A 25-year-old woman with chest pain and breathlessness

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Problem 29 A 25-year-old woman with chest pain and breathlessness

Fiona Kermeen

You are currently working in the emergency department on an evening shift. A 25-year-old woman has come to you for urgent assessment tonight with difficulty breathing and right-sided chest pain. The pain began suddenly 1 week ago. She describes it as sharp and worse on breathing in. It is now constant and has increased in severity. She has also become progressively more breathless on exertion over the last few days and is now unable to perform activities such as showering without feeling ‘out of puff’.
You ask her more history – she has not had a fever, cough or wheeze and she has never previously suffered any respiratory complaints. The woman has polycystic ovarian syndrome and has been using the oral contraceptive pill to help regulate her menses in the last couple of years. Her health has otherwise been good. She is an active smoker, averaging 10 cigarettes per day for the last 7 years.
You examine her – she is obese with a weight of 110 kg. She is sweaty and looking unwell. She is taking short shallow breaths and her respiratory rate is 30 breaths/minute. Her temperature is 37.5°C, her pulse is 120 beats/minute and feels regular. Her blood pressure is 125/60 mmHg with oximetry showing oxygen saturation on room air of 88%. Her jugular venous pressure is visualised at 5 cm. Both heart sounds are present with no murmurs or pericardial rub audible. There are reduced breath sounds at both lung bases. No crackles, wheeze or pleural rub are heard. You note that there is tenderness behind her left calf but no associated leg swelling. Her admission CXR is reported as having mild basal atelectasis, but as being otherwise normal.

Q.1

What are the most likely diagnoses? What further history would help?

On further questioning, the patient reports having had left calf pain for 1 month but she thought it was a ‘cramp’. She has had no episodes of haemoptysis or syncope. She has not had recent surgery. There is no known family history of heart or lung problems. She is compliant with her oral contraceptive pill and she is not pregnant. She has not embarked on any recent long distance travel. She has had a recent papsmear which was negative for malignancy.

Q.2

What further investigations are you going to organize now?

Complete blood picture and baseline electrolytes are normal.

Investigation 29.1 Arterial blood gas analysis

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Figure 29.1 Electrocardiograph.

Q.3

What do the above investigations show?

An imaging study is undertaken and two images from the sequence are shown (Figure 29.2). Her left Doppler showed an extensive clot into proximal femoral veins.

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Figure 29.2

Q.4

What do these images show? What clinical signs may reflect the underlying severity of the condition?

The nurse asks you to review the patient again because she is concerned that her BP is now 85/60 mmHg. Her pulse has increased to 128 beats/min with no central or peripheral cyanosis. She appears distressed and her oxygen saturations are 90% on 2 L/min O2 with use of nasal prong. In addition to her raised JVP, you palpate a left parasternal heave. A third heart sound is now heard (gallop rhythm). You order an urgent bedside echocardiogram and the sonographer tells you the right ventricle is moderately dilated with moderate RV dysfunction and RVSP of 40 mmHg.

Q.5

What actions do you take now?

Intravenous unfractionated heparin loading dose is given calculated to your institution’s weight-based protocol. O2 is increased to 10 L with non-rebreather mask. The patient is taken to ICU. Thrombolysis is given with alteplase. Within 4 hours the patient is normotensive, pulse rate 82 and O2 requirements have reduced and her JVP is not visible. The next day the patient is transferred to your ward with IV heparin running.

Q.6

How do you manage her ongoing anticoagulation?

Oral warfarin is commenced early, while on IV heparin. Once her INR has been within the therapeutic range for 2 days, the IV heparin is ceased. An echocardiogram is repeated and shows normalization of right ventricular size and function. Prior to discharge, her thrombophilic screen of tests is reported as showing no abnormalities.

Advice is provided about her condition and taking warfarin tablets. The hospital’s outpatient warfarin clinic is going to monitor her INR, and an alert bracelet is arranged for her to wear oral contraceptive pill is ceased and referal to gynaecologist regarding progestrone only contraception.

Q.7

What advice would you give her before discharge?

The woman returns to see you in the outpatient clinic after 3 months. She has been well and no longer experiences chest pain or breathlessness on exertion. Her INR has been well maintained within the therapeutic range. She has quit smoking.

