Oncological emergencies

Chapter 2
Oncological emergencies


Daniel L.Y. Lee


St James’ Institute of Oncology, UK


Anaphylaxis and hypersensitivity reactions


Definition



  • Hypersensitivity and anaphylaxis are immunologically triggered responses. Anaphylaxis can broadly be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.
  • There are two types of reaction, one is IgE mediated and the other is not. There has recently been a move away from these distinct diagnoses, that of anaphylaxis and anaphylactoid reactions respectively, to sub-categorisation within an overarching diagnosis of anaphylaxis.

Causes



  • All intravenous infusions are at some risk of a hypersensitivity reaction or anaphylaxis. The overall incidence is around 5%; however, some are much more high risk.
  • High risk infusions include: platinum and taxane chemotherapies (e.g. cisplatin, carboplatin, paclitaxel, docetaxel), some monoclonal antibody therapies (e.g. rituximab).
  • Other causes include: antibiotics, NSAIDs, vaccines, contrast media, foods, insect stings, skin preparations and latex.

Symptoms and signs



  • Patient education is paramount, and early symptoms may be as vague as feeling ‘unwell’ or ‘not normal’.
  • Early diagnosis improves outcomes and shortens the possible effects, so vigilance of the treating team is important.
  • Acute reactions can occur within seconds of exposure and can progress rapidly, slowly or in a biphasic manner. Rarely, reactions can occur after a few hours or persist for more than 24 hours.
  • Beta-blockers may increase the severity of the reaction and antagonise the effect of adrenaline. Adrenaline can cause severe hypertension and bradycardia in patients taking non-cardioselective beta-blockers.

Symptoms can range in severity and are most commonly divided into two groups:



  1. Mild symptoms only, without any respiratory symptoms.
  2. Clinical signs of shock with possible respiratory distress, stridor, wheeze or laryngeal oedema.

Management


Specific treatment will depend on the severity of the reaction and the drug which is being infused. Each department should have guidance on the local protocol, but general guidance is given below.


Localised hypersensitivity reaction



  • Assess symptoms and observations.
  • Consider antihistamine and/or corticosteroid use (see anaphylaxis treatment section below for doses).
  • Repeat observations every 15 minutes for one hour.

Anaphylaxis



  • Stop the IV infusion and keep the IV access.
  • Call for help and prepare resuscitation trolley for use.
  • Assess airway, breathing and circulation, along with consciousness (GCS).
  • Lay the patient flat or in the Trendelenberg position (i.e. feet elevated).
  • Oxygen – 15 litres/minute via a non-rebreath mask.
  • Adrenaline:

    • Intramuscular injection (1 mg/ml, 1:1000 dilution) into antero-lateral thigh, 0.5 mg every five minutes (treatment of choice).
    • Intravenous 50 mcg (0.5 ml, 1:10,000 dilution) boluses according to response – if repeated boluses required, start an adrenaline infusion. This is usually only given in specialist units (e.g. HDU, ITU or theatres) for patients with profound shock that is immediately life threatening.

  • Fluids: start with a fluid challenge of 500–1000 ml of crystalloid. Over two litres of fluid may extravasate within the first five minutes, so large volumes may be needed.
  • Corticosteroids: 200 mg hydrocortisone stat IM or slow IV.
  • Anti-histamines: 10 mg chlorpheniramine stat IM or slow IV.
  • Monitor pulse oximetry, blood pressure and perform an ECG.
  • Consider admission to a high-level bed if vasopressor or ventilatory support is needed.
  • Other drugs:

    • Glucagon may be useful in the treatment of anaphylaxis in patients on beta-blockers.
    • Atropine may be useful for bradycardia.
    • Bronchodilators (e.g. salbutamol, ipratropium) may be useful if a patient has asthmatic symptoms.

  • Investigations: mast cell tryptase – at least one sample after the onset of symptoms (do not delay resuscitation to take the sample). Ideally, also take another sample 1–2 hours after the start of symptoms and a third sample at convalescence or at 24 hours. This can help to confirm the diagnosis of anaphylaxis.

