0.95
-second trimester - 1.3
-third trimester - 1.7
*pregnancy adjusted d dimer levels have been proposed, however none prospectively validated
-first trimester - 0.75
-second trimester - 1
-third trimester - 1.12
*negative predictive value is still high so a negative D-dimer usually does not require further investigation
Imaging
*concern about exposure to radiation should not outweigh use of CTPA or VQ scan when indicated
-mortality associated with untreated PE > risk to the fetus than exposure to diagnostic imaging
*fetal radiation dose from a
-CXR at any gestational age is negligible (<0.1 mGy)
-CTPA (0.1 mGy) is less than the estimated fetal radiation exposure from VQ scanning (0.5 mGy)
-these exposures are well below the levels associated with carcinogensis
*where possible, use modified imaging protocols to reduce radiation exposure
Ultrasound
*despite low sensitivity may be reasonable first line test in suspected PE as it is fairly specific
*does not detect pelvic DVT
VQ scan
*investigation of choice for evaluation of PE in pregnant patients
*much less maternal radiation (especially to the maternal breasts), with slightly greater fetal radiation than CTPA
*radionuclide has minimal risk and is safe in pregnancy
*diagnostic quality VQ obtained in 97% of pregnant patients
-if CXR normal and no history of asthma or chronic lung disease
*73%–92% of V/Q scans in pregnant patients are normal
*radiation dose reduction possible
-ventilation scan omitted when perfusion normal
-decrease dose of perfusion component by 50%
*minimise radiation to the pelvis by
-high urine flow
-frequent voiding after injection of radionuclide
CTPA
*commonly used in pregnant patients with suspected PE
*less fetal radiation, more maternal radiation than VQ
*dose reduction methods possible
-alter CT acquisition parameters (maintaining diagnostic quality)
-bismuth breast shields to decrease maternal breast dose
-lead shielding to minimise fetal radiation exposure
*physiological changes of pregnancy may increase non diagnostic rate
*theoretical risk of iodinated contrast material to fetus
Management
*same initial approach as non pregnant patients
*LMWH preferred over UFH
*long-term anti-coagulation is with LMWH until 6 weeks post partum
-warfarin is a teratogen
-safety of DOACs uncertain, however are known to cross the placenta and may cause birth defects
LMWH
*drug clearance increases with increasing gestational age
*long-term use might result in an accumulation of dose effect
*monitor effect with anti-factor-Xa concentration weekly until stable
*does not cross the placenta
*minimally secreted in breast milk (safe in breast feeding)
*may reduce likelihood of epidural anaesthesia (reports of adverse events)
Thrombolysis
*consider for patients who are haemodynamically unstable
Resuscitative hysterotomy
*consider in arrested patients who have failed thrombolytic therapy
GOLD COPD Severity Classification
Intubation indications asthma/COPD
- Worsening hypoxia
- T2RF
- Altered conscious state
- NIV failed
- Medical therapies not working
- Reversible process
- Pt wishes / QOL
Massive haemoptysis
Def : >500 mls/24hrs or >100ml/hr + 1L loss
Causes
* Structural - Neoplasm, Trauma, FB
* Pulmonary - bronchitis, bronchiectasis, TB, pneumonia, lung abscess, fungal infection
* Iatrogenic - Post-lung biopsy, aorto-tracheal fistula, tracheostomy
* Thrombosis - PE, Coagulopathy, DIC, PLT
* Systemic - Cong heart disease, valvular heart disease, SLE, vasculitis, goodpasture’s
Re-expansion pulmonary oedema
Large PTx
Large volume pleural drainage > 3L
Young pts
Long duration > 7 days
Use of negative pressure (suction)
Mx Re-expansion Pulmonary oedema
CXR only - observation
Hypoxic / inc RR - supplemental O2
Mod-severe WOB - NIV with PEEP
Hypovolaemia + hypotension - IVF + inotropes
Hypervolaemia + volume overload - diuretics
Refractory resp failure or hypotension - ECMO
Transudate vs Exudate Pleural Effusion
Transudates:
* congestive cardiac failure or left ventricular (LV)
failure
* cirrhosis
* nephrotic syndrome
* superior vena cava obstruction
* myxoedema
* PE
Exudates:
* Parapneumonic effusions – bacterial pneumonia,
bronchiectasis, lung abscess, empyema
* Malignancy – 75% are due to lung carcinoma,
breast carcinoma and lymphoma
* Infective causes – tuberculosis, viral, fungal and parasitic infections
* Inflammaiton - pancreatitis
* Autoimmune - RA, SLE
* Post-MI
* Oesophageal perforation
* PE
Light’s Criteria + Transudate vs Exudate causes
Pleural Fluid Acidosis
Aspiration Pneumonitis
Chemical pneumonitis secondary to aspiration of sterile gastric contents
Direct lung injury and non-cardiogenic pulmonary oedema
May rapidly progress to ARDS
Early presentation w/in few hours
Initial CXR may be normal
3 mechanisms:
Aspiration gastric contents -> pneumonitis
Contaminated PO secretions and gastric contents
Particulate matter
Indications for ABX:
Failure to improve
Clinical deterioration
CXR suggesting pneumonia
Aspiration of contaminated fluid I.e. bowel contents
CXR PTX supine pt
Deep sulcus sign - air in the position
Pericardial fat tag sign - sharp outline pericardial fat due to air lower part pleural cavity
Lucency over upper abdomen - often visible liver
Pleural air - sharp appearance of mediastinal and diaphragm borders
SC emphysema without direct evidence PTX
CXR in PE
Westermark Sign = focal peripheral hyperlucency secondary to oligemia resulting in a collapsed appearance of vessels distal to the occlusion
Hampton’s Hump = dome-shaped, pleural-based opacification in the lung most commonly due to PE causing lung infarction
Fleischner sign = prominent central pulmonary artery caused by PAHTN or distension of the vessel by a large PE.