Q.8

How long should she be on warfarin, and are any tests required before stopping it?

Answers

A.1 This young lady has pleuritic chest pain, dyspnoea and hypoxia (based on pulse oximetry) unexplained by her chest X-ray.

• Pulmonary embolism (PE) is the most likely and important diagnosis to consider as it carries a significant mortality risk when untreated:

– her risk factors for PE are: obesity, smoking and use of the oral contraceptive pill
– the left calf tenderness on examination raises the possibility of deep vein thrombosis (DVT) which is found in 70% of patients with confirmed PE.

• Spontaneous pneumothorax has been excluded in this case with the chest X-ray.
• Inflammatory pleurisy from pneumonia is less likely because more infective symptoms would be expected a week after onset (sputum production and constitutional symptoms) along with definite features of consolidation on chest X-ray and/or on clinical examination (bronchial breath sounds).
• Pericarditis is another condition that sometimes mimics pleurisy but does not usually cause hypoxia, unless associated with acutely decompensated heart failure.

Further specific questions should be asked to determine her pre-test probability of DVT/PE:

• Recently abdominal/pelvic/orthopaedic surgery?
• Major trauma or lower limb fractures requiring casts?
• Pregnant or recently given birth?
• History of DVT or PE?
• History or family history of thrombophilia?
• Prolonged immobility such as long-haul air travel?
• History of any malignancy, (especially breast cancer in this case)?

A.2 The following investigations must be undertaken:

• Arterial blood gas analysis (to determine degree of hypoxia).
• ECG (looking for right-heart strain pattern).
• Complete blood picture (anaemia, leucocytosis).
• Biochemistry (baseline electrolytes).
• Specific imaging. The standard imaging studies used for the detection and assessment of PE are:

– Isotope ventilation–perfusion scan (‘V/Q scan’). The ventilation component of the scan is obtained when the patient breathes a radioactive gas (e.g. Xenon 133) and the perfusion scan obtained by injecting the patient with a gamma-emitting radionuclide (e.g. technetium-99m). A pulmonary embolus is detected through the identification of a ‘mismatch’ between ventilation (normal) and perfusion (reduced). This is the better investigation for detection of small peripheral embolic lesions. There are no concerns about contrast allergies, but it is of limited value in the presence of other forms of lung disease which can include atelectasis, pneumonia, COPD or pleural effusions.
– CT-pulmonary angiography (CTPA). This is the better tool if there is co-existent lung disease. These high-definition scans are capable of detecting small pieces of blood clot in the major pulmonary vessels. Some patients may be allergic to the contrast and there can be concerns about the contrast load in patients with renal impairment, particularly the elderly.
– Venous leg Doppler ultrasound (to exclude extensive venous thrombosis, which may require IVC filter).

A D-dimer blood test is not appropriate in this case as it is only useful in excluding a diagnosis of PE when there is a low pre-test clinical probability. This lady has known risk factors for and a clinical picture consistent with PE; therefore, specific imaging should be performed. A CTPA should be chosen in this setting because there is atelectasis on her chest X-ray which makes a V/Q scan difficult to interpret.

A.3 The arterial blood gases show the following:

• Hypoxia (low oxygen tension).
• Hypocapnia (low carbon dioxide tension).
• Respiratory alkalosis.
• Calculated A-a gradient of 55.

This is type 1 respiratory failure, and suggests an acute event, causing hypoxia. The patient then hyperventilates to compensate, and releases carbon dioxide leading to hypocapnia and an alkalosis. A similar pattern may be seen in acute asthma, pneumothorax and pulmonary oedema.

This ECG shows the classically quoted changes seen with PE of S-wave in lead I with a Q-wave and T-wave inversion in lead III (S1Q3T3). However, this is a rare occurrence and the most common abnormality seen is sinus tachycardia. More extensive emboli often result in new-onset atrial fibrillation.

A.4 This high-definition image confirms the diagnosis of PE showing clot at the bifurcation of the pulmonary artery into its right and left main branches (saddle PE).