Observation and biphasic reactions



  • A period of observation is recommended after an anaphylactic reaction. This may be from four to six hours, to an admission, depending on the severity of the reaction.
  • There is the possibility of the recurrence of symptoms after the effects of the adrenaline have worn off, although these are usually milder than the initial attack. A biphasic reaction is the recurrence of symptoms after the complete resolution of symptoms. This can occur in 3–20% of patients after an anaphylactic reaction.
  • At discharge, consider prescribing anti-histamines and oral steroids for up to three days to help treat urticaria (may also decrease the risk of a further reaction).

Ongoing management and retreatment


After the acute episode has abated further treatment with the offending drug may be considered. This is dependent on the grade of the reaction and the ‘value’ of pursuing further treatment with the same drug, or the benefits of any possible alternatives. There may be the possibility of increasing premedication regimens for the reaction or reducing the infusion rate. All such decisions should be undertaken by a senior member of the treating team. Refer to local guidelines regarding drug re-challenges and for desensitisation protocols.


References



  1. Gleich GJ, Leiferman KM. Anaphylaxis: implications of monoclonal antibody use in oncology. Oncology (Williston Park). 2009. 23(2 Suppl. 1): 7–13.
  2. Resuscitation Council (UK) Emergency treatment of anaphylactic reactions guidelines for healthcare providers (annotated July 2012). Available from: http://www.resus.org.uk/pages/reaction.htm (accessed 1 January 2014).
  3. Viale PH. Management of hypersensitivity reactions: a nursing perspective. Oncology (Williston Park). 2009. 23(2 Suppl. 1): 26–30.

Bleeding


Overview


Bleeding can occur in up to 10% of patients with advanced cancer. This may increase to up to 30% in those with a haematological malignancy.


There are multiple causes for bleeding in cancer patients:



  • Related to the cancer:

    • Varies dependent on the size, type and location of the primary tumour and the presence of lymphadenopathy or metastases.
    • Higher risk tumours include head and neck cancers, pelvic malignancies and fungating tumours, particularly if there is direct vascular invasion or damage from the cancer.

  • Related to cancer treatment:

    • Chemotherapy – thrombocytopenia.
    • Radiotherapy – bleeding secondary to inflammation or tumour shrinkage.
    • Surgery.

  • Related to comorbidities or other treatments:

    • Anticoagulants.
    • Liver impairment with subsequent coagulation deficiency.

    • Concurrent infection can raise the risk of bleeding due to inflammation.


      Antibiotic treatment may lower the risk.


Clinical presentation


The presentation can vary markedly:



  • Sub-acute or occult bleed:

    • Presenting as iron-deficiency anaemia
    • Anaemia beyond that expected from systemic therapies
    • Relating to the site of bleed, for example subarachnoid haemorrhage, intra-femoral bleed post fracture
    • Bleeding metastases (most commonly from malignant melanoma or RCC)

  • Visible bleed:

    • Bruising
    • Minor bleeding
    • Major/catastrophic bleeding

Clinical assessment


Appropriate management will depend on assessing:



  • Cancer history and treatment intent:

    • Prior surgery
    • Systemic treatment – discuss with senior if unsure of related bleeding risk

  • Time and severity of bleed:

    • Patient consciousness
    • Observations: pulse, BP, oxygen saturations, visible evidence of bleed


  • Identify the site of bleeding from history and examination.


    Note: a minor bleed may herald further more severe bleeding.


  • Bloods including: FBC, U&E, LFT, coagulation, group and save.

Management


General measures


Patients receiving adjuvant or curative treatment should be treated as per any other patient, with prompt assessment and intervention as needed. Major catastrophic haemorrhage is rare in cancer patients, but should be assessed in an acute environment and with the use of appropriate local protocols. Most emergency departments will have a specific catastrophic haemorrhage algorithm. Blood tests and IV access should be sought early and IV fluids administered as appropriate. IV fluids may further dilute the blood, so consider the use of blood products (see section on systemic interventions).


Particular consideration should be given to the patients’ prior treatment and the bleeding risk associated with this, for example after surgery. There are situations where patients at the end of life may have an unexpected or predicted catastrophic bleeding event. These should be managed with a very different approach, as detailed in the next section.


Local interventions



  • Packing:

    • Consider in nasal, vaginal or rectal bleed.
    • Haemostatic agents (e.g. topical sulcralfate, topical tranexamic acid) may be useful.
    • Dressings provide direct compression and can be soaked in tranexamic acid to try and stem the bleeding further.

