Tag Archives: PE

Pleurisy

Pleurisy (also referred to as pleuritis) is the inflammation of the pleural layers surrounding the lungs. Pain is caused when there is friction between the layers. Pleurisy is a symptom of an underlying condition, not a condition in itself.

There are two layers of epithelium, the visceral pleura encases the lungs, and the parietal pleura covers the mediastrinum and chest wall. The two pleuras meet at the hilum. The pleural space between the pleuras contains lubricating fluid which helps prevent friction occurring between the two layers. The visceral pleura has an autonomic nerve supply which gives no pain sensation, whereas the parietal pleura has sensory nerve endings supplied by the phrenic nerve and therefore can experience pain.

Accumulation of pleural fluid suggests and increase of fluid production that exceeds the ability of the lymphatic system to remove it, or an obstruction in the pleural space.

Pleurisy is often caused by viral infections, but when a patient presents with pleurisy it is important first to rule out any life-threatening conditions such as MI and PE first. Although pleurisy is generally a symptom of an underlying condition, sometimes pleurisy is idiopathic.

Patients present with pain, particularly on breathing, as the pleura surfaces become inflamed and cause friction, this pleural rub can sometimes be heard as a scratching sound on inspiration. A key feature of pleurisy is that the pain is sharp and is exacerbated on coughing, sneezing or taking a deep breath.

Other symptoms of pleurisy include fever, chills, rigors, shallow breathing, shortness of breath, productive cough, diminished breath sounds.

By determining how acute the pleurisy is the underlying cause is easier to discover; acute (minutes-hours), sub-acute (hours-days) chronic (days to weeks) or recurrent. Chest x-rays are normal diagnostic tests; not only will they show a pneumothorax but also will detect if there is pleural effusion. D-dimer tests are normal practice to rule out PE, ECG to detect MI and also a sputum sample should be sent for analysis.

A full history should be taken; previous chest pain, respiratory problems, long haul travel (immobility), how long the pain has been present, what the pain is like, what triggers it, what relieves it, accompanying symptoms, shortness of breath, syncope, cough, wheezing, past medical history. Observation should be taken; respiratory rate/quality, BP, pulse, temperature (ECG is also useful). The Early Warning System should be used if in an acute setting.

Pleurisy is generally treated initially with NSAIDs (use with caution in those with asthma, as with those with gastric ulcers,, patients over 65 and those on aspirin, anti-coagulants, corticosteroids or SSRIs). Indomethacin given 50-100mg daily can improve lung function and relieve pleuritic pain in chronic cases. If NSAIDs are unsuitable, or not tolerated narcotic analgesia can be given but caution is essential as it can cause respiratory depression. It must also be considered that pleurisy is a symptom of an underlying condition requires prompt diagnosis and treatment.

Inflammatory Bowel Disease and Venous Thromboembolism

Patients with inflammatory bowel disease such as Crohn’s or ulcerative colitis are twice as likely to develop a DVT or PE than the general population, according to researchers in Denmark. This may help to further inform how VTE risk is calculated for patients, and for which patients thromboprophylaxis should be indicated.

Kappleman, M.D. Et al (2011) Thrombo-embolic risk among Danish children and adults with inflammatory bowel diseases: a population–based nationwide study. Gut. Doi 10.1136/gut.2011.228585

The Use of Antiembolism Stockings

AE stockings are commonly used as a thrombolprophylaxis in secondary care settings. These may be prescribed after a patients’ risk of VTE has been assessed.

Patients are advised to wear them 24 hours daily from the time they are administered to the time the patient is no longer considered to be at an increased risk of developing VTE. AES may be prescribed in conjunction with pharmacological thromboprophylaxis for added protection in those assessed to be at greater risk.

Unless contraindicated, surgical patients are generally prescribed pharmacological thromboprophylaxis as well as mechanical thromboprophylaxis (AES or intermittent pneumatic compression – IPC).

CVA patient generally are not prescribed AES because they have not been shown to be effective in such patients and can increase the risk of skin breakdown.

Other patients to avoid AES are those with peripheral neuropathy or peripheral arterial disease, or friable skin.

AES need to be fitted correctly and the right size is essential. They work by exerting graduated circumferential pressure onto the legs which supports the veins and therefore improves venous return, which decreases venous stasis. They also decrease venous dilation and therefore help to prevent activation of clotting factors.

Summary of Chest Pain Triage in Primary Care

Urgent referral to A&E is needed for patients presenting with:

  • ACS: crushing/squeezing chest pain at rest, possibly accompanied by nausea, sweating, shortness of breath or dizziness, pain radiation from left arm to jaw may be present.
  • Aortic aneurysm dissection – symptoms include sharp tearing pain, dyspnoea, syncope, a feeling of impending doom.
  • PE – includes symptoms of sharp sudden pain in a patient with a history of recent inactivity/stasis – perhaps recent long-haul travel, recent surgical procedure under general anaesthetic or hospital admission which has restricted normal level of activity, breathlessness.

