Chapter 26: Acute oncology
Skip chapter table of contents and go to main content
Related theory
CNS malignancy accounts for only 2% of all cancers but its aggressive nature and proximity to vital CNS structure makes it the fourth leading cause of cancer‐related death in adults (Guilfoyle et al. [100], Lefebvre [140]). In general, CNS tumours have a poor prognosis. Both their anatomical position and pathology play an important role in prognosis and decisions about appropriate investigation and treatment. Sometimes, the risks of obtaining tissue for histopathological assessment are considered clinically unacceptable, and the patient is managed on the basis of a diagnosis made on neuroradiological features. The anatomical location influences symptoms that include physical, cognitive and psychological components. For this reason, adults with CNS tumours pose a unique challenge to healthcare professionals; the patient may not be the best person to explain his or her symptoms, and cognitive dysfunction may greatly increase the need for psychological/psychiatric, social and physical support. In view of the poor survival of many patients, even with optimal treatment, an important aspect of improving outcome is maximizing quality of life (NICE [202]).
Metastases in the brain occur in 20–40% of patients with other primary cancers. Brain metastases are usually associated with a poor prognosis. Adult‐onset epilepsy is a common feature of brain tumours and may present as either focal or generalized seizures. It usually presents without other neurological symptoms or signs (NICE [202]).
Diagnosis
Patients presenting with neurological deterioration require immediate assessment to determine the underlying cause (Lefebvre [140]). If the cause is a brain tumour (primary or metastatic), early identification allows measures to be initiated to control cerebral oedema and limit damage to CNS structures. As with any emergency situation, assessment of haemodynamic stability must be addressed first. If the patient is haemodynamically stable a comprehensive clinical history to identify the clinical signs and symptoms of CNS deterioration and exclude trauma, infection, drug or toxin exposure is the starting point (Lefebvre [140]). CNS symptoms and deterioration usually occur sequentially and will identify the urgency of the clinical situation. The chronology of symptoms should be acknowledged to assist rapid diagnosis. These can be generic such as headache (usually worse in the morning); nausea and vomiting; weakness; somnolence (radiotherapy‐induced fatigue); seizures; but can also be dependent on the area of the brain affected and include (Dunn [66], Lefebvre [140], NICE [202]):
- temporal lobe – dysphasia, contralateral homonymous hemianopia, amnesia
- frontal lobe – hemiparesis, personality change (irritability, lack of concentration, socially inappropriate behaviour), executive dysfunction
- parietal lobe – hemisensory loss, astereognosis (inability to recognize objects by touch alone), reduced two‐point discrimination, papilloedema
- occipital lobe – contralateral visual field defects, palinopsia (seeing things again once the stimulus has left the field of vision)
- cerebellum – DASHING: dysdiadochokinesis, ataxia, slurred speech, hypotonia, intention tremor, nystagmus, gait abnormalities.
A full neurological examination, including fundoscopy to assess for papilloedema, is an essential aspect of the physical examination (Lefebvre [140]). The minimum documented neurological observations should include vital observations, level of consciousness, pupillary activity and limb movements (NICE [202]). Vital observations include blood pressure, pulse, respiration, oxygen saturations and temperature monitoring (Pemberton and Waterhouse [226]). Blood glucose, ECG, FBC (including differentials) and electrolytes provide information regarding the acute nature of the situation and also information regarding possible reversible causes (Farrell and Dempsey [73], Lefebvre [140]).
If the patient has hypertension with a widening pulse pressure, bradycardia and bradypnoea, they are demonstrating the signs of Cushing's triad. This is seen when increased ICP decreases the cerebral blood flow significantly and triggers an increased arterial pressure in order to overcome the increased ICP (Farrell and Dempsey [73]). This is a medical emergency and requires treatment to stabilize the ICP. If this does not occur, herniation of the brainstem and occlusion of the cerebral blood flow can occur with dire consequences (Farrell and Dempsey [73]).