  • Endoscopy:

    • Particularly useful as it is able to visualise and treat multiple sources of bleeding.
    • Consider in upper GI, lung and bladder bleeds.


  • Interventional radiology:


    Transcutaneous arterial embolisation with beads/particles, glue or coils:



    • Restricted by patient factors and site of bleed.
    • Requires good patient selection to improve outcomes.
    • Benefit reported in patients with head and neck, pelvis, lung, liver and GI tract cancers.


  • Radiotherapy:

    • Most commonly used for bleeding in cancers of the lung, vagina, skin, rectum and bladder.
    • May be considered in head and neck cancers and in upper GI cancers.
    • There is a delay between treatment and effect, so not considered in the acute setting.

  • Surgery:

    • May be appropriate with good performance status and prognosis.
    • Particularly important in adjuvant patients with possible bleed secondary to resection.
    • Reserved for those who have failed conservative measures in advanced cancer.

Systemic interventions


Vitamin K:





    • IV is quicker but associated with more ‘over-correction’, usually at doses between 2.5 and 10 mg.
    • SC and oral administration are also effective if time is not of the essence.

  • Vasopressin/desmopressin:

    • Continuous infusions are reported to control half of patients with upper-GI malignancy-related bleeding.
    • Associated with myocardial, mesenteric and cerebral circulation ischaemia.

  • Somatostatin analogues (e.g. octreotide): used in upper GI bleeds, but no reports for efficacy in cancer patients.
  • Anti-fibrinolytic agents (e.g. tranexamic acid):

    • Act through reduced fibrin clot breakdown.
    • Cautious use in those with previous thrombotic event, renal failure (accumulation) and those with a cardiac stent.
    • Can be associated with GI side-effects (e.g. nausea, vomiting).

  • Blood products (e.g. platelets, fresh frozen plasma, coagulation factors, packed red blood cells):

    • Platelets – increased risk of bleeding if < 20, severe risk if < 10. May need four to six bags of platelets to reduce active bleeding – discuss with local bleed service or haematologist.
    • Fresh frozen plasma – selected for:

      • Coagulation deficiencies
      • Urgent reversal of INR in patients on warfarin
      • Urgent intervention needed (e.g. thoracic surgery)
      • Treatment of disseminated intravascular coagulation (DIC) when appropriate

Disseminated intravascular coagulopathy (DIC)


Associated with malignancy, sepsis and trauma. There is increased thrombin formation (with associated decreased fibrinogen, PT and APTT) and increased fibrinolysis (with associated increased d-dimer). There is an associated poor prognosis. The basis of treatment is:



  • Treatment of underlying condition (e.g. sepsis, malignancy)
  • Haemodynamic support
  • Platelet and FFP only if actively bleeding
  • Discussion with haematologist regarding further evaluation and management (e.g. use of heparin, blood films)

End of life considerations/catastrophic bleed


Advanced planning is crucial in palliation of expected catastrophic bleed. Patients undergoing palliation should have their chances of an acute catastrophic bleed identified early. An early, sensitive discussion with the family and patient about their wishes is paramount and can provide forewarning and reassurance. ‘Do not attempt resuscitation’ orders should be discussed and completed prior to any event.


Patients who are particularly at risk are those with:



  • Terminal head and neck cancer
  • Pelvic malignancy
  • Patients who presented with bleeding (e.g. haemoptysis)

The central focus of intervention is:



  • A calm approach to patient and family to reduce distress
  • Dark towels to soak up bleeding and provide direct pressure
  • Use of sedation (e.g. SC midazolam, lorazepam) for distress in the terminal event
  • Review of medications such as anticoagulation and NSAIDs
  • Care in a side room and timely ‘do not resuscitate’ decision

Other relevant sections of this book


Chapter 3, sections on anaemia, thrombocytopenia


References



  1. Hulme B, Wilcox S. Yorkshire Palliative Medicine Clinical Guidelines Group: Guidelines on the management of bleeding for palliative care patients with cancer (2008). Available at: http://www.palliativedrugs.com (registration required) (accessed 1 January 2014).
  2. Nauck F, Alt-Epping B. Crises in palliative care – a comprehensive approach. Lancet Oncology. 2008. 9(11): 1086–91.
  3. Pereira J, Phan T. Management of bleeding in patients with advanced cancer. The Oncologist. 2004. 9(5): 561–70.