The signs of PE will generally depend on the size of the embolus and underlying co-morbidities. Large, haemodynamically significant PE, as in this case, can be associated with:

• Tachycardia.
• Raised JVP.
• Left parasternal heave (consistent with right ventricular enlargement).
• Gallop rhythm (consistent with right ventricular third heart sound).
• Leg and sacral oedema (consistent with right heart failure).
• Cardiogenic shock with systemic hypotension.
• Cyanosis.
• Sudden cardiac arrest into pulseless electrical activity (PEA).

A.5 This patient requires emergency resuscitation. You need to increase the oxygen requirements, anticoagulate the patient with IV heparin and call for help from senior colleagues. Blood should be sent for thrombophilic screen to detect underlying abnormalities of coagulation prior to commencing heparin. These include:

Testing for Prothrombotic Disorders

• Factor V Leiden (activated protein C resistance).
• Protein C and S levels.
• Prothrombin gene mutation (20210A).
• Autoantibodies (ANA, ENA, anticardiolipin/lupus inhibitor).
• Homocystein MTHFR mutation.
• Plasminogen level.
• Fibrinogen levels.
• Factor XII (for deficiency).
• Factor VIII (for level >150%).
• CRP.

ANA, antinuclear antigen; CRP, C reactive protein; ENA, extractable nuclear antigen; MTHFR, methylenetetrahydrofolate reductase.

Immediate anticoagulation is the usual treatment for PE. In this case, unfractionated IV heparin should be given to achieve rapid anticoagulation.

Thrombolyis is indicated for life threatening PE when associated with one or more of the following features:

• Cardiogenic shock with systemic hypotension (<90 mmHg systolic or drop >40 mmHg from usual value).
• Circulatory collapse (including syncope or need for cardiopulmonary resuscitation).
• Echocardiographic findings indicating significant right ventricular systolic dysfunction.
• Severe, unresponsive hypoxia.

Thrombolysis should be performed in consultation with a major centre experienced in PE management.

This young woman is in impending cardiogenic shock (as defined above). Provided there are no contraindications, IV thrombolysis should be given and the patient should be transferred to HDU/ICU. Rarer treatment options that are only available in highly specialized centres include surgical embolectomy (where the clot is surgically removed) and catheter fragmentation (where the clot is broken up into smaller pieces with a special device) in patients with contraindications to thrombolysis.

Contraindications to Thrombolysis

Absolute

• Recent major trauma, major operation or non-compressible.
• Vascular puncture (within 10 days).
• Recent stroke (within 2 months) or any history of haemorrhagic stroke.
• Active internal bleeding.
• Significant bleeding diathesis.

Relative

• Prolonged cardiopulmonary resuscitation.
• Pregnancy.
• Diabetic proliferative retinopathy.

A.6 Intravenous (systemic) alteplase was chosen for thrombolysis as this has been shown in clinical trials to be effective in treatment of acute massive PE with right ventricular dysfunction.

Baseline coagulation studies are important (INR and APTT). A prolonged APTT prior to heparin is a common presentation of a lupus anticoagulant, and may indicate an underlying thrombophilic disorder. Thrombophlia is a very important diagnosis as it will mean the APTT cannot be used to monitor the heparin therapy if unfractionated heparin is to be used.

She requires ongoing anticoagulation both in the short and long terms.

• Unfractionated heparin (UFH) has the advantage of being rapidly reversible when given intravenously (by stopping the intravenous infusion and, if necessary, giving protamine). It can also be used in patients with renal impairment or obesity, and should be first-line therapy in massive PE. The disadvantages of UFH are need for more frequent APTT monitoring dose, and risks of both under-anticoagulation (under-treating the patient) versus over-anticoagulation (increasing the chance of haemorrhage).
• Low molecular weight heparins (LWMH such as enoxaparin) are convenient as they are dosed by weight and are administered subcutaneously. LWMH are well validated for use in acute coronary syndromes. However, there are significant disadvantages in the treatment of acute PE. Firstly, LWMH cannot be reversed if haemorrhage occur after thrombolysis. Also LWMH has been poorly studied in obese patients and there are concerns about efficacy, especially considering that PE is a life-threatening event.
• Warfarin (oral vitamin K antagnonist) should be commenced early. It should be given at the same time each day, usually in the evening. Hospitals have set guidelines as to warfarin loading and monitoring and you need to familiarize yourself with these. Heparin should not be stopped until a minimum of 48 hours (i.e. 2 consecutive days of overlap) have elapsed with the INR greater than 2.0. Plans must be made for close monitoring of the INR and specialized warfarin clinics exist to assist patient with this. In addition, any doctor involved in the patient’s care must be made aware that the patient is anticoagulated with warfarin, and a Medi-alert bracelet is advised.