Chest pain not necessarily requiring urgent transfer to A&E:

  • Angina – similar symptoms to ACS, but pain experienced on exertion and relieved at rest (possibly with a history of CVD). If the patient is unstable patient should be treated along the lines of ACS. Treat initially with GTN.
  • Chest infection/pleurisy; patient will present with pain on moving or breathing, presents as sharp central pain. Patient may also have a fever. This can be safely treated in primary care setting.
  • Pericarditis; again, symptoms as pleurisy, to be treated with NSAIDs if suitable for patient, consider outpatient ECG.
  • GORD – burning pain, retrosternal. May have a long history, possibly associated with particular foods. Not particularly urgent unless presenting with malaena or haematemesis. Patient may require gastroscopy; primary care may involve PPIs or H2 blockers.

It is vital to take a detailed history, as well as appropriate observations (BP, ECG, pulse, respiratory rate, temperature).

P – Provocation/palliation – what triggers the pain? What relieves it?

Q – Quality – what is the pain like? Stabbing, crushing, aching, dull, tearing. Also use pain scale.

R – Radiation – where does the pain begin, and where does it radiate to?

S – Site – what’s the location of the pain?

T – Timing – when did the pain start? What was the duration? How many episodes have there been? When did the episodes start? Is it getting better or worsening?

Also, record any accompanying symptoms such as dizziness, nausea/vomiting/burping, feeling of impending doom, syncope.

Symptoms suggesting ACS need urgent referral to hospital. If this is the case, the patient should be given 300mg aspirin and high-flow oxygen.

Thrombophilia

Thrombophilia, as the name implies is a blood disorder that increases the risk of clotting and therefore increases the risk of venous thromboembolism. It can be acquired through conditions such as heart failure, irritable bowel syndrome and nephritic syndrome. Or it may be inherited. Up to half of those treated for VTE are thought to have hereditary thrombophilia. This is known because patients who have had VTE are routines screened to see if there was an inherited factor in their episode. If a family member has had a previous VTE, genetic screening can be offered to identify and deal with the risk in others. Tests are carried out a month after anticoagulant treatment has finished as these interact with the antithrombin, protein S and protein C that are screened for deficiencies.

The risk of developing VTE in patients with thrombophilia is increased with dehydration and immobility/inactivity, surgery (particularly major general surgery and orthopaedic surgery to the legs) leg fractures, hip fractures, spinal cord inury, varicose veins or congestive heart or respiratory failure. Some forms of contraception can also increase the risk of VTE, therefore they are not normally recommended for patients with hereditary thrombophilia. The progestogen only pill (POP) is generally used instead of combined oral contraceptives. Pregnancy is also a risk factor, particularly if the mother is obese or more mature. This is the biggest cause of maternal mortality, especially after Caesarean section. Cancer patients are at increased risk too, but there’s also a secondary risk with chemotherapy.

In the acute setting, patients will generally be prescribed five days of anti-coagulation treatment with low molecular weight heparin (LMWH) or unfractionated heparin (if in renal failure). This is then followed by six months of oral anticoagulants. Because of the increased risk of haemorrhage, anticoagulants are not normally continued in such cases after six months.

VTE – Venous Thromboembolism

VTE is largely preventable in many cases. VTE is a term which includes PE and DVT. It doesn’t have ot be symptomatic.

DVT is most common in the lower leg, although it can occur further up or in the arms.  It can be caused by several factors; they form Virchow’s triad:

  • Pooling of blood (venous stasis) which occurs mainly in the extremities and is largely caused by immobility/inactivity
  • Injury or dilation of the vein wall which releases tissue factor and enables clotting
  • Hypercoaguability – increased ability for clotting – this may occur for a variety of reasons.

If any, or two, or all of the above factors are present the patient is at risk of VTE.

The thrombus becomes an embolus when it detaches and occludes a smaller vessel elsewhere, sometimes in the lung (PE). This prevents gaseous exchange, impeding the lung tissue’s blood supply which can cause chest pain, syncope, hypoxia, haemoptysis and shortness of breath. It is therefore important to monitory respiratory rate for tachpnea, tachycardia, and hypotension as PEs can be fatal.

Post-thrombotic syndrome (PTS) is cuased when a DVT causes long-term damage to venous values, this causes venous stasis which in turn increases the likelihood of developing a further DVT, causes erythema and swelling to the affected limb, discomfort, and sometimes venous leg ulcers. A third of DVT patients develop PTS.

On admission to hospital, all patients should be screened for their risk of developing TE and their care planned accordingly. This may involve anti-embolism stockings. Subcutaneous heparin, intermittent pneumatic compression (IPC), mobilisation as soon as possible or hydration.

Pharmacological prophylazis may involve low molecular weight heparin (LMMWH) fondaparinaz sodium, or if the patient has renal failure unfractionated heparin. Prophylaxis should begin as soon as possible and continue until the patient is no longer at the increased risk of VTE. As with all pharmacological thromboprophylaxis, the patient should be monitored for signs of bleeding/bruising. This needs to be documented and reported.