Central airway obstruction and stridor


Definition



  • Central airway obstruction (CAO): the central airways are defined as the trachea, main and lobular bronchi. These may become obstructed via an intraluminal, luminal or extraluminal pathology. The grading of tracheal obstruction is shown in Table 2.1.
  • Stridor: this is a harsh noise associated with respiration due to reduction in lumen of upper airway tracts. The grading of stridor is shown in Table 2.2.

    • If there is stridor and dyspnoea at rest, the central airways are usually narrowed to < 25% of their cross-sectional area.
    • The causes and treatment for stridor in children are very different from that seen in adults. This chapter will focus on adult cases only.

Table 2.1 CTCAE (V4.03) grading of tracheal obstruction.


From the website of the National Cancer Institute (http://www.cancer.gov).






















Grade Criteria
1 Partial symptomatic obstruction on examination (e.g. visual, radiologic or endoscopic).
2 Symptomatic (e.g. noisy airway breathing), no respiratory distress, medical intervention indicated (e.g. steroids), limiting ADL.
3 Stridor, radiologic or endoscopic intervention indicated (e.g. stent, laser); limiting self-care ADL.
4 Life-threatening airway compromise; urgent intervention indicated (e.g. tracheotomy or intubation).
5 Death.

Table 2.2 CTCAE (V4.03) grading of stridor.


From the website of the National Cancer Institute (http://www.cancer.gov).






















Grade Criteria
1 —
2 —
3 Respiratory distress limiting self-care ADL; medical intervention indicated.
4 Life-threatening airway compromise; urgent intervention indicated (e.g. tracheotomy or intubation).
5 Death.

Causes


CAO can be the result of malignant or non-malignant causes. Malignancy is the most common pathology, and the most common malignant pathology leading to CAO is lung cancer. Lung cancer can obstruct the airway intraluminally or through extraluminal compression.


Malignant causes include:



  • Lung cancer
  • Metastatic cancer – colon, breast, oesophagus, kidney and melanoma
  • Metastatic lymphadenopathy

Non-malignant processes include:



  • Laryngeal pathology – anaphylaxis, acute epiglottitis
  • Inhaled foreign bodies, food or blood clots
  • Chronic medical conditions affecting the lung – TB stricture, Wegener’s granulomatosis, sarcoidosis
  • Secondary to previous trauma to the airways – post-endotracheal tube insertion, post tracheostomy, chemical burns, post-bronchial sleeve resection
  • Idiopathic

Symptoms


Symptoms are dependent upon the degree of airway stenosis. In some cases, symptoms can develop rapidly and become life threatening. Symptoms include:



  • Wheeze
  • Stridor

    • Can be exertional or at rest
    • May be on inspiration, expiration or biphasic, depending on the site of cause

  • Haemoptysis
  • Chest pain
  • Post-stenotic pneumonia may be evident on CXR or suggested by recurrent episodes of pneumonia

Investigation



  • Radiology – most patients will have undergone a CXR as part of their initial assessment. A CT thorax will best determine the site and degree of stenosis. In patients who are not previously known to have cancer, it may also provide diagnostic use. 3D reconstruction sequences of the central airways have been cited as the gold standard, but are not readily available in all centres.
  • Bronchoscopy – allows direct visualisation of the airways to identify the site of stenosis and dimensions. It may allow intervention in some cases, such as clearing of mucous plugs. In undiagnosed cases, it may also provide histological confirmation of cancer.
  • Concomitant exacerbating factors, such as anaemia, COPD or asthma should also be sought and managed appropriately.

Management


There are multiple interventional procedures now available in the management of CAO. The optimum choice is dependent upon a number of patient factors (such as performance status and wishes), cancer and prognostic factors and local availability. Optimum intervention selection should involve an MDT, if time allows.


General management



  • Avoid respiratory depressants (e.g. sedatives) and muscle relaxants.
  • Oxygen supplementation may reduce respiratory effort.
  • High-dose steroids are commonly used (e.g. 8 mg OD dexamethasone IV/PO with PPI cover) but with little evidence.
  • Heliox (8:2 or 7:3) has been used in an attempt to reduce airway turbulence associated with CAO and stridor. Its use is supported by results from small case series, but further evidence is required. Any likely benefit should be seen at an early stage.
  • In severe cases (e.g. reduced pO2 or respiratory fatigue), discuss with ITU regarding extra respiratory support.
  • Early ENT input may be required for lesions around the epiglottis or vocal cords as patients may require a tracheostomy.
  • Do not attempt to instrument the airway without expert help.