Management
Patients who present with no prior cancer diagnosis must be referred to the neurosurgeons for immediate review, and management will depend on the type of malignancy (Lefebvre [140], NICE [202]). This section will focus on the management of patients with known cancer who present with raised ICP. As noted this can be caused by the cancer or its treatment.
Surgical decompression or debulking of the tumour is effective in reducing intracranial pressure and preventing further oedema (Raslan and Bhardwaj [244]). Unifocal brain tumours are potentially curable with radiation therapy. Radiation itself causes an increase in brain oedema but is used once the patient is stabilized to treat the underlying cause of oedema (Becker and Baehring [14]). Chemotherapy is limited in use due to its inability to cross the blood–brain barrier (Becker and Baehring [14]).
Objective management in the emergency setting is to treat promptly to prevent further deterioration. If the patient's neurological condition is deteriorating rapidly, IV access, oxygen and airway management is primary treatment. Aggressive therapy is necessary to sustain or restore optimal neurological function (Rangel‐Castillo et al. [243]). IV fluids should be limited unless the patient is hypotensive as they may worsen the situation (Lefebvre [140]). Sodium chloride 0.9% is the preferred fluid because dextrose can exacerbate cerebral oedema. If the patient has a fluctuating or depressed level of consciousness airway management should be considered, noting that coughing can increase ICP (Raslan and Bhardwaj [244]). Reversible causes of reduced conscious level such as hypoglycaemia or opioid toxicity should be reversed prior to commencing management of raised ICP (Lefebvre [140]).
Elevation of the patient's head (raising the head of the bed 30°) has been shown to decrease ICP due to the promotion of intracranial outflow (Hickey [107], Mestecky [179], Raslan and Bhardwaj [244]). Oxygenation of the patient should also be maximized through oxygen administration as guided by saturations which in turn reduces cerebral vasodilation and ICP (Raslan and Bhardwaj [244], Sippell [272]).
Osmotic therapy aims to drive excess water from the brain tissue (Rangel‐Castillo et al. [243]). Mannitol is recommended in acute deterioration at a dose of 0.25–1 g/kg IV as a 15–25% solution over 30–40 minutes with a maximum of 200 g/day (London Cancer Alliance [151], Raslan and Bhardwaj [244]). The effects should be seen within 20–40 minutes post infusion but provide a temporary solution. Mannitol can worsen an intracranial bleed and should not be used unless this has been ruled out (Raslan and Bhardwaj [244]).
Use of glucocorticoids in raised ICP is indicated if the cause is due to infection, a brain tumour or its treatment (Fields [78]). The dose of dexamethasone is dependent on the severity of symptoms. In the event of serious neurological deficit such as paralysis or seizures (more than three in a week) an initial dose of dexamethasone 10 mg intravenously with proton pump inhibitor cover should be given and then converted to 4 mg every 6 hours for 5–7 days (Fields [78], London Cancer Alliance [151]). The dose is tapered once neurological symptoms are controlled and reduced usually over a period of 2–3 weeks to avoid adrenal insufficiency. If symptoms occur during tapering then increasing the dose to its pre‐symptom level is recommended followed by clinical review (Cross and Glantz [50]).
If patients have seizures, they should be placed on anticonvulsant therapy as per local guidelines (Dunn [66], London Cancer Alliance [151], NICE [205]). Seizures cause an increase in cerebral metabolism thus increasing the risk of herniation due to a sudden rise in ICP, therefore prompt management and prophylaxis is imperative (Cross and Glantz [50]). Immediate discussion with the doctor is essential and additional support from the critical care outreach team may be required (Hickey [107]). The nurse should consider other pathologies as the cause of the seizure and exclude syncopal attacks, cardiac arrhythmias and transient ischaemic attacks. Reversible metabolic causes such as hypoglycaemia, hyponatraemia and hypoxia should be corrected and infective causes considered (Dunn [66]).
Bowel management is a simple but important aspect of raised ICP management. Constipation causes the patient to strain, therefore increasing intra‐abdominal pressure and thus raising ICP. Monitoring bowel habits, understanding the causes of constipation and use of laxatives are an important yet often forgotten aspect of nursing care in this patient group (Hickey [107]).