Chang sign = dilatation and abrupt change in caliber of the main pulmonary artery due to PE
Knuckle SIgn = abrupt tapering or cutoff of a pulmonary artery secondary to a PE
Palla sign = enlarged right descending pulmonary artery.
If Palla + Westermark suggests lobar or segmental pulmonary artery occlusion, or widespread occlusion of small arteries.
Echo in PE
Indirect signs indicating right heart strain:
RV > LV diameter
Septal flattening caused by increased Right sided pressures
Akinesia of the mid-free RV wall with preserved apical contractility = McConell’s sign
Dilated IVC and lask of inspiratory collapse
Inc TR
Inc Systolic PA pressures
PE ECG
RAD
New RBBB
STE or ST dep V1-3
TWI V1-4
S1Q3T3 (rare but poor prognostic sign)
P pulmonale
AF/A flutter /Atrial tachycardia
PE Investigation options
Bronchitis vs Emphsema
Empyema
Def: pus in thoracic cavity
50% pneumonia will have pleural effusion
5% dvp empyema
Cause
Bacterial transformation of effusion - haemo/chylo etc
Instrumentation - pleural tap or ICC
Bacterial / fungal / TB
Extension of lung abscess
**All require drainange and IV antibiotics **
Stages:
I - exudate < 48 hours - ICC
II - Fibrinopurulent / Locules - ICC + VATS + intra-pleural finbrinolytic agent
III - Organisation / extensive fibrosis - open lung surgery for pleural peel
Ix
Pleural fluid analysis
Turbid / purulent
pH < 7.2 - most important marker for drainage ICC or surgery
Glucose < 3.3mmol/l
WCC > 100,000 mm3
LDH > 1000 u/L
ABx
CAP vs HAP
Orgs
Kids - Staph, then Strep and Hib is decreasing
Adults - Pseudomonas, Klebsiella, Staph, Strep, TB, Fungal (rare)
Needle thoracocentesis
Diagnostic or therapeutic
Therapeutic indications
1. Respiratory compromise
2. Haemodynamic instability
3. Massive effusion with mediastinal shift
4. Some stable but symptomatic patients
Drian up to 1.5L stat
Drian larger effusions slower to prevent re-expansion pulmonary oedema
Cease drianage if chest pain, persitent cough or vasovagal symptoms
CI
Uncoperative Pt
coagulopathy unable to be corrected
Small effusion
Cases where aspiration could be catastrophic
- bullous lung disease
- ventilated with PEEP
- Single lung
- Elevated hemidiaphragm esp Left side
- Risk of bleeeding
- Cutaneous infection at site
Complications
PTc
SC emphysema
Infection
Haemothorax
Re-expansion pulmonary oedema
Visceral injury
Haemoperitoneum
Others: Vasovagal, hypoxia, hypovolaemia, cough, pain, allergy to LA
Pneumonia - Organisms
Strep - most common, CVS/ Resp disease, smoking, alcoholism, HIV, dementia, seizures, overcrowding
Staph - IVDU, Surgery of invasive procedure, recent measles or influenza
Legionella - aerosolised droplet contaminated water systems
Imuunosuppresion, DM, malignancy
Relative bradycardia
Constitutional symptoms
Assoc w/ Elelvated transaminases, low Na, Low PO4,
Mortality 75% if untreated
Mycoplasma - young 5-20yrs, later presentation and may have had antibiotics prior to presentation
Chlamydia - extremes of age
Non-penumonic findings - sinusitis, reactive airway disease, empyema
50% cases in infants have eosinophilia
Aerobic Gm -ve (Pseudomonas, klebsiella)
Rare but higher risk of mortality
RF - malginancy, resp disease - CF, bronchiectasis
COPD patients
H influenza, Moraxella catarrhalis, Pseudomonas, Klebsiella