Specific anti-cancer treatments



  • For those cases with a mild degree of CAO, usually without the presence of stridor, chemotherapy or radiotherapy may be the first choice of treatment.
  • Chemotherapy is particularly useful in SCLC or lymphoma, but also commonly used in non-severe cases with alternate cancer types that may respond to systemic treatment (e.g. NSCLC).
  • Radiosensitive tumours (e.g. NSCLC, thyroid and tracheal tumours) may be treated with radiotherapy, either prior to systemic therapy or concomitantly/sequentially with chemotherapy or endoscopic procedures.

Endoscopic procedures



  • Airway stent – available more readily in most areas than the alternatives discussed here.

    • The ability to place the stent will depend on the exact location of obstruction and whether a stent can be viably placed. Common contraindications include lesions proximal to bifurcation of the airways. However, Y-shaped stents have been developed for placement at the carina.

    • Stent related issues include: mucostasis, stent migration, colonisation with bacteria or fungi and possible subsequent pneumonia/lung abscesses.


      Re-stenosis due to tumour overgrowth or excessive granulation tissue formation may be overcome with a further stent, cryotherapy or argon plasma coagulation (APC).


  • Laser resection – particularly useful for central lesions with endobronchial tumour growth. This may be combined with stenting, brachytherapy or external beam radiotherapy to reduce tumour re-growth into the airway.
  • Electrocautery – APC, which is a form of electrocautery, may control local tumour growth and relieve obstruction as well as provide local haemostatic control.
  • Cryotherapy – a super-cooled tip (−89 °C) is placed in direct contact with the tumour and may debulk the mass so as to relieve the obstruction. It is less effective than either laser or electrocautery at controlling bleeding in the immediate to short term.
  • Intraluminal brachytherapy – effects are delayed, so not suitable in life-threatening circumstances. Usually used as part of a multi-modality treatment. Palliative brachytherapy may be considered in patients who have non-life threatening airway compromise, and are not able to undergo radiotherapy or surgery (either due to fitness or because they have already received maximal treatment with this modality).
  • Airway dilatation – short-lived in malignant processes, but may be useful in benign processes (such as post-surgical stenosis of the airways).

References



  1. Gompelmann D, Eberhardt R, Herth FJF. Advanced malignant lung disease: what the specialist can offer. Respiration. 2011. 82(2): 111–23.
  2. Feller-Kopman DJ, O’Donnell C. Physiology and clinical use of heliox. In: Hollingsworth H (ed.) UpToDate. UpToDate, Waltham, MA. 2013.
  3. Williamson JP, Phillips MJ, Hillman DR and Eastwood PR. Managing obstruction of the central airways. Internal Medicine Journal. 2010. 40(6): 399–410.

Extravasation


Definition


Extravasation is the leakage of a pharmacological or biological agent from the infusion site into the surrounding tissue. The grading of extravasation is shown in Table 2.3.


Table 2.3 CTCAE (V4.03) grading of extravasation.


From the website of the National Cancer Institute (http://www.cancer.gov).






















Grade Criteria
1 —
2 Erythema with associated symptoms (e.g. oedema, pain, induration, phlebitis).
3 Ulceration or necrosis; severe tissue damage; operative intervention indicated.
4 Life-threatening consequences; urgent intervention indicated.
5 Death.

The incidence of extravasation is unclear and there is variability in the guidelines of its management. Chemotherapeutic agents can be classified into categories based on their potential to cause damage and this is central to the management of extravasation. These categories are:



  • Vesicant: causes tissue necrosis leading to severe and lasting injury. It may affect the full thickness of the skin and underlying structures.
  • Irritant: causes a localised inflammatory response leading to discomfort, burning, tingling or phlebitis at the cannulation site or tracking along the vein. This is a short-term complication without the tissue necrosis seen with vesicant drugs.
  • Non-vesicant/irritant: no local inflammation.

