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
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