A.7 The patient should be issued with an information card about warfarin, a medical alert bracelet, and advised not to commence any new medications without first talking to a doctor. She must understand that warfarin can interact with many drugs. Alcohol, antibiotics, and non-steroidal anti-inflammatory drugs (NSAIDs) are common culprits in these instances. Also, contraception while on warfarin is essential as it is teratogenic in the first trimester. The oral contraceptive pill has been associated with increased risk of venous thrombosis, and expert opinion of alternative contraception methods should be sought (e.g. intra-uterine device, barrier methods, etc. depending on patient preference).

The patient should also be encouraged to lose weight through regular exercise and a good diet. She should have regular breast examinations and pap smears to ensure that an underlying malignancy does not become apparent. Furthermore, she should be helped to stop smoking.

A.8 The minimum treatment duration of warfarin therapy is 3 months which is appropriate in situations where there has been a short-lived risk factor such as recent surgery or orthopaedic injury.

A V/Q should be performed between 3 and 6 months after acute PE to reassure you that there has been resolution of thrombus as evidenced by normalization of perfusion.

A proportion of patients with life threatening PE go on to develop high blood pressure in the pulmonary circulation, known as chronic thromboembolic pulmonary hypertension (CTEPH). This is a rare but serious complication that can occur after acute PE and is often missed. CTEPH should be considered in patients who present with progressive breathlessness who have a distant history of PE or DVT. CTEPH is life-threatening but potentially curable with surgery called pulmonary thromboarterectomy.

Revision Points

Pulmonary Embolism

Definition

Venous thrombus which embolizes to the pulmonary circulation. Most arise from thromboses in the deep venous system of the legs and it follows that risk factors for pulmonary emboli are identical to those for deep vein thromboses.

Risk Factors

Divided into three groups as first described in Virchow’s triad:

Stasis: e.g. bed rest, immobility.
Endothelial damage: e.g. surgery, trauma.
Abnormalities of coagulation: e.g. inherited thrombophilia versus acquired (malignancy including myeloproliferative disorders, pregnancy, oral contraceptive pill, nephrotic syndrome, heparin-induced thrombocytopaenia, thrombotic thrombocytopaenic purpura).

Clinical Presentation

Varies greatly – from mild dyspnoea to sudden cardiovascular collapse and death – depending upon thrombus burden within the pulmonary circulation. The classic presentation includes sudden onset of shortness of breath and pleuritic chest pain. PE will have a greater impact on those with poor cardiovascular reserve (e.g. chronic obstructive pulmonary disease, congestive cardiac failure), and a sudden deterioration in breathing of such patients should raise suspicions of a PE.

Treatment

Long-term anticoagulation as outlined in Answer 6.

Patients with underlying malignancy have a high risk of developing thromboembolism, and unexplained DVT or pulmonary embolus in a previously well patient may be the first suggestion of occult malignancy. In patients with unexplained DVT/pulmonary embolus, a family history and personal history for previous episodes of clotting is very important in establishing whether they may have an inherited or acquired thrombophilia.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare but important complication to recognize. It can occur in the years following an acute PE resulting in breathlessness again. It is identified by an incomplete normalization of a V/Q scan with ongoing right ventricular systolic dysfunction and pulmonary hypertension on echocardiogram.

Issues to Consider

• What is the role of echocardiography in the management of PE?
• In what situations would you prefer unfractionated over low molecular weight heparin?
• Are you familiar with your local guidelines for heparin and warfarin?

Further Information

Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Guidelines on the diagnosis and management of acute pulmonary embolism. European Heart Journal. 2008;29:2276-2315.

Hamilton-Craig C.R., McNeil K., Dunning J.D., et al. Treatment options and strategies for acute severe pulmonary embolism. Internal Medicine Journal. 2008;38:657-667.

McNeil K., Dunning J.D. Chronic thromboembolic pulmonary hypertension (CTEPH). Heart. 2007;93:1152-1158.

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