However, these categories are not absolute and may depend on the volume of drug extravasated and the concentration of the infusion (e.g. a classically irritant drug can cause a vesicant reaction). Chemotherapeutic agents and their extravasation potential are listed in Table 2.4.


Table 2.4 Chemotherapeutic categories


Adapted from Perez Fidalgo JA et al. Ann Oncol 2012; 23:vii167–73. Reproduced with permission of Oxford University Press.






























































































































DNA-binding Vesicants Non-DNA-binding Vesicants Irritants Non-Vesicants
Alkylating Agents Vinca Alkaloids Alkylating Agents Asparaginase
Mecholretamine Vinblastine Ifosfamide Bleomycin3
Bendamustine1 Vincristine Streptozocin Bortezomib
Carmustine2 Vindesine Dacarbazine2 Cladiribine

Vinorelbine Melphalan Cytarabine
Anthracyclines

Cyclophosphamide
Doxorubicin Taxanes Anthracyclines (other) Fludarabine
Daunorubicin Docetaxel (rare) Liposomal doxorubicin Gemcitabine
Epirubicin Paclitaxel (rare) Liposomal daunorubicin Interferons
Idarubicin
Mitoxantrone Interleukin-2

Others
Methotrexate
Others (Antibiotics) Trabectedin Topoisomerase II inhibitors Monoclonal antibodies
Amsacrine
Etoposide Pemetrexed
Dactinomycin
Teniposide Raltitrexed
Mitomycin C

Temsirolimus
Mitoxantrone2
Antimetabolites Thiothepa3


5-FU


 


Platinum Salts


Carboplatin


Cisplatin2


Oxaliplatin2


 


Topoisomerase I inhibitors


Irinotecan


Topotecan


 


Others


Ixabepilone


Arsenic trioxide


Melphalan


Trastuzumab

1 Bendamustine is classified as a vesicant but reports have since described soft tissue damage on extravasation.


2 May have vesicant or irritant properties, dependent upon the volume of the drug extravasated. Greater volume or concentration of the drug is associated with higher vesicant potential.


3 May have irritant properties, dependent upon the volume of the drug extravasated.


Risk factors and prevention of extravasation



  • Risk factors include:

    • Difficult IV access (e.g. small, mobile or fragile veins, obesity)
    • Long infusion times
    • Site of cannulation

  • Prevention of extravasation: choice of cannulation site, if these cannot be avoided then consider a central line:

    • Choose a new site rather than a previous site
    • Choose a large vein in the forearm
    • Use local warming to dilate the vein
    • Never place the cannula in the inner wrist
    • Never place over a joint or in an area affected by lymphoedema
    • Avoid sites of previous radiation therapy or surgery

Diagnosis


Early signs that a drug may be extravasating include:





    • Tingling, burning, erythema/blanching and discomfort or swelling at the cannulation site.
    • Medical staff may notice a reduction in the flow rate or increased resistance on manual administration of medications via the cannula. Many infusion devices are set up to alarm in this scenario.
    • Patients should be informed to alert staff quickly if these symptoms occur. This is particularly important for vesicant drugs.

  • Late signs include blistering, necrosis and ulceration around the site of cannulation. This can occur up to two to three days after the infusion, or later in some instances.
  • Care should be taken with the following patients during the infusion or bolus:

    • Patients with peripheral neuropathy (and thus reduced sensation).
    • Patients with thrombosed veins from previous treatments.
    • When cannulation is ipsilateral to a mastectomy, axillary lymph node clearance or in an arm affected by lymphoedema.

Differential diagnoses



  • Extravasation is the most important diagnosis if local site irritation or reaction occurs.
  • Some drugs may cause a local reaction or a chemical phlebitis which is not related to extravasation. These are listed in Table 2.5.

Table 2.5 Chemotherapeutic agents that may cause a local reaction.






























Local skin reactions Chemical phlebitis
Aspariginase Amsacrin
Cisplatin Carmustine
Daunorubicin Dacarbazine
Epirubicin Epirubicin
Fludarabine 5-FU (as continual infusion in combination with cisplatin)
Mechlorethamine Gemcitabine
Melphalan Mechlorethamine

Vinorelbine

Management

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Jun 13, 2016 | Posted by in ONCOLOGY | Comments Off on Oncological emergencies

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